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{{CMG}} {{AE}} [[User:Mohammed Salih|Mohammed Salih, M.D.]] {{sali}}


==overview==
==overview==
A cardiac abscess is a suppurative infection of the myocardium, endocardium, native or prosthetic valve tissue. Similar to other abscesses, it develops either by dissemination from a distant source such as bacteremia or sepsis or by direct extension of a pre-existing cardiac infective focus. Infective endocarditis has long been identified as the main cause of the latter. Although the incidence of cardiac abscesses continues to be investigated, it is presumably higher than noted postmortem and is of great importance when deciding the prognosis and management of patients. A single organism causes cardiac abscesses, usually Staphylococcus aureus or Escherichia coli. Less typically, polymicrobial abscesses have been noted. Important complications of a cardiac abscess, whether alone or with valve tissue, are conduction abnormalities on electrocardiogram (ECG). The incidence of perivalvular abscess among patients with infective endocarditis is between 30% to 40%, with the aortic valve having a higher predisposition than the mitral valve and annulus. Native aortic valve endocarditis, usually located in a weak part of the annulus near the atrioventricular node (AV), clearly demonstrates the anatomic predisposition and exemplifies why abscesses and heart block presents as frequent sequelae.
A [[cardiac abscess]] is a [[suppurative]] infection of the [[myocardium]], [[endocardium]], native or [[prosthetic]] valve tissue. Similar to other [[abscesses]], it develops either by dissemination from a distant source such as [[bacteremia]] or [[sepsis]] or by direct extension of a pre-existing [[cardiac]] [[infective]] focus. [[Infective]] [[endocarditis]] has long been identified as the main cause of the latter. Although the [[incidence]] of [[cardiac]] [[abscesses]] continues to be investigated, it is presumably higher than noted postmortem and is of great importance when deciding the prognosis and management of patients. A single organism causes [[cardiac]] abscesses, usually [[Staphylococcus aureus]] or [[Escherichia coli]]. Less typically, [[polymicrobial]] [[abscesses]] have been noted. Important complications of a cardiac abscess, whether alone or with valve tissue, are conduction abnormalities on [[electrocardiogram]] ([[ECG]]). The incidence of [[perivalvular]] [[abscess]] among patients with [[infective]] [[endocarditis]] is between 30% to 40%, with the [[aortic valve]] having a higher predisposition than the [[mitral valve]] and [[annulus]]. Native [[aortic valve]] [[endocarditis]], usually located in a weak part of the [[annulus]] near the [[atrioventricular node]] (AV), clearly demonstrates the anatomic predisposition and exemplifies why [[abscesses]] and [[heart block]] presents as frequent sequelae.
Perivalvular abscesses are also more common with prosthetic valves. In this case, the annulus instead of the leaflet is usually the primary site of infection. The degree of conduction disruption, therefore, depends on the extent of the involvement of the conduction system and is more commonly seen in perivalvular aortic abscesses. Additionally, the severe extension of perivalvular infection can also result in extrinsic coronary compression, or disruption, leading to an acute coronary syndrome. Thus far, only aortic valve involvement and current IV drug use have been prospectively identified as independent risk factors for a perivalvular abscess. Any patient with a cardiac abscess, regardless of all other factors, has an increased risk of embolization, morbidity, and mortality. Prophylaxis remains a longstanding subject in the matter of prevention of IE or cardiac abscess. Thus far, prophylaxis is mostly based on observational studies and, in fact, places such as the United Kingdom no longer endorse antibiotic prophylaxis for dental procedures to prevent IE, the leading source of the cardiac abscess. One point against prophylaxis is the fact that tooth brushing has been proven to cause bacteremia and, therefore, makes it difficult to assess the rare versus high magnitude transient bacteremia and its effect on IE and its sequelae. For this reason, the United States and European countries have agreed that the use of prophylaxis is reserved only for those at "highest risk."
[[Perivalvular]] [[abscesses]] are also more common with [[prosthetic]] valves. In this case, the [[annulus]] instead of the leaflet is usually the primary site of infection. The degree of conduction disruption, therefore, depends on the extent of the involvement of the conduction system and is more commonly seen in [[perivalvular aortic abscesses]]. Additionally, the severe extension of [[perivalvular infection]] can also result in extrinsic [[coronary]] compression, or disruption, leading to an [[acute coronary syndrome]]. Thus far, only [[aortic valve]] involvement and current [[IV drug]] use have been prospectively identified as independent risk factors for a [[perivalvular]] abscess. Any patient with a cardiac abscess, regardless of all other factors, has an increased risk of [[embolization]], [[morbidity]], and [[mortality]]. [[Prophylaxis]] remains a longstanding subject in the matter of prevention of [[IE]] or [[cardiac]] [[abscess]]. Thus far, [[prophylaxis]] is mostly based on observational studies and, in fact, places such as the United Kingdom no longer endorse antibiotic prophylaxis for dental procedures to prevent IE, the leading source of the [[cardiac]] [[abscess]]. One point against prophylaxis is the fact that [[tooth]] [[brushing]] has been proven to cause [[bacteremia]] and, therefore, makes it difficult to assess the rare versus high [[magnitude]] transient [[bacteremia]] and its effect on IE and its sequelae. For this reason, the United States and European countries have agreed that the use of prophylaxis is reserved only for those at "highest risk."
On that same matter, the widespread use of antibiotics for the prevention and treatment of IE and abscesses could potentially create a setting where there will be an increased incidence of polymicrobial infection and antibiotic resistance, especially in immunocompromised patients.
On that same matter, the widespread use of antibiotics for the prevention and treatment of IE and abscesses could potentially create a setting where there will be an increased incidence of [[polymicrobial]] infection and antibiotic resistance, especially in [[immunocompromised]] patients.


==Historical perspective==
==Historical perspective==
*In 1933, Cossio and Berconsky reported a case of coronary occlusion with myocardial infarction in which an abscess was found in the infarcted area at post-mortem examination.<ref name="pmid28482860">{{cite journal |vauthors=Kim JS, Kang MK, Cho AJ, Seo YB, Kim KI |title=Complicated infective endocarditis: a case series |journal=J Med Case Rep |volume=11 |issue=1 |pages=128 |date=May 2017 |pmid=28482860 |pmc=5423006 |doi=10.1186/s13256-017-1274-7 |url=}}</ref>
*In 1933, Cossio and Berconsky reported a case of [[coronary]] occlusion with [[myocardial infarction]] in which an [[abscess]] was found in the [[infarcted]] area at [[post-mortem]] examination.<ref name="pmid28482860">{{cite journal |vauthors=Kim JS, Kang MK, Cho AJ, Seo YB, Kim KI |title=Complicated infective endocarditis: a case series |journal=J Med Case Rep |volume=11 |issue=1 |pages=128 |date=May 2017 |pmid=28482860 |pmc=5423006 |doi=10.1186/s13256-017-1274-7 |url=}}</ref>


==Pathophysiology==
==Pathophysiology==


Myocardial abscess is a pus-containing infection of the endocardium, myocardium, prosthetic or native valves, perivalvular structures or the cardiac conduction system. <ref>Howitt T: Remarkable case of abscess of the heart. Lancet 1, 684-685 (1846)</ref> <ref>Abela GS, B. Majmudar, J.M. Felner: Myocardial abscess unassociated with infective endocarditis. South Med J 74, 432-434 (1981)</ref> <ref>Saphir O: Myocarditis: A general review, with an analysis of two hundred and forty cases. Arch Pathol 32,1000-1051 (1941)</ref> <ref>Flaxman N: Myocardial abscess. JAMA 122, 804-806 (1943)</ref> <ref>Sanson J, S. Slodki, J.G. Gruhn: Myocardial abscesses. Am Heart J 66, 301-308 (1963)</ref> <ref>Weiss S, R.W. Wilkins: Myocardial abscess with perforation of the heart. Am J Med Sci 194,199-205 (1937)</ref> <ref>Tedeschi CG, T.D. Stevenson, H.M. Levenson. Abscess formation in myocardial infarction. NEJM 243,1024-7
[[Myocardial abscess]] is a pus-containing [[infection]] of the [[endocardium]], [[myocardium]], [[prosthetic]] or [[native valves]], [[perivalvular]] structures or the [[cardiac]] [[conduction system]].   <ref>Tennant R, H.W. Parks: Myocardial abscesses. Arch Pathol 68,112-6 (1959)</ref> <ref>Narula J, B.A. Khaw, W. Dec, I.F. Palacios, J.F. Southern, J.T. Fallon, H.W. Strauss, E. Haber, T. Yasuda: Recognition of acute myocarditis masquerading as acute myocardial infarction. NEJM 328,100-4 (1993)</ref>
(1950)</ref> <ref>Bateman AC, M. Richards, A.P. Pallett. Fatal myocarditis associated with a Lancefield Group B Streptococcus. J Infect 36,354-5 (1998)</ref> <ref>Von Kurnatowski HA, J.L.Sierra-Callejas, W. Henkel: Foudroyant todlich verlaufende myokarditis durch streptokokken der gruppe B. Dtsch Med Wschr 103,439-41 (1977)</ref> <ref>Saphir O: Meningococcus myocarditis. Am J Pathol 12,677-87 (1936)</ref> <ref>McCue MJ, E.E. Moore: Myocarditis with
microabscess formation caused by Listeria monocytogenes associated with myocardial infarct. Human Pathol 10:469-72 (1979)</ref> <ref>Lewis JF: Myocardial infarction during pregnancy: With associated myocardial Bacteroides abscess. South Med J 66,379-1 (1973)</ref> <ref>Tennant R, H.W. Parks: Myocardial abscesses. Arch Pathol 68,112-6 (1959)</ref> <ref>Narula J, B.A. Khaw, W. Dec, I.F. Palacios, J.F. Southern, J.T. Fallon, H.W. Strauss, E. Haber, T. Yasuda: Recognition of acute myocarditis masquerading as acute myocardial infarction. NEJM 328,100-4 (1993)</ref>


'''Pathogenesis'''
'''Pathogenesis'''
*Development of infective endocarditis and subsequent myocardial abscess involves interaction of multiple factors, as follows:
*Development of [[infective endocarditis]] and subsequent [[myocardial]] [[abscess]] involves interaction of multiple factors, as follows<ref name="pmid29617499">{{cite journal |vauthors=Oliveira JLR, Santos MAD, Arnoni RT, Ramos A, Togna DD, Ghorayeb SK, Kroll RTM, Souza LCB |title=Mortality Predictors in the Surgical Treatment of Active Infective Endocarditis |journal=Braz J Cardiovasc Surg |volume=33 |issue=1 |pages=32–39 |date=2018 |pmid=29617499 |pmc=5873776 |doi=10.21470/1678-9741-2017-0132 |url=}}</ref>:
**Vascular endothelium
**[[Vascular endothelium]]
**Hemostatic mechanisms
**[[Hemostatic]] mechanisms
**Host immune system
**Host [[immune]] system
**Gross anatomic abnormalities in the heart
**Gross [[anatomic]] abnormalities in the heart
**Surface properties of microorganisms
**Surface properties of microorganisms
**Extracardiac events that introduce bacteremia
**Extracardiac events that introduce [[bacteremia]]
*The rarity of endocarditis despite the relatively high prevalence of transient asymptomatic and symptomatic bacteremia suggests that the intact endothelium is resistant to infection.If the endothelium on the valve surface is damaged, hemostasis is stimulated and the deposition of platelets and fibrin complex begins. This complex, called non-bacterial thrombotic endocarditis (NBTE), is more susceptible to bacterial colonization when bacteremia develops from an extracardiac source that allows the organisms access to the NBTE.
*The rarity of [[endocarditis]] despite the relatively high prevalence of transient asymptomatic and symptomatic [[bacteremia]] suggests that the intact [[endothelium]] is [[resistant]] to infection.If the endothelium on the valve surface is damaged, hemostasis is stimulated and the deposition of platelets and fibrin complex begins. This complex, called [[non-bacterial thrombotic endocarditis]] ([[NBTE]]), is more susceptible to [[bacterial]] colonization when [[bacteremia]] develops from an [[extracardiac]] source that allows the organisms access to the [[NBTE]]<ref>Howitt T: Remarkable case of abscess of the heart. Lancet 1, 684-685 (1846)</ref> <ref>Abela GS, B. Majmudar, J.M. Felner: Myocardial abscess unassociated with infective endocarditis. South Med J 74, 432-434 (1981)</ref>.
*The intracardiac consequences of endocarditis range from trivial, characterized by an infected vegetation with no attendant tissue damage, to catastrophic, when infection is locally destructive or extends beyond the valve leaflet. Distortion or perforation of valve leaflets, rupture of chordae tendineae, and perforations or fistulas may result in progressive congestive heart failure (CHF). Infection, particularly that involving the aortic valve or prosthetic valves, may extend into paravalvular tissue and result in myocardial abscesses and persistent fever due to the infection's unresponsiveness to the antibiotic; disruption of the conduction system, with electrocardiographic conduction abnormalities; and clinically relevant arrhythmias or purulent pericarditis.
*The intracardiac consequences of endocarditis range from trivial, characterized by an infected vegetation with no attendant tissue damage, to catastrophic, when [[infection]] is locally destructive or extends beyond the [[valve]] leaflet. Distortion or perforation of valve [[leaflets]], rupture of [[chordae tendineae]], and perforations or fistulas may result in progressive [[congestive heart failure]] ([[CHF]]). Infection, particularly that involving the [[aortic valve]] or [[prosthetic valves]], may extend into [[paravalvular]] [[tissue]] and result in [[myocardial abscesses]] and persistent [[fever]] due to the infection's unresponsiveness to the antibiotic; disruption of the conduction system, with electrocardiographic conduction abnormalities; and clinically relevant [[arrhythmias]] or purulent [[pericarditis]]<ref>Howitt T: Remarkable case of abscess of the heart. Lancet 1, 684-685 (1846)</ref> <ref>Abela GS, B. Majmudar, J.M. Felner: Myocardial abscess unassociated with infective endocarditis. South Med J 74, 432-434 (1981)</ref> <ref>Saphir O: Myocarditis: A general review, with an analysis of two hundred and forty cases. Arch Pathol 32,1000-1051 (1941)</ref>.


'''Post-mortem examination,of myocardial abscess, showed following pathological changes:'''
'''Post-mortem examination,of myocardial abscess, showed following pathological changes:'''


'''Macroscopic finding'''
'''Macroscopic finding'''
*The cardiac area was greatly enlarged, and when the pericardial sac was opened, it was found to contain 600 cc of partially clotted blood.
*The [[cardiac]] area was greatly enlarged, and when the [[pericardial]] sac was opened, it was found to contain 600 cc of partially clotted blood.
*The parietal pericardium was blood tinged but smooth and glistening throughout.  
*The [[parietal]] [[pericardium]] was blood tinged but smooth and glistening throughout <ref>Flaxman N: Myocardial abscess. JAMA 122, 804-806 (1943)</ref> <ref>Sanson J, S. Slodki, J.G. Gruhn: Myocardial abscesses. Am Heart J 66, 301-308 (1963)</ref> <ref>Weiss S, R.W. Wilkins: Myocardial abscess with perforation of the heart. Am J Med Sci 194,199-205 (1937)</ref> .  
*The epicardium was normal in appearance over the anterior aspect of the heart but glassy and coated with a thin layer of fibrinous exudate in the posterior aspect.
*The [[epicardium]] was normal in appearance over the anterior aspect of the [[heart]] but [[glassy]] and coated with a thin layer of [[fibrinous]] [[exudate]] in the posterior aspect.
*The tear involved the entire thickness of the myocardium so that a probe could be passed through it into the left ventricular cavity without resistance.  
*The tear involved the entire thickness of the [[myocardium]] so that a probe could be passed through it into the [[left ventricular]] cavity without resistance.  
*The surrounding myocardium was infiltrated by blood and flabby in consistence in an area about 6 cm in diameter.
*The surrounding myocardium was infiltrated by blood and flabby in consistence in an area about 6 cm in diameter.
*Externally and on cut section this area displayed a variegated tinge from reddish brown to yellowish gray.
*Externally and on cut section this area displayed a variegated tinge from reddish brown to yellowish gray.
*Clusters of honey-combed pockets, each pin head in size or larger, were scattered throughout this area.  
*Clusters of honey-combed pockets, each pin head in size or larger, were scattered throughout this area.  
*Grossly, these pockets were suggestive of small abscesses and contained a thick, golden-yellow material.
*Grossly, these pockets were suggestive of small abscesses and contained a thick, golden-yellow material.
*The coronary arteries were diffusely narrowed, with atheroma formation and calcification.  
*The coronary arteries were diffusely narrowed, with [[atheroma]] formation and [[calcification]].  
*The right coronary artery was occluded a short distance below its main stem by a firmly adherent, friable, yellowish-brown thrombotic mass.  
*The [[right coronary artery]] was occluded a short distance below its main stem by a firmly adherent, friable, yellowish-brown [[thrombotic]] mass.  
*Examination of the cardiac chambers revealed a laminated thrombus on the posterior aspect of the left ventricle<ref name="pmid14785774">{{cite journal |vauthors=TEDESCHI CG, STEVENSON TD, LEVENSON HM |title=Abscess formation in myocardial infarction |journal=N. Engl. J. Med. |volume=243 |issue=26 |pages=1024–7 |date=December 1950 |pmid=14785774 |doi=10.1056/NEJM195012282432602 |url=}}</ref>.
*Examination of the [[cardiac]] chambers revealed a laminated thrombus on the posterior aspect of the left ventricle<ref name="pmid14785774">{{cite journal |vauthors=TEDESCHI CG, STEVENSON TD, LEVENSON HM |title=Abscess formation in myocardial infarction |journal=N. Engl. J. Med. |volume=243 |issue=26 |pages=1024–7 |date=December 1950 |pmid=14785774 |doi=10.1056/NEJM195012282432602 |url=}}</ref>.
[http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
[http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
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'''Microscopic finding'''
'''Microscopic finding'''
*Myocardial infarct the microscopical sections showed an almost complete obliteration of the normal architecture.  
*[[Myocardial infarct]] the [[microscopical]] sections showed an almost complete obliteration of the normal architecture<ref>Bateman AC, M. Richards, A.P. Pallett. Fatal myocarditis associated with a Lancefield Group B Streptococcus. J Infect 36,354-5 (1998)</ref> <ref>Von Kurnatowski HA, J.L.Sierra-Callejas, W. Henkel: Foudroyant todlich verlaufende myokarditis durch streptokokken der gruppe B. Dtsch Med Wschr 103,439-41 (1977)</ref>.  
*The muscle fibers displayed loss of striations and of nuclear patterns and seemed fused together into an amorphous mass of eosinophilic material.
*The [[muscle]] [[fibers]] displayed loss of [[striations]] and of [[nuclear]] patterns and seemed fused together into an [[amorphous]] mass of [[eosinophilic]] material.
*The capillaries in the area were congested, and extravasated red cells were present throughout.  
*The capillaries in the area were congested, and extravasated red cells were present throughout.  
*There was a concomitant marked infiltration of polymorphonuclear leukocytes either scattered or in clusters, and this extended into the epicardium.
*There was a concomitant marked infiltration of polymorphonuclear leukocytes either scattered or in clusters, and this extended into the epicardium.
*The leukocytes were not well preserved; the majority were fused together or showed karyorrhexis and karyolysis resulting in a scattering of cellular débris.  
*The leukocytes were not well preserved; the majority were fused together or showed karyorrhexis and karyolysis resulting in a scattering of cellular débris.  
*The endocardial mural thrombus consisted of amorphous eosinophilic material and was interspersed with white cells and cellular débris.  
*The endocardial mural thrombus consisted of amorphous eosinophilic material and was interspersed with white cells and cellular débris.  
*The mural thrombus merged indistinctly into the adjacent necrotic myocardium.  
*The [[mural]] [[thrombus]] merged indistinctly into the adjacent [[necrotic]] [[myocardium]].  
*The thrombotic mass in the lumen of the right coronary artery showed incipient organization with intimal histiocytic and fibroblastic proliferation and atheromatous changes.
*The thrombotic mass in the lumen of the [[right coronary artery]] showed incipient organization with intimal [[histiocytic]] and [[fibroblastic]] [[proliferation]] and [[atheromatous]] changes<ref>Tedeschi CG, T.D. Stevenson, H.M. Levenson. Abscess formation in myocardial infarction. NEJM 243,1024-7
(1950)</ref>.
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==Causes==
==Causes==
*Cardiac abscesses are rare in the United States. Cardiac abscesses are most commonly thought to occur primarily by the extent of a pre-existing cardiac infection, as it is with the case of infective endocarditis (IE). Secondary causes of cardiac abscess are believed to be due to bacteremia (persistent or transient) without a known cardiac source, as well as susceptible heart tissue soon after myocardial infarction (MI), or prosthetic valve disease, usually in the setting of bacteremia. Staphylococcus aureus is the most common pathogen when the disease is present.The following are organisms noted to be involved in cardiac abscess formation:
*[[Cardiac]] [[abscesses]] are rare in the United States. [[Cardiac]] abscesses are most commonly thought to occur primarily by the extent of a pre-existing [[cardiac] [[infection]], as it is with the case of [[infective]] [[endocarditis]] ([[IE]]) <ref>Saphir O: Meningococcus myocarditis. Am J Pathol 12,677-87 (1936)</ref> <ref>McCue MJ, E.E. Moore: Myocarditis with microabscess formation caused by Listeria monocytogenes associated with myocardial infarct. Human Pathol 10:469-72 (1979)</ref> <ref>Lewis JF: Myocardial infarction during pregnancy: With associated myocardial Bacteroides abscess. South Med J 66,379-1 (1973)</ref>. Secondary causes of [[cardiac]] [[abscess]] are believed to be due to [[bacteremia]] (persistent or transient) without a known [[cardiac]] source, as well as susceptible [[heart]] [[tissue]] soon after [[myocardial infarction]] ([[MI]]), or [[prosthetic valve disease]], usually in the setting of [[bacteremia]]. [[Staphylococcus aureus]] is the most common pathogen when the disease is present.The following are organisms noted to be involved in cardiac abscess formation<ref name="pmid29083576">{{cite journal |vauthors=Ramos Tuarez FJ, Law MA |title= |journal= |volume= |issue= |pages= |date= |pmid=29083576 |doi= |url=}}</ref>:
**Staphylococcus aureus
**[[Staphylococcus aureus]]
**Haemophilus species
**[[Haemophilus]] species
**Enterococci  
**[[Enterococci]]
**Escherichia coli
**[[Escherichia coli]]
**Beta-hemolytic streptococci  
**Beta-hemolytic [[streptococci]]
**Streptococcus pneumoniae
**[[Streptococcus]] pneumoniae
'''Endocarditis'''
'''[[Endocarditis]]'''
*The most common clinical setting for myocardial abscess is as a complication of endocarditis involving either native or prosthetic valves.  
*The most common clinical setting for [[myocardial]] [[abscess]] is as a complication of [[endocarditis]] involving either native or [[prosthetic valves]].  
*In a review of 40 cases of infective endocarditis, Gonzalez Vilchez et al (1991) found that 67.5% (27 cases) involved native valves.  
*In a review of 40 cases of [[infective]] [[endocarditis]], Gonzalez Vilchez et al (1991) found that 67.5% (27 cases) involved native valves.  
*The most common site was the aortic valve, followed in descending order by the ventricular septa, mitral valves, and papillary muscles.  
*The most common site was the [[aortic valve]], followed in descending order by the [[ventricular septa]], [[mitral valves]], and [[papillary muscles]].  
*Approximately one third of cases involved the base of the aortic valve.  
*Approximately one third of cases involved the base of the aortic valve.  
*Staphylococcus was the most prevalent species involved, isolated from one third of all cases.  
*[[Staphylococcus]] was the most prevalent species involved, isolated from one third of all cases.  
*Prosthetic valve abscess comprised 34% of cases, and 50% of these were caused by staphylococcal infection.  
*[[Prosthetic valve]] abscess comprised 34% of cases, and 50% of these were caused by [[staphylococcal]] infection.  
*An infected coronary artery stent may be a rare source of multiple myocardial abscesses.
*An infected [[coronary artery]] stent may be a rare source of multiple [[myocardial]] abscesses<ref name="pmid3389387">{{cite journal |vauthors=Zeineddin M, Stewart JA |title=Echocardiographic detection of non-valve-ring myocardial abscess complicating aortic valve endocarditis |journal=Am. J. Med. |volume=85 |issue=1 |pages=97–9 |date=July 1988 |pmid=3389387 |doi=10.1016/0002-9343(88)90510-4 |url=}}</ref>.


'''Bacteremia'''
'''Bacteremia'''
*In the past, the most common setting for myocardial abscess was generalized bacteremia, as described in older autopsy reports.  
*In the past, the most common setting for [[myocardial]] [[abscess]] was generalized [[bacteremia]], as described in older autopsy reports.  
*Sanson and colleagues (1963) described 23 cases, 21 of which exhibited multiple abscesses in lungs, kidneys, brain, and myocardium. Myocardial abscesses were small in these patients, and the authors postulated that the patients died too early to develop larger abscesses.
*Sanson and colleagues (1963) described 23 cases, 21 of which exhibited multiple abscesses in [[lungs]], [[kidneys]], [[brain]], and [[myocardium]]. [[Myocardial]] [[abscesses]] were small in these patients, and the authors postulated that the patients died too early to develop larger [[abscesses]]<ref name="pmid2028858">{{cite journal |vauthors=Akins EW, Slone RM, Wiechmann BN, Browning M, Martin TD, Mayfield WR |title=Perivalvular pseudoaneurysm complicating bacterial endocarditis: MR detection in five cases |journal=AJR Am J Roentgenol |volume=156 |issue=6 |pages=1155–8 |date=June 1991 |pmid=2028858 |doi=10.2214/ajr.156.6.2028858 |url=}}</ref>.


'''Myocardial infarction'''
'''[[Myocardial infarction]]'''
*Myocardial abscess may develop at the site of a myocardial infarction (MI) but usually develops in the setting of bacteremia.  
*[[Myocardial]] [[abscess]] may develop at the site of a [[myocardial infarction]] ([[MI]]) but usually develops in the setting of [[bacteremia]]<ref name="pmid696668">{{cite journal |vauthors=Kim HS, Weilbaecher DG, Lie JT, Titus JL |title=Myocardial abscesses |journal=Am. J. Clin. Pathol. |volume=70 |issue=1 |pages=18–23 |date=July 1978 |pmid=696668 |doi=10.1093/ajcp/70.1.18 |url=}}</ref>.  
*Cossio et al (1933) reported a myocardial abscess at the site of an acute MI.  
*Cossio et al (1933) reported a [[myocardial]] [[abscess]] at the site of an acute [[MI]].  
*In the case records of the Massachusetts General Hospital, Castleman and McNeely (1970) reported a secondary infection within an inferior wall MI in a patient with Bacteroides bacteremia following genitourinary surgery and placement of an infected indwelling catheter.
*In the case records of the Massachusetts General Hospital, Castleman and McNeely (1970) reported a secondary infection within an inferior wall [[MI]] in a patient with Bacteroides bacteremia following genitourinary surgery and placement of an infected indwelling catheter.
*In a review of 13 cases of myocardial abscess in acute MI, Weisz and Young (1977) found bronchopneumonia to be the probable source in 4 cases, gastrointestinal and renal sepsis in 2, and no definable source in the others. Organisms included Staphylococcus aureus, Clostridium perfringens, Bacteroides species, Escherichia coli, beta-hemolytic streptococci, and Streptococcus pneumoniae, in order of decreasing frequency.  
*In a review of 13 cases of [[myocardial]] [[abscess]] in acute [[MI]], Weisz and Young (1977) found [[bronchopneumonia]] to be the probable source in 4 cases, [[gastrointestinal]] and [[renal]] [[sepsis]] in 2, and no definable source in the others. Organisms included [[Staphylococcus aureus]], [[Clostridium perfringens]], [[Bacteroides]] species, [[Escherichia coli]], [[beta-hemolytic streptococci]], and [[Streptococcus pneumoniae]], in order of decreasing frequency.  
*The propensity of cardiac muscle to develop myocardial abscess in the setting of acute MI and septicemia may be due to the presence of necrosis of the muscular fibers and surrounding inflammatory exudates, decreased or absent perfusion, and lack of cell-mediated immunity secondary to decreased blood flow. Such myocardium also appears to be at a greater risk of rupture than healthy myocardium (7-fold higher per Weisz and Young [1977], with a catastrophic outcome.
*The propensity of [[cardiac muscle]] to develop [[myocardial abscess]] in the setting of acute MI and [[septicemia]] may be due to the presence of [[necrosis]] of the [[muscular fibers]] and surrounding [[inflammatory]] [[exudates]], decreased or absent perfusion, and lack of [[cell-mediated immunity]] secondary to decreased [[blood]] flow. Such [[myocardium]] also appears to be at a greater risk of rupture than [[healthy]] [[myocardium]] (7-fold higher per Weisz and Young [1977], with a catastrophic outcome.


'''Other settings associated with myocardial abscesses that have been reported in the literature include the following:'''
'''Other settings associated with myocardial abscesses that have been reported in the literature include the following:'''


*Trauma
*[[Trauma]]
*Deep penetrating wounds
*Deep [[penetrating wounds]]
*Deep burns
*Deep [[burns]]
*Infected pseudoaneurysms
*Infected [[pseudoaneurysms]]
*Suppurative pericarditis
*[[Suppurative]] [[pericarditis]]
*Infected transplanted hearts
*Infected [[transplanted]] [[hearts]]
*Extension from sternal abscess
*Extension from [[sternal]] [[abscess]]
*HIV-associated myocarditis and suppuration
*HIV-associated [[myocarditis]] and [[suppuration]]
*Parasitic infections
*[[Parasitic]] infections
*Infection of a left ventricular aneurysm or tumor
*Infection of a [[left ventricular aneurysm]] or [[tumor]]
 
==Differential Diagnosis==
:*[[Thrombotic nonbacterial endocarditis]]/[[Marantic endocarditis]]
:*[[Vasculitis]]
:*[[Temporal arteritis]]
:*[[SLE]]/[[Libman-Sacks endocarditis]]
:*[[Connective tissue disease]]
:*[[Fever of unknown origin]] ([[FUO]])
:*[[Intra-abdominal]] [[infection]]s
:*[[Septic]] [[pulmonary]] [[infarction]]
 
Myocardial Abscess should be differentiated from other diseases presenting with [[fever]], [[chest pain]] and [[anorxia]]. The differentials include the following:<ref name="pmid24550636">{{cite journal |vauthors=Brenes-Salazar JA |title=Westermark's and Palla's signs in acute and chronic pulmonary embolism: Still valid in the current computed tomography era |journal=J Emerg Trauma Shock |volume=7 |issue=1 |pages=57–8 |year=2014 |pmid=24550636 |pmc=3912657 |doi=10.4103/0974-2700.125645 |url=}}</ref><ref name="urlCT Angiography of Pulmonary Embolism: Diagnostic Criteria and Causes of Misdiagnosis | RadioGraphics">{{cite web |url=http://pubs.rsna.org/doi/full/10.1148/rg.245045008 |title=CT Angiography of Pulmonary Embolism: Diagnostic Criteria and Causes of Misdiagnosis &#124; RadioGraphics |format= |work= |accessdate=}}</ref><ref name="pmid23940438">{{cite journal |vauthors=Bĕlohlávek J, Dytrych V, Linhart A |title=Pulmonary embolism, part I: Epidemiology, risk factors and risk stratification, pathophysiology, clinical presentation, diagnosis and nonthrombotic pulmonary embolism |journal=Exp Clin Cardiol |volume=18 |issue=2 |pages=129–38 |year=2013 |pmid=23940438 |pmc=3718593 |doi= |url=}}</ref><ref name="urlPulmonary Embolism: Symptoms - National Library of Medicine - PubMed Health">{{cite web |url=https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0022657/ |title=Pulmonary Embolism: Symptoms - National Library of Medicine - PubMed Health |format= |work= |accessdate=}}</ref><ref name="pmid20118395">{{cite journal |vauthors=Ramani GV, Uber PA, Mehra MR |title=Chronic heart failure: contemporary diagnosis and management |journal=Mayo Clin. Proc. |volume=85 |issue=2 |pages=180–95 |year=2010 |pmid=20118395 |pmc=2813829 |doi=10.4065/mcp.2009.0494 |url=}}</ref><ref name="pmid18215495">{{cite journal |vauthors=Blinderman CD, Homel P, Billings JA, Portenoy RK, Tennstedt SL |title=Symptom distress and quality of life in patients with advanced congestive heart failure |journal=J Pain Symptom Manage |volume=35 |issue=6 |pages=594–603 |year=2008 |pmid=18215495 |pmc=2662445 |doi=10.1016/j.jpainsymman.2007.06.007 |url=}}</ref><ref name="pmid19168510">{{cite journal |vauthors=Hawkins NM, Petrie MC, Jhund PS, Chalmers GW, Dunn FG, McMurray JJ |title=Heart failure and chronic obstructive pulmonary disease: diagnostic pitfalls and epidemiology |journal=Eur. J. Heart Fail. |volume=11 |issue=2 |pages=130–9 |year=2009 |pmid=19168510 |pmc=2639415 |doi=10.1093/eurjhf/hfn013 |url=}}</ref><ref name="pmid9465867">{{cite journal |vauthors=Takasugi JE, Godwin JD |title=Radiology of chronic obstructive pulmonary disease |journal=Radiol. Clin. North Am. |volume=36 |issue=1 |pages=29–55 |year=1998 |pmid=9465867 |doi= |url=}}</ref><ref name="pmid14651761">{{cite journal |vauthors=Wedzicha JA, Donaldson GC |title=Exacerbations of chronic obstructive pulmonary disease |journal=Respir Care |volume=48 |issue=12 |pages=1204–13; discussion 1213–5 |year=2003 |pmid=14651761 |doi= |url=}}</ref><ref name="pmid23833163">{{cite journal |vauthors=Nakawah MO, Hawkins C, Barbandi F |title=Asthma, chronic obstructive pulmonary disease (COPD), and the overlap syndrome |journal=J Am Board Fam Med |volume=26 |issue=4 |pages=470–7 |year=2013 |pmid=23833163 |doi=10.3122/jabfm.2013.04.120256 |url=}}</ref><ref name="pmid20511488">{{cite journal |vauthors=Khandaker MH, Espinosa RE, Nishimura RA, Sinak LJ, Hayes SN, Melduni RM, Oh JK |title=Pericardial disease: diagnosis and management |journal=Mayo Clin. Proc. |volume=85 |issue=6 |pages=572–93 |year=2010 |pmid=20511488 |pmc=2878263 |doi=10.4065/mcp.2010.0046 |url=}}</ref><ref name="pmid23610095">{{cite journal |vauthors=Bogaert J, Francone M |title=Pericardial disease: value of CT and MR imaging |journal=Radiology |volume=267 |issue=2 |pages=340–56 |year=2013 |pmid=23610095 |doi=10.1148/radiol.13121059 |url=}}</ref><ref name="pmid11680112">{{cite journal |vauthors=Gharib AM, Stern EJ |title=Radiology of pneumonia |journal=Med. Clin. North Am. |volume=85 |issue=6 |pages=1461–91, x |year=2001 |pmid=11680112 |doi= |url=}}</ref><ref name="pmid23507061">{{cite journal |vauthors=Schmidt WA |title=Imaging in vasculitis |journal=Best Pract Res Clin Rheumatol |volume=27 |issue=1 |pages=107–18 |year=2013 |pmid=23507061 |doi=10.1016/j.berh.2013.01.001 |url=}}</ref><ref name="pmid16891436">{{cite journal |vauthors=Suresh E |title=Diagnostic approach to patients with suspected vasculitis |journal=Postgrad Med J |volume=82 |issue=970 |pages=483–8 |year=2006 |pmid=16891436 |pmc=2585712 |doi=10.1136/pgmj.2005.042648 |url=}}</ref><ref name="pmid123074">{{cite journal |vauthors=Stein PD, Dalen JE, McIntyre KM, Sasahara AA, Wenger NK, Willis PW |title=The electrocardiogram in acute pulmonary embolism |journal=Prog Cardiovasc Dis |volume=17 |issue=4 |pages=247–57 |year=1975 |pmid=123074 |doi= |url=}}</ref><ref name="pmid23413894">{{cite journal |vauthors=Warnier MJ, Rutten FH, Numans ME, Kors JA, Tan HL, de Boer A, Hoes AW, De Bruin ML |title=Electrocardiographic characteristics of patients with chronic obstructive pulmonary disease |journal=COPD |volume=10 |issue=1 |pages=62–71 |year=2013 |pmid=23413894 |doi=10.3109/15412555.2012.727918 |url=}}</ref><ref name="pmid23000104">{{cite journal |vauthors=Stein PD, Matta F, Ekkah M, Saleh T, Janjua M, Patel YR, Khadra H |title=Electrocardiogram in pneumonia |journal=Am. J. Cardiol. |volume=110 |issue=12 |pages=1836–40 |year=2012 |pmid=23000104 |doi=10.1016/j.amjcard.2012.08.019 |url=}}</ref><ref name="pmid26209947">{{cite journal |vauthors=Hazebroek MR, Kemna MJ, Schalla S, Sanders-van Wijk S, Gerretsen SC, Dennert R, Merken J, Kuznetsova T, Staessen JA, Brunner-La Rocca HP, van Paassen P, Cohen Tervaert JW, Heymans S |title=Prevalence and prognostic relevance of cardiac involvement in ANCA-associated vasculitis: eosinophilic granulomatosis with polyangiitis and granulomatosis with polyangiitis |journal=Int. J. Cardiol. |volume=199 |issue= |pages=170–9 |year=2015 |pmid=26209947 |doi=10.1016/j.ijcard.2015.06.087 |url=}}</ref><ref name="pmid20112390">{{cite journal |vauthors=Dennert RM, van Paassen P, Schalla S, Kuznetsova T, Alzand BS, Staessen JA, Velthuis S, Crijns HJ, Tervaert JW, Heymans S |title=Cardiac involvement in Churg-Strauss syndrome |journal=Arthritis Rheum. |volume=62 |issue=2 |pages=627–34 |year=2010 |pmid=20112390 |doi=10.1002/art.27263 |url=}}</ref>
 
<small>
{|
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
! rowspan="2" |<small>Diseases</small>
! colspan="3" |<small>Diagnostic tests</small>
! colspan="3" |<small>Physical Examination</small>
| colspan="7" |<small>Symptoms
! colspan="1" rowspan="2" |<small>Past medical history</small>
! rowspan="2" |<small>Other Findings</small>
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
!<small>CT scan and MRI</small>
!<small>EKG</small>
!<small>Chest X-ray</small> 
!<small>Tachypnea</small>
!<small>Tachycardia</small>
!<small>Fever</small>
!<small>Chest Pain</small>
!<small>Hemoptysis</small>
!<small>Dyspnea on Exertion</small>
!<small>Wheezing</small>
!<small>Chest Tenderness</small>
!<small>Nasalopharyngeal Ulceration</small>
!<small>Carotid Bruit</small>
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Pulmonary embolism]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |
* On [[CT angiography]]:
** Intra-luminal filling defect
*On [[MRI]]:
** Narrowing of involved [[Blood vessel|vessel]]
** No contrast seen distal to [[obstruction]]
** Polo-mint sign (partial filling defect surrounded by contrast)
| style="background: #F5F5F5; padding: 5px;" |
* [[Pulmonary embolism electrocardiogram|S1Q3T3]] pattern representing acute [[right heart]] strain
| style="background: #F5F5F5; padding: 5px;" |
* [[Fleischner sign]] (enlarged pulmonary artery), [[Hampton's hump|Hampton hump]], [[Westermark's sign]]
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔ (Low grade)
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔ (In case of massive PE)
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*Hypercoagulating conditions ([[Factor V Leiden]], [[thrombophilia]], [[deep vein thrombosis]], immobilization, [[malignancy]], [[pregnancy]])
| style="background: #F5F5F5; padding: 5px;" |
* May be associated with [[metabolic alkalosis]] and [[syncope]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" | [[Infective Endocarditis]]
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*Previous [[myocardial infarction]]
*[[Hypertension]] ([[Systemic hypertension|systemic]] and [[Pulmonary hypertension|pulmonary]])
*[[Cardiac arrhythmia|Cardiac arrythmias]]
*[[Viral]] infections ([[myocarditis]])
*[[Congenital heart disease|Congenital heart defects]]
| style="background: #F5F5F5; padding: 5px;" |
*[[Right heart failure]] associated with:
**[[Hepatomegaly]]
**Positive hepato-jugular reflex
**Increased [[jugular venous pressure]]
**[[Peripheral edema]]
*[[Left heart failure]] associated with:
**[[Pulmonary edema]]
**Eventual [[right heart failure]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Non-Bacterial Thrombotic Endocarditis]]
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔ (Low grade)
| style="background: #F5F5F5; padding: 5px;" |✔ (Relieved by sitting up and leaning forward)
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*Idiopathic in a large number of cases
*[[Autoimmune]]
*[[Uremia]]
*[[Malignancy]]
*Previous [[myocardial infarction]]
| style="background: #F5F5F5; padding: 5px;" |
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Libman Sack Endocarditis]]
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*SLE
| style="background: #F5F5F5; padding: 5px;" |
*Requires [[Sputum|sputum stain]] and culture for diagnosis
*[[Empiric therapy|Empiric management]] usually started before [[Culture collection|culture]] results
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Vasculitis]]
| style="background: #F5F5F5; padding: 5px;" |
*On [[Computed tomography|CT scan]]: ([[Takayasu's arteritis|Takayasu arteritis]])
**[[Blood vessel|Vessel]] wall thickening
**Luminal narrowing of [[pulmonary artery]]
**Masses or nodules ([[Anti-neutrophil cytoplasmic antibody|ANCA]]-associated granulomatous vasculitis)
*On [[Magnetic resonance imaging|MRI]]:
Homogeneous, circumferential [[Blood vessel|vessel]] wall [[swelling]]
| style="background: #F5F5F5; padding: 5px;" |
*[[Bundle branch block|Right or left bundle-branch block]] ([[Churg-Strauss syndrome]])
*[[Atrial fibrillation]] ([[Churg-Strauss syndrome]])
*Non-specific [[ST interval|ST segment]] and [[T wave]] changes
| style="background: #F5F5F5; padding: 5px;" |
*[[Nodule (medicine)|Nodules]]
*[[Cavitation]]
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |
*[[Takayasu's arteritis|Takayasu arteritis]] usually found in persons aged 4-60 years with a mean of 30
*[[Giant-cell arteritis]] usually occurrs in persons aged > 60 years
*[[Churg-Strauss syndrome]] may present with [[asthma]], [[sinusitis]], transient [[pulmonary]] infiltrates and neuropathy alongwith [[cardiac]] involvement
*Granulomatous vasculitides may present with [[nephritis]] and [[upper airway]] ([[nasopharyngeal]]) destruction
| style="background: #F5F5F5; padding: 5px;" |
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Fever of unknown origin]] (FUO)
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" |✔
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*Fever, anorexia
*[[Cough]]
| style="background: #F5F5F5; padding: 5px;" |
*[[Alpha 1-antitrypsin deficiency|Alpha 1 antitrypsin deficiency]] may be associated with [[hepatomegaly]]
|}


==Epidemiology and Demographics==
==Epidemiology and Demographics==
*Myocardial abscess rarely occurs in the United States.
*[[Myocardial]] [[abscess]] rarely occurs in the [[United States]].
*Murdoch et al (2009) published a contemporary report on the presentation, etiology, and outcome of infective endocarditis in a large patient cohort from multiple locations worldwide.
*Seventy-seven percent of the [[patient]]s presented early in the [[disease]] course (ie, within the first month), with few of the classic [[clinical]] hallmarks of [[infective]] [[endocarditis]]<ref name="pmid19273776">{{cite journal |vauthors=Murdoch DR, Corey GR, Hoen B, Miró JM, Fowler VG, Bayer AS, Karchmer AW, Olaison L, Pappas PA, Moreillon P, Chambers ST, Chu VH, Falcó V, Holland DJ, Jones P, Klein JL, Raymond NJ, Read KM, Tripodi MF, Utili R, Wang A, Woods CW, Cabell CH |title=Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study |journal=Arch. Intern. Med. |volume=169 |issue=5 |pages=463–73 |date=March 2009 |pmid=19273776 |pmc=3625651 |doi=10.1001/archinternmed.2008.603 |url=}}</ref>.
*They analyzed a prospective cohort study of 2781 adults (median age 57.9 y) with definite infective endocarditis (72.1% of the native valve) who were admitted to 58 hospitals in 25 countries over a 5-year period.  
*S [[aureus]] was the most common pathogen found (31.2% of patients). The [[mitral valve]] was found to be [[infected]] in 41.1% of cases and the [[aortic valve]] in 37.6%. The common complications included [[stroke]] (16.9%), [[embolization]] other than [[stroke]] (22.6%), [[heart failure]] (32.3%), and [[intracardiac]] [[abscess]] (14.4%). [[Surgical]] [[therapy]] was performed in 48.2% of the patients, and in-hospital [[mortality]] rates were high (17.7%).
*Seventy-seven percent of the patients presented early in the disease course (ie, within the first month), with few of the classic clinical hallmarks of infective endocarditis. Recent health care exposure was found in one quarter of the patients.
*In the early 21st century, [[infective]] [[endocarditis]] continues to be more often an [[acute]] [[disease]], characterized by a high rate of S aureus [[infection]] and an unacceptably high [[mortality rate]].
*S aureus was the most common pathogen found (31.2% of patients). The mitral valve was found to be infected in 41.1% of cases and the aortic valve in 37.6%. The common complications included stroke (16.9%), embolization other than stroke (22.6%), heart failure (32.3%), and intracardiac abscess (14.4%). Surgical therapy was performed in 48.2% of the patients, and in-hospital mortality rates were high (17.7%).
*The [[incidence]] of [[infective]] [[endocarditis]] remained relatively stable from 1950-1987, at approximately 4.2 cases per 100,000 patient-years.
*Several factors portended a high fatality risk, including prosthetic valve involvement (odds ratio [OR], 1.47), increasing age (OR, 1.30), pulmonary edema (OR, 1.79), S aureus infection (OR, 1.54), coagulase-negative staphylococcal infection (OR, 1.50), mitral valve vegetation (OR, 1.34), and paravalvular complications (OR, 2.25). Streptococcus viridans infection (OR, 0.52) and surgery (OR, 0.61) were associated with a decreased fatality risk. In summary, in the early 21st century, infective endocarditis continues to be more often an acute disease, characterized by a high rate of S aureus infection and an unacceptably high mortality rate. [7]
*During the early 1980s, the yearly incidence of [[infective]] [[endocarditis]] was 2 cases per 100,000 population in the [[United Kingdom]] and Wales.
*The incidence of infective endocarditis remained relatively stable from 1950-1987, at approximately 4.2 cases per 100,000 patient-years. [8] During the early 1980s, the yearly incidence of infective endocarditis was 2 cases per 100,000 population in the United Kingdom and Wales and 1.9 cases per 100,000 population in the Netherlands. A higher incidence was noted from 1984-1990; 5.9 and 11.6 episodes per 100,000 population were reported from Sweden and metropolitan Philadelphia, respectively. [9]
*1.9 cases per 100,000 population in the Netherlands. A higher [[incidence]] was noted from 1984-1990; 5.9 and 11.6 [[episodes]] per 100,000 population were reported from Sweden and metropolitan Philadelphia, respectively.  
*Infections involving prosthetic valves, especially mechanical prostheses, in which the infection is entirely periannular, often extend into the adjacent myocardium, resulting in paravalvular abscess formation and partial dehiscence of the prosthetic valve with paravalvular regurgitation.
*[[Infection]]s involving [[prosthetic valves]], especially [[mechanical]] prostheses, in which the [[infection]] is entirely [[periannular]], often extend into the adjacent [[myocardium]], resulting in [[paravalvular]] [[abscess]] formation and partial [[dehiscence]] of the [[prosthetic valve]] with [[paravalvular]] [[regurgitation]].
*Among 85 patients with endocarditis involving a mechanical prosthesis, annulus invasion and myocardial abscess were noted in 42% and 14% of patients, respectively. [10]
*Ben Ismail et al (1987) found [[annulus]] [[infection]] and [[valve]] [[dehiscence]] in (82%) [[infected]] [[mechanical]] [[valves]] examined at [[surgery]] or [[autopsy]].
*Ben Ismail et al (1987) found annulus infection and valve dehiscence in 38 of 41 (82%) infected mechanical valves examined at surgery or autopsy. [11]
*[[Myocardial]] [[abscess]] formation profoundly worsens the prognosis in patients with [[infective]][[endocarditis]].
*Myocardial abscess formation profoundly worsens the prognosis in patients with infective endocarditis.
*The [[mortality rate]] associated with [[S aureus]] [[infective]] [[endocarditis]] is 42% overall. If treated with [[antibiotics]] only, the [[mortality rate]] is 75%, while a regimen that combines [[antibiotics]] and [[surgery]] reduces the [[mortality rate]] to 25%.
*The mortality rate associated with S aureus infective endocarditis is 42% overall. If treated with antibiotics only, the mortality rate is 75%, while a regimen that combines antibiotics and surgery reduces the mortality rate to 25%.
*[[Myocardial]] [[abscess]] have more prevalent in [[African American]]s in urban setting.
*The presence of an intracardiac abscess or complications increases the mortality rate 13.7-fold.
*[[Myocardial]] [[abscess]] is also more common in women than in men. Among persons who abuse [[intravenous]] [[drugs]], [[myocardial]] [[abscess]] is more prevalent in men (65%-80%).
*Myocardial abscess has no substantial racial predilection. However, the condition may be more prevalent in African Americans in urban settings.
 
*The relative risk ranges from 3.5-8.2. Because mitral valve prolapse (MVP) is more common in women than in men, myocardial abscess is also more common in women than in men. Among persons who abuse intravenous drugs, myocardial abscess is more prevalent in men (65%-80%).
*In adults, MVP has emerged as a prominent predisposing structural abnormality that may account for 7%-30% of cases of nonvalvular endocarditis (NVE). However, myocardial abscess developing in such cases is exceedingly rare.
*Involvement of cardiac structures with endocarditis and myocardial abscess mainly depends on the incidence of various underlying structural heart conditions among different age groups.
*The incidence of infective endocarditis among hospitalized children ranges from 1 case in 4500 to 1 case in 1280. In the Netherlands, incidences of 1.7 cases per 100,000 persons in boys and 1.2 cases per 100,000 persons in girls have been noted. [8] In neonates, the rate has been increasing because of contaminated intravenous lines and the increased use of right-sided heart catheters. Infective endocarditis usually involves the tricuspid valve and is caused primarily by S aureus. Congenital heart defects are predisposing conditions in toddlers and older children.
*In adults, MVP is the most common structural heart abnormality associated with infectious endocarditis, found in as many as 7%-30% of patients with NVE, and the risk increases in patients older than 45 years.
*Those who abuse intravenous drugs are increasingly susceptible (2%-5% per patient-year).
==Risk Factors==
==Risk Factors==


Any septic focus can theoretically lead to myocardial abscess. These are the primary foci in order of frequency of causing myocardial abscess.
Any septic focus can theoretically lead to myocardial abscess. These are the primary foci in order of frequency of causing myocardial abscess.


*[[Renal]] infections:
*[[Renal]] infections<ref name="pmid17897252">{{cite journal |vauthors=Khan B, Strate RW, Hellman R |title=Myocardial abscess and fatal cardiac arrhythmia in a hemodialysis patient with an arterio-venous fistula infection |journal=Semin Dial |volume=20 |issue=5 |pages=452–4 |date=2007 |pmid=17897252 |doi=10.1111/j.1525-139X.2007.00247.x |url=}}</ref>
:Spread from the urinary tract is the most common cause.
:Spread from the urinary tract is the most common cause.
*[[Gastrointestinal tract|Gastrointestinal]] diseases:
*[[Gastrointestinal tract|Gastrointestinal]] diseases:
:Spread from the [[gastrointestinal tract]] is the second common cause (e.g. perforated [[appendix]], <nowiki/>perforated [[colon cancer]], [[diverticulitis]] ,and [[Crohn’s disease|cohn’s disease]].)                                 
:Spread from the [[gastrointestinal tract]] is the second common cause (e.g. perforated [[appendix]], <nowiki/>perforated [[colon cancer]], [[diverticulitis]] ,and [[Crohn’s disease|cohn’s disease]].)                                 
*[[Bone]] infection:
*[[Bone]] infection<ref name="pmid2602260">{{cite journal |vauthors=Smith RE, Martin JE, Mills PG |title=Myocardial abscess and sternal osteomyelitis following myocardial infarction and resuscitation |journal=Postgrad Med J |volume=65 |issue=766 |pages=589–90 |date=August 1989 |pmid=2602260 |pmc=2429504 |doi=10.1136/pgmj.65.766.589 |url=}}</ref>
:e.g. [[pott's disease]] or [[osteomyelitis]]
:e.g. [[pott's disease]] or [[osteomyelitis]]
*Hematogenous spread:
*Hematogenous spread<ref name="pmid8062808">{{cite journal |vauthors=Debelian GJ, Olsen I, Tronstad L |title=Systemic diseases caused by oral microorganisms |journal=Endod Dent Traumatol |volume=10 |issue=2 |pages=57–65 |date=April 1994 |pmid=8062808 |doi=10.1111/j.1600-9657.1994.tb00061.x |url=}}</ref>
:From distant septic foci.
:From distant septic foci.<ref name="pmid9081801">{{cite journal |vauthors=Omran H, Reichel H, Wirtz P, Jung W, Rabahieh R, Pfeifer U, Pfeiffer D, Lüderitz B |title=[Septic myocardial aneurysm in mitral valve endocarditis. Clinical and pathological-anatomical findings] |language=German |journal=Dtsch. Med. Wochenschr. |volume=122 |issue=6 |pages=156–60 |date=February 1997 |pmid=9081801 |doi=10.1055/s-2008-1047590 |url=}}</ref>
*[[Iatrogenic]]:
 
:Following [[chest]] [[abdominal]] or [[pelvic]] surgery.


Any condition compromising the [[immune system]] is a [[risk factor]] for developing myocardial abscess. The following were the [[Risk factor|risk factors]] in observed patients. <ref name="pmid1492717">{{cite journal| author=Grollier G, Burucoa C, Bonnin M, de Rautlin de La Roy Y| title=Identification and susceptibility testing for obligate anaerobic bacteria using a semi-automated API ATB plus system. | journal=Ann Biol Clin (Paris) | year= 1992 | volume= 50 | issue= 6-7 | pages= 393-7 | pmid=1492717 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1492717  }} </ref>
Any condition compromising the [[immune system]] is a [[risk factor]] for developing myocardial abscess. The following were the [[Risk factor|risk factors]] in observed patients. <ref name="pmid1492717">{{cite journal| author=Grollier G, Burucoa C, Bonnin M, de Rautlin de La Roy Y| title=Identification and susceptibility testing for obligate anaerobic bacteria using a semi-automated API ATB plus system. | journal=Ann Biol Clin (Paris) | year= 1992 | volume= 50 | issue= 6-7 | pages= 393-7 | pmid=1492717 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1492717  }} </ref>
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===Complications :===
===Complications :===
'''The following are potential complications of myocardial abscess:'''
'''The following are potential [[complication]]s of [[myocardial]] [[abscess]]<ref name="pmid29083576">{{cite journal |vauthors=Ramos Tuarez FJ, Law MA |title= |journal= |volume= |issue= |pages= |date= |pmid=29083576 |doi= |url=}}</ref>:'''
:*Myocardial perforation
:*[[Myocardial]] perforation<ref name="pmid11515915">{{cite journal |vauthors=Shackcloth MJ, Dihmis WC |title=Contained rupture of a myocardial abscess in the free wall of the left ventricle |journal=Ann. Thorac. Surg. |volume=72 |issue=2 |pages=617–9 |date=August 2001 |pmid=11515915 |doi=10.1016/s0003-4975(00)02530-3 |url=}}</ref>
:*Significant clinical deterioration
:*Significant [[clinical]] deterioration
:*Worsening CHF
:*Worsening [[CHF]]
:*Worsening heart sounds and murmurs
:*Worsening [[heart]] [[sound]] and [[murmur]]s
:*New-onset valvular regurgitation (100% of cases) [12]
:*New-onset [[valvular]] [[regurgitation]] (100% of cases)  
:*Poor response to antibiotics
:*Poor response to [[antibiotic]]s
:*Development of conduction defects or progression of heart block, such as bundle-branch block and atrioventricular block (45%) [2]
:*Development of [[conduction]] defects or progression of [[heart block]], such as [[bundle-branch block]] and [[atrioventricular block]] (45%)  
:*Sudden onset of complete heart block or Mobitz type II block (highly specific)
:*Sudden onset of [[complete heart block]] or [[Mobitz type II block]] (highly specific)
:*Type of valve involvement, eg, aortic valve endocarditis (40%-85%)
:*Type of valve involvement, eg, [[aortic]] valve [[endocarditis]] (40%-85%)
:*Miscellaneous (severe recurrent ventricular arrhythmias, pericarditis [uncommon], infection of the prosthetic valves, right-sided endocarditis in patients with congenital heart disease)
:*Miscellaneous (severe recurrent [[ventricular]] [[arrhythmias]], [[pericarditis]] [uncommon], [[infection]] of the [[prosthetic]] [[valves]], [[right-sided]] [[endocarditis]] in patients with [[congenital heart disease]])


===Prognosis ===
===Prognosis ===
:*Depending on the extent of the [[abscess]] at the time of [[diagnosis]], the [[prognosis]] may vary.
:*Depending on the extent of the [[abscess]] at the time of [[diagnosis]], the [[prognosis]] may vary<ref name="pmid29526056">{{cite journal |vauthors=Grant R, Page S, Iyer A |title=Contained myocardial abscess following a myocardial infarction |journal=J Card Surg |volume=33 |issue=3 |pages=144–145 |date=March 2018 |pmid=29526056 |doi=10.1111/jocs.13555 |url=}}</ref> .
:*The condition carries a very high mortality ranging from 30% to 75% without treatment. To reduce the morbidity and mortality of this disorder, it is imperative that a structured approach is developed to make an early diagnosis and begin treatment.[10]
:*The condition carries a very high [[mortality]] ranging from 30% to 75% without treatment. To reduce the [[morbidity]] and [[mortality]] of this disorder, it is imperative that a structured approach is developed to make an early [[diagnosis]] and begin treatment.
:*Even with therapy, mortality rates of 5% to 15% are not uncommon.
:*Even with [[therapy]], [[mortality rate]]s of 5% to 15% are not uncommon.


==Diagnosis==  
==Diagnosis==  
===History===
===History===
* A detailed history should be obtained from the patient presenting with infective endocarditis and chest pain.  
* A detailed history should be obtained from the [[patient]] presenting with [[infective]] [[endocarditis]] and [[chest pain]].  
* Patients who have longstanding persistent bacteremia and who do not respond to antibiotic therapy.
* Patients who have longstanding persistent [[bacteremia]] and who do not respond to [[antibiotic]] [[therapy]].
* Myocardial abscess is more prevalent in the period following mechanical interventions or surgery and in patients with HIV/AIDS-related myocarditis.
* [[Myocardial]] [[abscess]] is more prevalent in the period following [[mechanical]] [[interventions]] or [[surgery]] and in patients with [[HIV]]/[[AIDS]]-related [[myocarditis]]<ref name="pmid3232134">{{cite journal |vauthors=Borowski A, Korb H, Voth E, de Vivie ER |title=Asymptomatic myocardial abscess |journal=Thorac Cardiovasc Surg |volume=36 |issue=6 |pages=338–40 |date=December 1988 |pmid=3232134 |doi=10.1055/s-2007-1022976 |url=}}</ref>.


===Symptoms===
===Symptoms===
One must bear in mind certain constellations of symptoms that may raise the suggestion of myocardial abscess. For example, fever is the most common symptom, presenting in 80%-85% of patients. It is absent in some patients who are elderly; those who have CHF, severe debility, or chronic renal failure; and in patients with coagulase-negative staphylococcal infection and abscess. Another characteristic symptom is chills, which occurs in 42%-75% of cases.
One must bear in mind certain constellations of symptoms that may raise the suggestion of [[myocardial]] [[abscess]]. For example, [[fever]] is the most common symptom, presenting in 80%-85% of patients. It is absent in some patients who are elderly; those who have [[CHF]], severe [[debility]], or [[chronic]] [[renal failure]]; and in patients with [[coagulase-negative]] [[staphylococcal]] [[infection]] and [[abscess]]. Another characteristic symptom is chills, which occurs in 42%-75% of cases<ref name="pmid20149397">{{cite journal |vauthors=Crespo EP, Bertrán DV, Martínez CB, Foradada JT, Diz FW |title=[Myocardial abscess] |language=Spanish; Castilian |journal=Med Clin (Barc) |volume=136 |issue=9 |pages=415 |date=April 2011 |pmid=20149397 |doi=10.1016/j.medcli.2009.11.015 |url=}}</ref>.
====Common symptoms:====
====Common symptoms:====
:*[[Fever]] is the most common complaint and usually it is more than 101 F.
:*[[Fever]] is the most common complaint and usually it is more than 101 F.
:*Constitutional symptoms : [[chills]], [[malaise]], [[anorexia]] and [[weight loss]].
:*Constitutional symptoms : [[chills]], [[malaise]], [[anorexia]] and [[weight loss]]<ref name="pmid15145849">{{cite journal |vauthors=Chikwe J, Barnard J, Pepper JR |title=Myocardial abscess |journal=Heart |volume=90 |issue=6 |pages=597 |date=June 2004 |pmid=15145849 |pmc=1768256 |doi=10.1136/hrt.2003.024646 |url=}}</ref>.


====Less common symptoms:====
====Less common symptoms:====
:*Myalgia
:*[[Myalgia]]
:*Arthralgia
:*[[Arthralgia]]
:*Abdominal pain
:*[[Abdominal pain]]
:*Back pain
:*[[Back pain]]
:*Confusion
:*[[Confusion]]
:*Sweats
:*[[Sweats]]


==Physical Exam==
==Physical Exam==
===General Appearance===
===General Appearance===
Physical examination findings commonly encountered in myocardial abscess are mainly due to the underlying infective endocarditis. These include the following:
[[Physical examination]] findings commonly encountered in [[myocardial abscess]] are mainly due to the underlying [[infective endocarditis]]. These include the following:
Fever, Tachycardia, Murmur, especially changing or new murmur, Neurological abnormalities, Embolic event, Splenomegaly, Clubbing, Peripheral manifestations,Osler nodes, Splinter hemorrhages, Petechiae, Janeway lesions, Retinal lesions (Roth spots),Widening pulse pressure, especially with involvement of the aortic valve and progression of aortic regurgitation
[[Fever]], [[Tachycardia]], [[Murmur]], especially changing or new murmur, Neurological abnormalities, [[Embolic]] event, [[Splenomegaly]], [[Clubbing]], [[Peripheral]] manifestations,[[Osler nodes]], [[Splinter hemorrhages]], [[Petechiae]], [[Janeway lesions]], [[Retinal lesions]] ([[Roth spots]]),Widening [[pulse]] pressure, especially with involvement of the [[aortic valve]] and progression of [[aortic regurgitation]]
The patient is usually fatigued & looking ill due to the preexisting risk factor. In advanced cases with [[septicemia]], the patient may be drowsy with [[decreased level of consciousness]].<ref name="pmid1492717">{{cite journal| author=Grollier G, Burucoa C, Bonnin M, de Rautlin de La Roy Y| title=Identification and susceptibility testing for obligate anaerobic bacteria using a semi-automated API ATB plus system. | journal=Ann Biol Clin (Paris) | year= 1992 | volume= 50 | issue= 6-7 | pages= 393-7 | pmid=1492717 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1492717  }} </ref>
The patient is usually fatigued & looking ill due to the preexisting risk factor. In advanced cases with [[septicemia]], the patient may be drowsy with [[decreased level of consciousness]].<ref name="pmid1492717">{{cite journal| author=Grollier G, Burucoa C, Bonnin M, de Rautlin de La Roy Y| title=Identification and susceptibility testing for obligate anaerobic bacteria using a semi-automated API ATB plus system. | journal=Ann Biol Clin (Paris) | year= 1992 | volume= 50 | issue= 6-7 | pages= 393-7 | pmid=1492717 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1492717  }} </ref>
===Vital signs===
===Vital signs===
*[[Fever]]
*[[Fever]]<ref name="pmid15145849">{{cite journal |vauthors=Chikwe J, Barnard J, Pepper JR |title=Myocardial abscess |journal=Heart |volume=90 |issue=6 |pages=597 |date=June 2004 |pmid=15145849 |pmc=1768256 |doi=10.1136/hrt.2003.024646 |url=}}</ref>
*[[Tachycardia]]
*[[Tachycardia]]
*[[Tachypnea]]
*[[Tachypnea]]
*[[Hypotension]] (if patient is presenting with [[shock]])
*[[Hypotension]] (if patient is presenting with [[shock]])
===Chest Examination===
===Chest Examination===
*[[Chest tenderness]] is often present (localized).
*[[Chest]] [[tenderness]] is often present ([[localized]]).
*Alteration of heart sounds and murmurs (new-onset valvular regurgitation [100% of cases]) [12]
*Alteration of [[heart]] [[sound]]s and [[murmur]]s (new-onset [[valvular]] [[regurgitation]] [100% of cases])
 
===Lab Findings===
===Lab Findings===
*Complete blood cell count findings commonly are abnormal.
*[[Complete blood cell]] count findings commonly are abnormal.
*Anemia with normochromic normocytic red cell indices is present.  
*[[Anemia]] with [[normochromic normocytic red cell]] indices is present.  
*A low serum iron level is also observed. A low serum iron-binding capacity is observed in 70-90% of patients.
*A low [[serum]] [[iron]] level is also observed. A low [[serum]] [[iron-binding capacity]] is observed in 70-90% of patients.
*Anemia worsens with increased duration of illness.
*Anemia worsens with increased duration of illness.
*In subacute endocarditis, the white blood cell count is usually normal.  
*In [[subacute]] [[endocarditis]], the white blood cell count is usually normal.  
*In contrast, a leukocytosis with increased segmented granulocytes is common in acute endocarditis and myocardial abscess.
*In contrast, a [[leukocytosis]] with increased segmented [[granulocytes]] is common in acute [[endocarditis]] and [[myocardial]] [[abscess]].
*The erythrocyte sedimentation rate (ESR) is elevated (on average approximately 55 mm/h) in almost all patients with endocarditis and myocardial abscess; the exceptions are those with CHF, renal failure, or disseminated intravascular coagulation.
*The [[erythrocyte sedimentation rate]] ([[ESR]]) is elevated (on average approximately 55 mm/h) in almost all patients with endocarditis and myocardial abscess; the exceptions are those with [[CHF]], [[renal failure]], or disseminated intravascular [[coagulation]].
*Blood cultures are the crucial laboratory tests for confirming the diagnosis of the underlying endocarditis.
*[[Blood cultures]] are the crucial laboratory tests for confirming the diagnosis of the underlying [[endocarditis]].
*Urinalysis results are often abnormal, even when renal function remains normal. Proteinuria and microscopic hematuria are noted in 50% of patients. Urinalysis also plays a standard role in the evaluation of azotemia, which is frequently associated with myocardial abscess.
*[[Urinalysis]] results are often abnormal, even when [[renal]] function remains normal. [[Proteinuria]] and [[microscopic]] [[hematuria]] are noted in 50% of patients. [[Urinalysis]] also plays a standard role in the evaluation of [[azotemia]], which is frequently associated with [[myocardial]] [[abscess]]<ref name="pmid15145849">{{cite journal |vauthors=Chikwe J, Barnard J, Pepper JR |title=Myocardial abscess |journal=Heart |volume=90 |issue=6 |pages=597 |date=June 2004 |pmid=15145849 |pmc=1768256 |doi=10.1136/hrt.2003.024646 |url=}}</ref>.


==Radiological Findings==
==Radiological Findings==
*In the past, most cases of myocardial abscess were found during autopsy. however, detection of myocardial abscess can now be achieved antemortem using multiple noninvasive imaging modalities, including transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE), indium In 111 radionuclide scintigraphy, computed tomography (CT) scan, and magnetic resonance imaging (MRI).
*In the past, most cases of [[myocardial]] [[abscess]] were found during [[autopsy]]. however, detection of [[myocardial]] [[abscess]] can now be achieved antemortem using multiple [[noninvasive]] [[imaging]] modalities, including [[transthoracic echocardiography]] ([[TTE]]) and [[transesophageal echocardiography]] ([[TEE]]), [[indium]] In 111 [[radionuclide scintigraphy]], [[computed tomography]] ([[CT]]) [[scan]], and [[magnetic resonance imaging]] ([[MRI]]).


'''Chest radiography'''
'''[[Chest]] [[radiography]]'''
*chest radiography is perform to look for associated pulmonary infection.
*[[chest]] [[radiography]] is perform to look for associated [[pulmonary]] [[infection]].
Chest radiographic findings help assess for CHF.
*[[Chest]] [[radiographic]] findings help assess for [[CHF]].


'''Transthoracic echocardiography'''
'''[[Transthoracic echocardiography]]'''
*TTE helps evaluate patients in whom endocarditis or myocardial abscess is suggested clinically. Findings frequently allow the morphologic confirmation of infection and increasingly aid in making decisions regarding management.
*[[TTE]] helps evaluate patients in whom [[endocarditis]] or [[myocardial]] [[abscess]] is suggested clinically. Findings frequently allow the morphologic confirmation of infection and increasingly aid in making decisions regarding management.
*One must perform an echocardiographic evaluation in all patients suspected of having an intracardiac or pericardial infection, including those with negative blood culture findings.
*One must perform an [[echocardiographic]] evaluation in all patients suspected of having an intracardiac or [[pericardial infection]], including those with negative blood culture findings<ref name="pmid3389387">{{cite journal |vauthors=Zeineddin M, Stewart JA |title=Echocardiographic detection of non-valve-ring myocardial abscess complicating aortic valve endocarditis |journal=Am. J. Med. |volume=85 |issue=1 |pages=97–9 |date=July 1988 |pmid=3389387 |doi=10.1016/0002-9343(88)90510-4 |url=}}</ref>.
*TTE has a sensitivity of 23% and specificity of 98.6%.
*[[TTE]] has a sensitivity of 23% and specificity of 98.6%.
*According to Ellis et al (1985), the following 5 criteria are 86% sensitive and 88% specific for myocardial abscess: [13]
*According to Ellis et al (1985), the following 5 criteria are 86% sensitive and 88% specific for [[myocardial]] [[abscess]]:  
**Evidence of prosthetic valve rocking
**Evidence of [[prosthetic]] valve rocking
**Aneurysmal dilatation of the sinus of Valsalva
**[[Aneurysmal]] dilatation of the [[sinus]] of [[Valsalva]]
**Posterior aortic root thickness greater than 10 mm
**Posterior [[aortic root]] thickness greater than 10 mm
**Perivalvular density in the septum of greater than 14 mm
**[[Perivalvular]] density in the septum of greater than 14 mm
**The presence of "echo-free space" - Very specific but found relatively infrequently
**The presence of "echo-free space" - Very specific but found relatively infrequently
*Walker et al report a rare case of a myocardial abscess in valvular endocarditis that was difficult to assess with 2-dimensional TTE; however, real-time 3-dimensional contrast TTE allowed visualization of the full extent of the defect and its precise anatomical location, prior to successful surgical resection. [14]
*Walker et al report a rare case of a [[myocardial]] [[abscess]] in [[valvular]] [[endocarditis]] that was difficult to assess with 2-dimensional [[TTE]]; however, real-time 3-dimensional contrast [[TTE]] allowed [[visualization]] of the full extent of the defect and its precise [[anatomical]] location, prior to successful surgical resection.  


'''Transesophageal echocardiography'''
'''[[Transesophageal echocardiography]]'''
*Although many patients with NVE involving the aortic or mitral valve can be adequately assessed using TTE, TEE with color flow and continuous pulsed Doppler is the state-of-the-art technique. Doppler and color-flow Doppler or contrast 2-dimensional echocardiography helps optimally define fistulas and abscess pockets and extensions. See the image below.
*Although many patients with NVE involving the [[aortic]] or [[mitral valve]] can be adequately assessed using [[TTE]], [[TEE]] with color flow and continuous pulsed [[Doppler]] is the state-of-the-art technique. [[Doppler]] and color-flow Doppler or contrast 2-dimensional [[echocardiography]] helps optimally define fistulas and [[abscess]] pockets and extensions. See the image below.
*TEE has a sensitivity of 87% and specificity of 94.6%. Patients in whom an abscess is suggested but has not been detected using TEE should undergo MRI, including magnetic resonance angiography. ADD PIC
*[[TEE]] has a sensitivity of 87% and [[specificity]] of 94.6%. Patients in whom an [[abscess]] is suggested but has not been detected using [[TEE]] should undergo MRI, including [[magnetic resonance angiography]].<ref name="pmid17967599">{{cite journal |vauthors=Hill EE, Herijgers P, Claus P, Vanderschueren S, Peetermans WE, Herregods MC |title=Abscess in infective endocarditis: the value of transesophageal echocardiography and outcome: a 5-year study |journal=Am. Heart J. |volume=154 |issue=5 |pages=923–8 |date=November 2007 |pmid=17967599 |doi=10.1016/j.ahj.2007.06.028 |url=}}</ref>


'''Scintigraphy'''
'''[[Scintigraphy]]'''
*Indium In 111 leukocyte scintigraphy is especially useful in prosthetic valve endocarditis, in which echocardiography shows too much scatter.
*[[Indium]] In 111 [[leukocyte]] [[scintigraphy]] is especially useful in [[prosthetic]] [[valve]] [[endocarditis]], in which [[echocardiography]] shows too much scatter<ref name="pmid9735977">{{cite journal |vauthors=Campeau RJ, Ingram C |title=Perivalvular abscess complicating infective endocarditis: complementary role of echocardiography and indium-111-labeled leukocytes |journal=Clin Nucl Med |volume=23 |issue=9 |pages=582–4 |date=September 1998 |pmid=9735977 |doi=10.1097/00003072-199809000-00003 |url=}}</ref>.
*A few milliliters of venous blood is drawn and mixed with an anticoagulant solution. The white blood cells are separated and labeled with radioactive isotope111 In, centrifuged, resuspended in isotonic sodium chloride solution, and reinjected into the patient. Images are then obtained with a gamma-ray camera within 16-24 hours. *The viable radioactive leukocytes potentially accumulate in the areas of inflammation or abscess. Obtain oblique views to avoid overshadowing by sternal accumulation.
*A few milliliters of [[venous]] [[blood]] is drawn and mixed with an [[anticoagulant]] solution. The [[white blood cell]]s are separated and labeled with [[radioactive]] isotope111 In, centrifuged, resuspended in [[isotonic]] [[sodium chloride]] solution, and reinjected into the patient. Images are then obtained with a [[gamma-ray]] camera within 16-24 hours. *The viable [[radioactive]] [[leukocytes]] potentially accumulate in the areas of [[inflammation]] or [[abscess]]. Obtain oblique views to avoid overshadowing by sternal accumulation<ref name="pmid10230285">{{cite journal |vauthors=Ivancević V, Munz DL |title=Nuclear medicine imaging of endocarditis |journal=Q J Nucl Med |volume=43 |issue=1 |pages=93–9 |date=March 1999 |pmid=10230285 |doi= |url=}}</ref>.
*The need for111 In scintigraphy is very low if TEE is used.
*The need for111 In [[scintigraphy]] is very low if [[TEE]] is used.


'''MRI'''
'''[[MRI]]'''
*This is a good modality for helping delineate myocardial abscess. However, the portability and excellent resolution of echocardiography make it more practical than MRI.
*This is a good modality for helping delineate [[myocardial]] [[abscess]]. However, the portability and excellent resolution of [[echocardiography]] make it more practical than [[MRI]]<ref name="pmid12638334">{{cite journal |vauthors=Pasowicz M, Klimeczek P, Wicher-Muniak E, Podolec P, Kapelak B, Sadowski J, Tracz W |title=[Usefulness of magnetic resonance imaging in diagnosis of mitral valve anulus abscess--case report] |language=Polish |journal=Prz. Lek. |volume=59 |issue=8 |pages=623–5 |date=2002 |pmid=12638334 |doi= |url=}}</ref>.


'''CT scan'''
'''[[CT scan]]'''
*Only anecdotal reports of diagnosis are available. It is not very sensitive.
*Only anecdotal reports of diagnosis are available. It is not very sensitive<ref name="pmid11449169">{{cite journal |vauthors=Reynier C, Garcier J, Legault B, Motreff P, Ponsonnaille J, Ravel A, De Riberolles C, Boyer L |title=[Cross-sectional imaging of post endocarditis paravalvular myocardial abscesses of native mitral valves: 4 cases] |language=French |journal=J Radiol |volume=82 |issue=6 Pt 1 |pages=665–9 |date=June 2001 |pmid=11449169 |doi= |url=}}</ref>.


'''Intraoperative echocardiography'''
'''Intraoperative [[echocardiography]]'''
*Although invasive, small abscesses can be detected in the operating room by means of intraoperative echocardiography, which may enable the operating surgeon to drain the abscess effectively.
*Although invasive, small [[abscess]]es can be detected in the operating room by means of [[intraoperative]] [[echocardiography]], which may enable the operating [[surgeon]] to drain the [[abscess]] effectively.


==Other Diagnostic Studies==
==Other Diagnostic Studies==


'''Electrocardiography'''
'''Electrocardiography'''
*New-onset and persistent electrocardiographic conduction abnormalities may be observed. Gradual PR prolongation may be observed, and it may suggest development of valve ring abscess.
*New-onset and persistent [[electrocardiographic]] [[conduction]] abnormalities may be observed. Gradual [[PR]] prolongation may be observed, and it may suggest development of [[valve]] ring [[abscess]].
*Although not a sensitive indicator of perivalvular infection or abscess (28%), these findings are relatively specific (85-90%). See the image below.
*Although not a [[sensitive]] indicator of [[perivalvular]] [[infection]] or [[abscess]] (28%), these findings are relatively [[specific]] (85-90%)<ref name="pmid2028858">{{cite journal |vauthors=Akins EW, Slone RM, Wiechmann BN, Browning M, Martin TD, Mayfield WR |title=Perivalvular pseudoaneurysm complicating bacterial endocarditis: MR detection in five cases |journal=AJR Am J Roentgenol |volume=156 |issue=6 |pages=1155–8 |date=June 1991 |pmid=2028858 |doi=10.2214/ajr.156.6.2028858 |url=}}</ref>.


'''Tests of immune system stimulation'''
'''Tests of [[immune system]] stimulation'''
*Tests results may show disease activity, but the tests are costly and not very efficient for diagnosis or monitoring response to therapy
*Tests results may show disease activity, but the [[test]]s are costly and not very efficient for [[diagnosis]] or [[monitoring]] response to [[therapy]]
*These may include testing of circulating immune complexes, rheumatoid factor, quantitative immune globulin, cryoglobulins, and C-reactive protein.
*These may include testing of circulating [[immune complex]]es, [[rheumatoid factor]], quantitative [[immune globulin]], [[cryoglobulin]]s, and [[C-reactive protein]]<ref name="pmid10648113">{{cite journal |vauthors=Singh B |title=Stimulation of the developing immune system can prevent autoimmunity |journal=J. Autoimmun. |volume=14 |issue=1 |pages=15–22 |date=February 2000 |pmid=10648113 |doi=10.1006/jaut.1999.0349 |url=}}</ref>.


'''Serologic tests'''
'''[[Serologic]] tests'''
*Serological test findings are used to evaluate cardiac sepsis in which blood culture findings are negative.
*[[Serological]] test findings are used to evaluate [[cardiac]] [[sepsis]] in which [[blood culture]] findings are negative.
*Tests to detect antibodies to ribitol teichoic acids from staphylococci may help distinguish uncomplicated S aureus bacteremia from that associated with cardiac involvement.
*Tests to detect antibodies to [[ribitol teichoic acid]]s from [[staphylococci]] may help distinguish uncomplicated [[S aureus]] [[bacteremia]] from that associated with [[cardiac]] involvement.
*These tests have not been used in clinical applications because of their lack of adequate specificity or predictive value.
*These tests have not been used in [[clinical]] applications because of their lack of adequate [[specificity]] or [[predictive value]].


'''Procedures'''
'''Procedures'''
*Cardiac catheterization may add very little to the imaging studies and is not recommended unless coronary angiography is needed for patients undergoing valve surgery who also may have significant coronary artery disease.
*[[Cardiac]] [[catheterization]] may add very little to the [[imaging studies]] and is not recommended unless [[coronary angiography]] is needed for patients undergoing [[valve]] [[surgery]] who also may have significant [[coronary artery disease]].


==Treatment==
==Treatment==
'''Medical treatment'''
'''[[Medical]] [[treatment]]'''
*Intravenous antibiotics should be administered in a timely fashion once a patient is suspected of IE or a cardiac abscess. Empiric broad-spectrum antibiotics until further characterization of infective species should be monitored for at least 6 weeks of therapy in this patient population. [9]
*[[Intravenous]] [[antibiotic]]s should be administered in a timely fashion once a patient is suspected of [[IE]] or a [[cardiac]] [[abscess]]. [[Empiric]] broad-spectrum [[antibiotic]]s until further characterization of [[infective]] species should be monitored for at least 6 weeks of therapy in this patient [[population]]<ref name="pmid22176644">{{cite journal |vauthors=Yamamoto S, Hosokawa N, Sogi M, Inakaku M, Imoto K, Ohji G, Doi A, Iwabuchi S, Iwata K |title=Impact of infectious diseases service consultation on diagnosis of infective endocarditis |journal=Scand. J. Infect. Dis. |volume=44 |issue=4 |pages=270–5 |date=April 2012 |pmid=22176644 |doi=10.3109/00365548.2011.638317 |url=}}</ref><ref name="pmid1047088">{{cite journal |vauthors=Sande MA, Courtney KB |title=Nafcillin-gentamicin synergism in experimental staphylococcal endocarditis |journal=J. Lab. Clin. Med. |volume=88 |issue=1 |pages=118–24 |date=July 1976 |pmid=1047088 |doi= |url=}}</ref>.  


*Supportive treatment includes the following:
*Supportive [[treatment]] includes the following:
**Fluid and electrolyte balance
**[[Fluid]] and [[electrolyte]] balance
**Nutritional support
**[[Nutritional]] support


'''Surgical Treatment'''
'''[[Surgical]] [[Treatment]]'''
*Surgery consult and the time of surgical intervention is of high importance when approaching a patient with a cardiac abscess.  
*[[Surgery]] consult and the time of [[surgical]] [[intervention]] is of high importance when approaching a patient with a [[cardiac]] [[abscess]].  
*There is increased morbidity and mortality in patients in whom surgery is delayed. Thus early surgery is recommended. Surgery for these patients aims toward the eradication of the infection and correction of hemodynamic abnormalities.
*There is increased [[morbidity]] and [[mortality]] in patients in whom [[surgery]] is delayed. Thus early [[surgery]] is recommended. [[Surgery]] for these [[patient]]s aims toward the eradication of the [[infection]] and correction of [[hemodynamic]] abnormalities<ref name="pmid4009931">{{cite journal |vauthors=Arita M, Kusuyama Y, Takatsuji M, Kawazoe K, Masuyama Y |title=Septal myocardial abscess and infectious pericarditis in a case of bacterial endocarditis |journal=Jpn. Circ. J. |volume=49 |issue=4 |pages=451–5 |date=April 1985 |pmid=4009931 |doi=10.1253/jcj.49.451 |url=}}</ref>.
*However, some patients with periannular extension of infection or myocardial abscess could potentially be treated without surgical intervention. These patients include:
*However, some patients with [[periannular]] extension of [[infection]] or [[myocardial]] [[abscess]] could potentially be treated without [[surgical]] [[intervention]]. These patients include<ref name="pmid610417">{{cite journal |vauthors=Mildvan D, Goldberg E, Berger M, Altchek MR, Lukban SB |title=Diagnosis and successful management of septal myocardial abscess: a complication of bacterial endocarditis |journal=Am. J. Med. Sci. |volume=274 |issue=3 |pages=311–6 |date=1977 |pmid=610417 |doi=10.1097/00000441-197711000-00010 |url=}}</ref>:
**Patients with smaller (less than 1 cm) abscesses
**[[Patient]]s with smaller (less than 1 cm) [[abscess]]es
**Patients who do not have complications of heart block, an echocardiographic progression of abscess during antibiotic therapy
**[[Patient]]s who do not have [[complication]]s of [[heart block]], an [[echocardiographic]] progression of [[abscess]] during [[antibiotic]] [[therapy]]
**Patients who do not have valvular dehiscence or insufficiency
**[[Patient]]s who do not have [[valvular]] [[dehiscence]] or [[insufficiency]].
*It is recommended that patients who do not undergo surgery are monitored closely with serial TEE repeated at 2, 4, and 8 weeks after completion of antibiotic therapy.
*It is recommended that patients who do not undergo [[surgery]] are monitored closely with serial [[TEE]] repeated at 2, 4, and 8 weeks after completion of [[antibiotic]] [[therapy]].


==References==
==References==

Latest revision as of 21:25, 1 April 2020

Myocardial abscess
Myocardial abscess: Candida: Gross, natural color excellent depiction myocardial abscesses caused by Candida tropicalis. A 51yo man with acute monocytic leukemia.
Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohammed Salih, M.D. Syed Musadiq Ali M.B.B.S.[2]

overview

A cardiac abscess is a suppurative infection of the myocardium, endocardium, native or prosthetic valve tissue. Similar to other abscesses, it develops either by dissemination from a distant source such as bacteremia or sepsis or by direct extension of a pre-existing cardiac infective focus. Infective endocarditis has long been identified as the main cause of the latter. Although the incidence of cardiac abscesses continues to be investigated, it is presumably higher than noted postmortem and is of great importance when deciding the prognosis and management of patients. A single organism causes cardiac abscesses, usually Staphylococcus aureus or Escherichia coli. Less typically, polymicrobial abscesses have been noted. Important complications of a cardiac abscess, whether alone or with valve tissue, are conduction abnormalities on electrocardiogram (ECG). The incidence of perivalvular abscess among patients with infective endocarditis is between 30% to 40%, with the aortic valve having a higher predisposition than the mitral valve and annulus. Native aortic valve endocarditis, usually located in a weak part of the annulus near the atrioventricular node (AV), clearly demonstrates the anatomic predisposition and exemplifies why abscesses and heart block presents as frequent sequelae. Perivalvular abscesses are also more common with prosthetic valves. In this case, the annulus instead of the leaflet is usually the primary site of infection. The degree of conduction disruption, therefore, depends on the extent of the involvement of the conduction system and is more commonly seen in perivalvular aortic abscesses. Additionally, the severe extension of perivalvular infection can also result in extrinsic coronary compression, or disruption, leading to an acute coronary syndrome. Thus far, only aortic valve involvement and current IV drug use have been prospectively identified as independent risk factors for a perivalvular abscess. Any patient with a cardiac abscess, regardless of all other factors, has an increased risk of embolization, morbidity, and mortality. Prophylaxis remains a longstanding subject in the matter of prevention of IE or cardiac abscess. Thus far, prophylaxis is mostly based on observational studies and, in fact, places such as the United Kingdom no longer endorse antibiotic prophylaxis for dental procedures to prevent IE, the leading source of the cardiac abscess. One point against prophylaxis is the fact that tooth brushing has been proven to cause bacteremia and, therefore, makes it difficult to assess the rare versus high magnitude transient bacteremia and its effect on IE and its sequelae. For this reason, the United States and European countries have agreed that the use of prophylaxis is reserved only for those at "highest risk." On that same matter, the widespread use of antibiotics for the prevention and treatment of IE and abscesses could potentially create a setting where there will be an increased incidence of polymicrobial infection and antibiotic resistance, especially in immunocompromised patients.

Historical perspective

Pathophysiology

Myocardial abscess is a pus-containing infection of the endocardium, myocardium, prosthetic or native valves, perivalvular structures or the cardiac conduction system. [2] [3]

Pathogenesis

Post-mortem examination,of myocardial abscess, showed following pathological changes:

Macroscopic finding

  • The cardiac area was greatly enlarged, and when the pericardial sac was opened, it was found to contain 600 cc of partially clotted blood.
  • The parietal pericardium was blood tinged but smooth and glistening throughout [10] [11] [12] .
  • The epicardium was normal in appearance over the anterior aspect of the heart but glassy and coated with a thin layer of fibrinous exudate in the posterior aspect.
  • The tear involved the entire thickness of the myocardium so that a probe could be passed through it into the left ventricular cavity without resistance.
  • The surrounding myocardium was infiltrated by blood and flabby in consistence in an area about 6 cm in diameter.
  • Externally and on cut section this area displayed a variegated tinge from reddish brown to yellowish gray.
  • Clusters of honey-combed pockets, each pin head in size or larger, were scattered throughout this area.
  • Grossly, these pockets were suggestive of small abscesses and contained a thick, golden-yellow material.
  • The coronary arteries were diffusely narrowed, with atheroma formation and calcification.
  • The right coronary artery was occluded a short distance below its main stem by a firmly adherent, friable, yellowish-brown thrombotic mass.
  • Examination of the cardiac chambers revealed a laminated thrombus on the posterior aspect of the left ventricle[13].

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Microscopic finding

  • Myocardial infarct the microscopical sections showed an almost complete obliteration of the normal architecture[14] [15].
  • The muscle fibers displayed loss of striations and of nuclear patterns and seemed fused together into an amorphous mass of eosinophilic material.
  • The capillaries in the area were congested, and extravasated red cells were present throughout.
  • There was a concomitant marked infiltration of polymorphonuclear leukocytes either scattered or in clusters, and this extended into the epicardium.
  • The leukocytes were not well preserved; the majority were fused together or showed karyorrhexis and karyolysis resulting in a scattering of cellular débris.
  • The endocardial mural thrombus consisted of amorphous eosinophilic material and was interspersed with white cells and cellular débris.
  • The mural thrombus merged indistinctly into the adjacent necrotic myocardium.
  • The thrombotic mass in the lumen of the right coronary artery showed incipient organization with intimal histiocytic and fibroblastic proliferation and atheromatous changes[16].

Causes

Endocarditis

Bacteremia

Myocardial infarction

Other settings associated with myocardial abscesses that have been reported in the literature include the following:

Differential Diagnosis

Myocardial Abscess should be differentiated from other diseases presenting with fever, chest pain and anorxia. The differentials include the following:[24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43]

Diseases Diagnostic tests Physical Examination Symptoms Past medical history Other Findings
CT scan and MRI EKG Chest X-ray Tachypnea Tachycardia Fever Chest Pain Hemoptysis Dyspnea on Exertion Wheezing Chest Tenderness Nasalopharyngeal Ulceration Carotid Bruit
Pulmonary embolism
  • On CT angiography:
    • Intra-luminal filling defect
  • On MRI:
    • Narrowing of involved vessel
    • No contrast seen distal to obstruction
    • Polo-mint sign (partial filling defect surrounded by contrast)
 ✔ ✔ ✔ (Low grade) ✔ ✔ (In case of massive PE) ✔ - - - -
Infective Endocarditis ✔ ✔ ✔ - - ✔ - - - -
Non-Bacterial Thrombotic Endocarditis ✔ ✔ ✔ (Low grade) ✔ (Relieved by sitting up and leaning forward) - ✔ - - - -
Libman Sack Endocarditis ✔ ✔ ✔ ✔ - ✔ ✔ - - -
  • SLE
Vasculitis

Homogeneous, circumferential vessel wall swelling

✔ ✔ ✔ ✔ ✔ ✔ - ✔ ✔ ✔
Fever of unknown origin (FUO) ✔ ✔ - - - ✔ ✔ - - -

Epidemiology and Demographics

Risk Factors

Any septic focus can theoretically lead to myocardial abscess. These are the primary foci in order of frequency of causing myocardial abscess.

Spread from the urinary tract is the most common cause.
Spread from the gastrointestinal tract is the second common cause (e.g. perforated appendix, perforated colon cancer, diverticulitis ,and cohn’s disease.)
e.g. pott's disease or osteomyelitis
  • Hematogenous spread[47]
From distant septic foci.[48]


Any condition compromising the immune system is a risk factor for developing myocardial abscess. The following were the risk factors in observed patients. [49]

Screening

According to the USPSTF, screening for retroperitoneal abscess is not recommended.

Natural History, Complications and Prognosis:

Natural history

If left untreated, myocardial abscess may cause heart block, septal rupture with very high incidence of morbidity and mortality.

Complications :

The following are potential complications of myocardial abscess[20]:

Prognosis

Diagnosis

History

Symptoms

One must bear in mind certain constellations of symptoms that may raise the suggestion of myocardial abscess. For example, fever is the most common symptom, presenting in 80%-85% of patients. It is absent in some patients who are elderly; those who have CHF, severe debility, or chronic renal failure; and in patients with coagulase-negative staphylococcal infection and abscess. Another characteristic symptom is chills, which occurs in 42%-75% of cases[53].

Common symptoms:

Less common symptoms:

Physical Exam

General Appearance

Physical examination findings commonly encountered in myocardial abscess are mainly due to the underlying infective endocarditis. These include the following: Fever, Tachycardia, Murmur, especially changing or new murmur, Neurological abnormalities, Embolic event, Splenomegaly, Clubbing, Peripheral manifestations,Osler nodes, Splinter hemorrhages, Petechiae, Janeway lesions, Retinal lesions (Roth spots),Widening pulse pressure, especially with involvement of the aortic valve and progression of aortic regurgitation The patient is usually fatigued & looking ill due to the preexisting risk factor. In advanced cases with septicemia, the patient may be drowsy with decreased level of consciousness.[49]

Vital signs

Chest Examination

Lab Findings

Radiological Findings

Chest radiography

Transthoracic echocardiography

  • TTE helps evaluate patients in whom endocarditis or myocardial abscess is suggested clinically. Findings frequently allow the morphologic confirmation of infection and increasingly aid in making decisions regarding management.
  • One must perform an echocardiographic evaluation in all patients suspected of having an intracardiac or pericardial infection, including those with negative blood culture findings[21].
  • TTE has a sensitivity of 23% and specificity of 98.6%.
  • According to Ellis et al (1985), the following 5 criteria are 86% sensitive and 88% specific for myocardial abscess:
  • Walker et al report a rare case of a myocardial abscess in valvular endocarditis that was difficult to assess with 2-dimensional TTE; however, real-time 3-dimensional contrast TTE allowed visualization of the full extent of the defect and its precise anatomical location, prior to successful surgical resection.

Transesophageal echocardiography

Scintigraphy

MRI

CT scan

  • Only anecdotal reports of diagnosis are available. It is not very sensitive[59].

Intraoperative echocardiography

Other Diagnostic Studies

Electrocardiography

Tests of immune system stimulation

Serologic tests

Procedures

Treatment

Medical treatment

Surgical Treatment

References

  1. ↑ Kim JS, Kang MK, Cho AJ, Seo YB, Kim KI (May 2017). "Complicated infective endocarditis: a case series". J Med Case Rep. 11 (1): 128. doi:10.1186/s13256-017-1274-7. PMC 5423006. PMID 28482860.
  2. ↑ Tennant R, H.W. Parks: Myocardial abscesses. Arch Pathol 68,112-6 (1959)
  3. ↑ Narula J, B.A. Khaw, W. Dec, I.F. Palacios, J.F. Southern, J.T. Fallon, H.W. Strauss, E. Haber, T. Yasuda: Recognition of acute myocarditis masquerading as acute myocardial infarction. NEJM 328,100-4 (1993)
  4. ↑ Oliveira J, Santos M, Arnoni RT, Ramos A, Togna DD, Ghorayeb SK, Kroll R, Souza L (2018). "Mortality Predictors in the Surgical Treatment of Active Infective Endocarditis". Braz J Cardiovasc Surg. 33 (1): 32–39. doi:10.21470/1678-9741-2017-0132. PMC 5873776. PMID 29617499. Vancouver style error: initials (help)
  5. ↑ Howitt T: Remarkable case of abscess of the heart. Lancet 1, 684-685 (1846)
  6. ↑ Abela GS, B. Majmudar, J.M. Felner: Myocardial abscess unassociated with infective endocarditis. South Med J 74, 432-434 (1981)
  7. ↑ Howitt T: Remarkable case of abscess of the heart. Lancet 1, 684-685 (1846)
  8. ↑ Abela GS, B. Majmudar, J.M. Felner: Myocardial abscess unassociated with infective endocarditis. South Med J 74, 432-434 (1981)
  9. ↑ Saphir O: Myocarditis: A general review, with an analysis of two hundred and forty cases. Arch Pathol 32,1000-1051 (1941)
  10. ↑ Flaxman N: Myocardial abscess. JAMA 122, 804-806 (1943)
  11. ↑ Sanson J, S. Slodki, J.G. Gruhn: Myocardial abscesses. Am Heart J 66, 301-308 (1963)
  12. ↑ Weiss S, R.W. Wilkins: Myocardial abscess with perforation of the heart. Am J Med Sci 194,199-205 (1937)
  13. ↑ TEDESCHI CG, STEVENSON TD, LEVENSON HM (December 1950). "Abscess formation in myocardial infarction". N. Engl. J. Med. 243 (26): 1024–7. doi:10.1056/NEJM195012282432602. PMID 14785774.
  14. ↑ Bateman AC, M. Richards, A.P. Pallett. Fatal myocarditis associated with a Lancefield Group B Streptococcus. J Infect 36,354-5 (1998)
  15. ↑ Von Kurnatowski HA, J.L.Sierra-Callejas, W. Henkel: Foudroyant todlich verlaufende myokarditis durch streptokokken der gruppe B. Dtsch Med Wschr 103,439-41 (1977)
  16. ↑ Tedeschi CG, T.D. Stevenson, H.M. Levenson. Abscess formation in myocardial infarction. NEJM 243,1024-7 (1950)
  17. ↑ Saphir O: Meningococcus myocarditis. Am J Pathol 12,677-87 (1936)
  18. ↑ McCue MJ, E.E. Moore: Myocarditis with microabscess formation caused by Listeria monocytogenes associated with myocardial infarct. Human Pathol 10:469-72 (1979)
  19. ↑ Lewis JF: Myocardial infarction during pregnancy: With associated myocardial Bacteroides abscess. South Med J 66,379-1 (1973)
  20. ↑ 20.0 20.1 Ramos Tuarez FJ, Law MA. PMID 29083576. Missing or empty |title= (help)
  21. ↑ 21.0 21.1 Zeineddin M, Stewart JA (July 1988). "Echocardiographic detection of non-valve-ring myocardial abscess complicating aortic valve endocarditis". Am. J. Med. 85 (1): 97–9. doi:10.1016/0002-9343(88)90510-4. PMID 3389387.
  22. ↑ 22.0 22.1 Akins EW, Slone RM, Wiechmann BN, Browning M, Martin TD, Mayfield WR (June 1991). "Perivalvular pseudoaneurysm complicating bacterial endocarditis: MR detection in five cases". AJR Am J Roentgenol. 156 (6): 1155–8. doi:10.2214/ajr.156.6.2028858. PMID 2028858.
  23. ↑ Kim HS, Weilbaecher DG, Lie JT, Titus JL (July 1978). "Myocardial abscesses". Am. J. Clin. Pathol. 70 (1): 18–23. doi:10.1093/ajcp/70.1.18. PMID 696668.
  24. ↑ Brenes-Salazar JA (2014). "Westermark's and Palla's signs in acute and chronic pulmonary embolism: Still valid in the current computed tomography era". J Emerg Trauma Shock. 7 (1): 57–8. doi:10.4103/0974-2700.125645. PMC 3912657. PMID 24550636.
  25. ↑ "CT Angiography of Pulmonary Embolism: Diagnostic Criteria and Causes of Misdiagnosis | RadioGraphics".
  26. ↑ Bĕlohlávek J, Dytrych V, Linhart A (2013). "Pulmonary embolism, part I: Epidemiology, risk factors and risk stratification, pathophysiology, clinical presentation, diagnosis and nonthrombotic pulmonary embolism". Exp Clin Cardiol. 18 (2): 129–38. PMC 3718593. PMID 23940438.
  27. ↑ "Pulmonary Embolism: Symptoms - National Library of Medicine - PubMed Health".
  28. ↑ Ramani GV, Uber PA, Mehra MR (2010). "Chronic heart failure: contemporary diagnosis and management". Mayo Clin. Proc. 85 (2): 180–95. doi:10.4065/mcp.2009.0494. PMC 2813829. PMID 20118395.
  29. ↑ Blinderman CD, Homel P, Billings JA, Portenoy RK, Tennstedt SL (2008). "Symptom distress and quality of life in patients with advanced congestive heart failure". J Pain Symptom Manage. 35 (6): 594–603. doi:10.1016/j.jpainsymman.2007.06.007. PMC 2662445. PMID 18215495.
  30. ↑ Hawkins NM, Petrie MC, Jhund PS, Chalmers GW, Dunn FG, McMurray JJ (2009). "Heart failure and chronic obstructive pulmonary disease: diagnostic pitfalls and epidemiology". Eur. J. Heart Fail. 11 (2): 130–9. doi:10.1093/eurjhf/hfn013. PMC 2639415. PMID 19168510.
  31. ↑ Takasugi JE, Godwin JD (1998). "Radiology of chronic obstructive pulmonary disease". Radiol. Clin. North Am. 36 (1): 29–55. PMID 9465867.
  32. ↑ Wedzicha JA, Donaldson GC (2003). "Exacerbations of chronic obstructive pulmonary disease". Respir Care. 48 (12): 1204–13, discussion 1213–5. PMID 14651761.
  33. ↑ Nakawah MO, Hawkins C, Barbandi F (2013). "Asthma, chronic obstructive pulmonary disease (COPD), and the overlap syndrome". J Am Board Fam Med. 26 (4): 470–7. doi:10.3122/jabfm.2013.04.120256. PMID 23833163.
  34. ↑ Khandaker MH, Espinosa RE, Nishimura RA, Sinak LJ, Hayes SN, Melduni RM, Oh JK (2010). "Pericardial disease: diagnosis and management". Mayo Clin. Proc. 85 (6): 572–93. doi:10.4065/mcp.2010.0046. PMC 2878263. PMID 20511488.
  35. ↑ Bogaert J, Francone M (2013). "Pericardial disease: value of CT and MR imaging". Radiology. 267 (2): 340–56. doi:10.1148/radiol.13121059. PMID 23610095.
  36. ↑ Gharib AM, Stern EJ (2001). "Radiology of pneumonia". Med. Clin. North Am. 85 (6): 1461–91, x. PMID 11680112.
  37. ↑ Schmidt WA (2013). "Imaging in vasculitis". Best Pract Res Clin Rheumatol. 27 (1): 107–18. doi:10.1016/j.berh.2013.01.001. PMID 23507061.
  38. ↑ Suresh E (2006). "Diagnostic approach to patients with suspected vasculitis". Postgrad Med J. 82 (970): 483–8. doi:10.1136/pgmj.2005.042648. PMC 2585712. PMID 16891436.
  39. ↑ Stein PD, Dalen JE, McIntyre KM, Sasahara AA, Wenger NK, Willis PW (1975). "The electrocardiogram in acute pulmonary embolism". Prog Cardiovasc Dis. 17 (4): 247–57. PMID 123074.
  40. ↑ Warnier MJ, Rutten FH, Numans ME, Kors JA, Tan HL, de Boer A, Hoes AW, De Bruin ML (2013). "Electrocardiographic characteristics of patients with chronic obstructive pulmonary disease". COPD. 10 (1): 62–71. doi:10.3109/15412555.2012.727918. PMID 23413894.
  41. ↑ Stein PD, Matta F, Ekkah M, Saleh T, Janjua M, Patel YR, Khadra H (2012). "Electrocardiogram in pneumonia". Am. J. Cardiol. 110 (12): 1836–40. doi:10.1016/j.amjcard.2012.08.019. PMID 23000104.
  42. ↑ Hazebroek MR, Kemna MJ, Schalla S, Sanders-van Wijk S, Gerretsen SC, Dennert R, Merken J, Kuznetsova T, Staessen JA, Brunner-La Rocca HP, van Paassen P, Cohen Tervaert JW, Heymans S (2015). "Prevalence and prognostic relevance of cardiac involvement in ANCA-associated vasculitis: eosinophilic granulomatosis with polyangiitis and granulomatosis with polyangiitis". Int. J. Cardiol. 199: 170–9. doi:10.1016/j.ijcard.2015.06.087. PMID 26209947.
  43. ↑ Dennert RM, van Paassen P, Schalla S, Kuznetsova T, Alzand BS, Staessen JA, Velthuis S, Crijns HJ, Tervaert JW, Heymans S (2010). "Cardiac involvement in Churg-Strauss syndrome". Arthritis Rheum. 62 (2): 627–34. doi:10.1002/art.27263. PMID 20112390.
  44. ↑ Murdoch DR, Corey GR, Hoen B, Miró JM, Fowler VG, Bayer AS, Karchmer AW, Olaison L, Pappas PA, Moreillon P, Chambers ST, Chu VH, Falcó V, Holland DJ, Jones P, Klein JL, Raymond NJ, Read KM, Tripodi MF, Utili R, Wang A, Woods CW, Cabell CH (March 2009). "Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study". Arch. Intern. Med. 169 (5): 463–73. doi:10.1001/archinternmed.2008.603. PMC 3625651. PMID 19273776.
  45. ↑ Khan B, Strate RW, Hellman R (2007). "Myocardial abscess and fatal cardiac arrhythmia in a hemodialysis patient with an arterio-venous fistula infection". Semin Dial. 20 (5): 452–4. doi:10.1111/j.1525-139X.2007.00247.x. PMID 17897252.
  46. ↑ Smith RE, Martin JE, Mills PG (August 1989). "Myocardial abscess and sternal osteomyelitis following myocardial infarction and resuscitation". Postgrad Med J. 65 (766): 589–90. doi:10.1136/pgmj.65.766.589. PMC 2429504. PMID 2602260.
  47. ↑ Debelian GJ, Olsen I, Tronstad L (April 1994). "Systemic diseases caused by oral microorganisms". Endod Dent Traumatol. 10 (2): 57–65. doi:10.1111/j.1600-9657.1994.tb00061.x. PMID 8062808.
  48. ↑ Omran H, Reichel H, Wirtz P, Jung W, Rabahieh R, Pfeifer U, Pfeiffer D, Lüderitz B (February 1997). "[Septic myocardial aneurysm in mitral valve endocarditis. Clinical and pathological-anatomical findings]". Dtsch. Med. Wochenschr. (in German). 122 (6): 156–60. doi:10.1055/s-2008-1047590. PMID 9081801.
  49. ↑ 49.0 49.1 Grollier G, Burucoa C, Bonnin M, de Rautlin de La Roy Y (1992). "Identification and susceptibility testing for obligate anaerobic bacteria using a semi-automated API ATB plus system". Ann Biol Clin (Paris). 50 (6–7): 393–7. PMID 1492717.
  50. ↑ Shackcloth MJ, Dihmis WC (August 2001). "Contained rupture of a myocardial abscess in the free wall of the left ventricle". Ann. Thorac. Surg. 72 (2): 617–9. doi:10.1016/s0003-4975(00)02530-3. PMID 11515915.
  51. ↑ Grant R, Page S, Iyer A (March 2018). "Contained myocardial abscess following a myocardial infarction". J Card Surg. 33 (3): 144–145. doi:10.1111/jocs.13555. PMID 29526056.
  52. ↑ Borowski A, Korb H, Voth E, de Vivie ER (December 1988). "Asymptomatic myocardial abscess". Thorac Cardiovasc Surg. 36 (6): 338–40. doi:10.1055/s-2007-1022976. PMID 3232134.
  53. ↑ Crespo EP, Bertrán DV, Martínez CB, Foradada JT, Diz FW (April 2011). "[Myocardial abscess]". Med Clin (Barc) (in Spanish; Castilian). 136 (9): 415. doi:10.1016/j.medcli.2009.11.015. PMID 20149397.
  54. ↑ 54.0 54.1 54.2 Chikwe J, Barnard J, Pepper JR (June 2004). "Myocardial abscess". Heart. 90 (6): 597. doi:10.1136/hrt.2003.024646. PMC 1768256. PMID 15145849.
  55. ↑ Hill EE, Herijgers P, Claus P, Vanderschueren S, Peetermans WE, Herregods MC (November 2007). "Abscess in infective endocarditis: the value of transesophageal echocardiography and outcome: a 5-year study". Am. Heart J. 154 (5): 923–8. doi:10.1016/j.ahj.2007.06.028. PMID 17967599.
  56. ↑ Campeau RJ, Ingram C (September 1998). "Perivalvular abscess complicating infective endocarditis: complementary role of echocardiography and indium-111-labeled leukocytes". Clin Nucl Med. 23 (9): 582–4. doi:10.1097/00003072-199809000-00003. PMID 9735977.
  57. ↑ Ivancević V, Munz DL (March 1999). "Nuclear medicine imaging of endocarditis". Q J Nucl Med. 43 (1): 93–9. PMID 10230285.
  58. ↑ Pasowicz M, Klimeczek P, Wicher-Muniak E, Podolec P, Kapelak B, Sadowski J, Tracz W (2002). "[Usefulness of magnetic resonance imaging in diagnosis of mitral valve anulus abscess--case report]". Prz. Lek. (in Polish). 59 (8): 623–5. PMID 12638334.
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  61. ↑ Yamamoto S, Hosokawa N, Sogi M, Inakaku M, Imoto K, Ohji G, Doi A, Iwabuchi S, Iwata K (April 2012). "Impact of infectious diseases service consultation on diagnosis of infective endocarditis". Scand. J. Infect. Dis. 44 (4): 270–5. doi:10.3109/00365548.2011.638317. PMID 22176644.
  62. ↑ Sande MA, Courtney KB (July 1976). "Nafcillin-gentamicin synergism in experimental staphylococcal endocarditis". J. Lab. Clin. Med. 88 (1): 118–24. PMID 1047088.
  63. ↑ Arita M, Kusuyama Y, Takatsuji M, Kawazoe K, Masuyama Y (April 1985). "Septal myocardial abscess and infectious pericarditis in a case of bacterial endocarditis". Jpn. Circ. J. 49 (4): 451–5. doi:10.1253/jcj.49.451. PMID 4009931.
  64. ↑ Mildvan D, Goldberg E, Berger M, Altchek MR, Lukban SB (1977). "Diagnosis and successful management of septal myocardial abscess: a complication of bacterial endocarditis". Am. J. Med. Sci. 274 (3): 311–6. doi:10.1097/00000441-197711000-00010. PMID 610417.


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