Left ventricular aneurysm overview: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Left ventricular aneurysm}} | {{Left ventricular aneurysm}} | ||
{{CMG}} | {{CMG}};{{AE}}{{MehdiP}} | ||
== | ==Historical perspective== | ||
Left ventricular aneurysm ( | *John and William Hunter, Britanian vascular surgeons first described the aneurysm in 1880. | ||
*In 1967, Gorlin and colleagues reported that a strong suspicion of aneurysm could be obtained in 75% of patients with myocardial infarction.<ref name="pmid6024720">{{cite journal |vauthors=Gorlin R, Klein MD, Sullivan JM |title=Prospective correlative study of ventricular aneurysm. Mechanistic concept and clinical recognition |journal=Am. J. Med. |volume=42 |issue=4 |pages=512–31 |year=1967 |pmid=6024720 |doi= |url=}}</ref> | |||
==Classification== | |||
Based on the wall nature and its components, left ventricular aneurysms are classified as ''true'' or ''false [[aneurysm|aneurysms]]''.<ref name="pmid18809796">{{cite journal |vauthors=Maron MS, Finley JJ, Bos JM, Hauser TH, Manning WJ, Haas TS, Lesser JR, Udelson JE, Ackerman MJ, Maron BJ |title=Prevalence, clinical significance, and natural history of left ventricular apical aneurysms in hypertrophic cardiomyopathy |journal=Circulation |volume=118 |issue=15 |pages=1541–9 |year=2008 |pmid=18809796 |doi=10.1161/CIRCULATIONAHA.108.781401 |url=}}</ref> | |||
===True Left Ventricular Aneurysm=== | |||
A true left ventricular aneurysm has an aneurysmal sac which contains the [[endocardium]], [[epicardium]], and thinned fibrous tissue ([[scar]]) that is a remnant of the left ventricular muscle. | |||
===False Left Ventricular Aneurysm or Pseudoaneurysm=== | |||
Unlike a true [[aneurysm]], which contains some [[myocardial]] elements in its wall, the walls of a false aneurysm are composed of organized [[hematoma]] and [[pericardium]] and lack any element of the original myocardial wall. | |||
==Pathophysiology== | |||
Aneurysm forms when intraventricular tension stretches the noncontracting infarcted heart muscle, producing expansion of the thin layer of necrotic muscle and fibrous tissue that bulges with each cardiac contraction. The wall of a mature aneurysm is a white fibrous scar. It becomes more densely fibrotic as the time passages, but bulges outward with each cardiac contraction and causes some of the left ventricular stroke volume to be ineffective. On microscopic histopathological analysis, hyalinized fibrous tissue is the predominant finding. It usually takes 1 month for fibrous tissue to form. <ref name="pmid6024720">{{cite journal |vauthors=Gorlin R, Klein MD, Sullivan JM |title=Prospective correlative study of ventricular aneurysm. Mechanistic concept and clinical recognition |journal=Am. J. Med. |volume=42 |issue=4 |pages=512–31 |year=1967 |pmid=6024720 |doi= |url=}}</ref><ref name="pmid5842520">{{cite journal |vauthors=Dubnow MH, Burchell HB, Titus JL |title=Postinfarction ventricular aneurysm. A clinicomorphologic and electrocardiographic study of 80 cases |journal=Am. Heart J. |volume=70 |issue=6 |pages=753–60 |year=1965 |pmid=5842520 |doi= |url=}}</ref> | |||
==Causes== | |||
[[Myocardial infarction]] is the most common cause of Left ventricular (LV) aneurysm formation. Less common causes include [[Hypertrophic cardiomyopathy|HCM]], [[trauma]], and [[idiopathic]] and [[Congenital disorder|congenital abnormalities]].<ref>{{cite book | last = Mann | first = Douglas | title = Braunwald's heart disease : a textbook of cardiovascular medicine | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2015 | isbn = 978-1455751341 }}</ref> | |||
Other less common causes include:<ref name="pmid24674752">{{cite journal |vauthors=Ichida M, Nishimura Y, Kario K |title=Clinical significance of left ventricular apical aneurysms in hypertrophic cardiomyopathy patients: the role of diagnostic electrocardiography |journal=J Cardiol |volume=64 |issue=4 |pages=265–72 |year=2014 |pmid=24674752 |doi=10.1016/j.jjcc.2014.02.011 |url=}}</ref><ref name="pmid18809796">{{cite journal |vauthors=Maron MS, Finley JJ, Bos JM, Hauser TH, Manning WJ, Haas TS, Lesser JR, Udelson JE, Ackerman MJ, Maron BJ |title=Prevalence, clinical significance, and natural history of left ventricular apical aneurysms in hypertrophic cardiomyopathy |journal=Circulation |volume=118 |issue=15 |pages=1541–9 |year=2008 |pmid=18809796 |doi=10.1161/CIRCULATIONAHA.108.781401 |url=}}</ref><ref name="pmid20087451">{{cite journal |vauthors=Xia S, Wu B, Zhang X, Hu X |title=Left ventricular aneurysm in patients with idiopathic dilated cardiomyopathy: clinical analysis of six cases |journal=Neth Heart J |volume=17 |issue=12 |pages=475–80 |year=2009 |pmid=20087451 |pmc=2804080 |doi= |url=}}</ref> | |||
==Differential diagnosis== | |||
True LV aneurysm must be differentiated from false aneurysms.<ref name="pmid17053370">{{cite journal |vauthors=Cho MN, Mehta SK, Matulevicius S, Weinstein D, Wait MA, McGuire DK |title=Differentiating true versus pseudo left ventricular aneurysm: a case report and review of diagnostic strategies |journal=Cardiol Rev |volume=14 |issue=6 |pages=e27–30 |year=2006 |pmid=17053370 |doi=10.1097/01.crd.0000233756.66532.45 |url=}}</ref> <ref name="pmid21224951">{{cite journal |vauthors=Makkuni P, Kotler MN, Figueredo VM |title=Diverticular and aneurysmal structures of the left ventricle in adults: report of a case within the context of a literature review |journal=Tex Heart Inst J |volume=37 |issue=6 |pages=699–705 |year=2010 |pmid=21224951 |pmc=3014120 |doi= |url=}}</ref> | |||
==Epidemiology== | |||
It was estimated that LV aneurysm develops in 30%-35% of patients with Q wave MI. But it has been decreased significantly due to introduction of improvements in the management of patients with acute MI.<ref name="pmid8452458">{{cite journal |vauthors=Mills NL, Everson CT, Hockmuth DR |title=Technical advances in the treatment of left ventricular aneurysm |journal=Ann. Thorac. Surg. |volume=55 |issue=3 |pages=792–800 |year=1993 |pmid=8452458 |doi= |url=}}</ref> Currently it is estimated that true left ventricular aneurysms develop in less than 5% of all patients with STEMI.<ref name="pmid19145116">{{cite journal |vauthors=Napodano M, Tarantini G, Ramondo A, Cacciavillani L, Corbetti F, Marra MP, Fraccaro C, Peluso D, Razzolini R, Iliceto S |title=Myocardial abnormalities underlying persistent ST-segment elevation after anterior myocardial infarction |journal=J Cardiovasc Med (Hagerstown) |volume=10 |issue=1 |pages=44–50 |year=2009 |pmid=19145116 |doi=10.2459/JCM.0b013e32831967b2 |url=}}</ref> | |||
According to this report, the use of thrombolytic agents has decreased the incidence of LV aneurysm from 18.8% to 7.2%.<ref name="pmid19145116">{{cite journal |vauthors=Napodano M, Tarantini G, Ramondo A, Cacciavillani L, Corbetti F, Marra MP, Fraccaro C, Peluso D, Razzolini R, Iliceto S |title=Myocardial abnormalities underlying persistent ST-segment elevation after anterior myocardial infarction |journal=J Cardiovasc Med (Hagerstown) |volume=10 |issue=1 |pages=44–50 |year=2009 |pmid=19145116 |doi=10.2459/JCM.0b013e32831967b2 |url=}}</ref> | |||
==Risk Factors== | |||
The most potent risk factor for development of the LV aneurysm is '''[[ST elevation myocardial infarction|ST elevation MI]]'''. Other risk factors include:<ref name="pmid19145116">{{cite journal |vauthors=Napodano M, Tarantini G, Ramondo A, Cacciavillani L, Corbetti F, Marra MP, Fraccaro C, Peluso D, Razzolini R, Iliceto S |title=Myocardial abnormalities underlying persistent ST-segment elevation after anterior myocardial infarction |journal=J Cardiovasc Med (Hagerstown) |volume=10 |issue=1 |pages=44–50 |year=2009 |pmid=19145116 |doi=10.2459/JCM.0b013e32831967b2 |url=}}</ref><ref name="pmid18809796">{{cite journal |vauthors=Maron MS, Finley JJ, Bos JM, Hauser TH, Manning WJ, Haas TS, Lesser JR, Udelson JE, Ackerman MJ, Maron BJ |title=Prevalence, clinical significance, and natural history of left ventricular apical aneurysms in hypertrophic cardiomyopathy |journal=Circulation |volume=118 |issue=15 |pages=1541–9 |year=2008 |pmid=18809796 |doi=10.1161/CIRCULATIONAHA.108.781401 |url=}}</ref><ref name="pmid4812079">{{cite journal |vauthors=Bulkley BH, Roberts WC |title=Steroid therapy during acute myocardial infarction. A cause of delayed healing and of ventricular aneurysm |journal=Am. J. Med. |volume=56 |issue=2 |pages=244–50 |year=1974 |pmid=4812079 |doi= |url=}}</ref><ref name="pmid5659397">{{cite journal |vauthors=Mourdjinis A, Olsen E, Raphael MJ, Mounsey JP |title=Clinical diagnosis and prognosis of ventricular aneurysm |journal=Br Heart J |volume=30 |issue=4 |pages=497–513 |year=1968 |pmid=5659397 |pmc=487659 |doi= |url=}}</ref> | |||
*[[Hypertrophic cardiomyopathy]] (HCM) | |||
*[[Dilated cardiomyopathy]] (DCM) | |||
*Advanced age | |||
*[[Hypertension]] | |||
*Use of [[corticosteroids]] | |||
==Screening== | |||
Clue for diagnosis LV aneurysm after MI is, persistant ST elevation without chest pain and there is no recommendation to screen patients for LV aneurysm. | |||
==Natural History== | |||
If left untreated it may lead to heart failure and persistent anginal pain. For false aneurysms rupture and hemodynamic compromise are the outcomes if left untreated. Improvements in STEMI management, control of hypertension and avoidance of corticosteroids in STEMI have led to better prognosis and decreased mortality.<ref name="pmid5659397">{{cite journal |vauthors=Mourdjinis A, Olsen E, Raphael MJ, Mounsey JP |title=Clinical diagnosis and prognosis of ventricular aneurysm |journal=Br Heart J |volume=30 |issue=4 |pages=497–513 |year=1968 |pmid=5659397 |pmc=487659 |doi= |url=}}</ref> | |||
==Complications== | |||
Mural thrombosis, heart failure, persistent angina and arrhythmia are it's major complications. | |||
==Symptoms== | |||
Symptoms of aneurysm depend on it's size. Small and medium sized are usually asymptomatic but large size aneurysms may present as persistent chest pain and dyspnea despite the proper treatment of underlying cardiac condition. | |||
==Physical exam== | |||
Physical findings on cardiac examination in patients with LV aneurysms include diffuse displaced apical impulse, S3 and/or S4 heart sounds and mitral regurgitation murmur. | |||
==Electrocardiography== | |||
Persistent ST elevation is suggestive finding for LV aneurysm.<ref name="pmid5659397">{{cite journal |vauthors=Mourdjinis A, Olsen E, Raphael MJ, Mounsey JP |title=Clinical diagnosis and prognosis of ventricular aneurysm |journal=Br Heart J |volume=30 |issue=4 |pages=497–513 |year=1968 |pmid=5659397 |pmc=487659 |doi= |url=}}</ref> | |||
==Chest X ray== | |||
A bulge of the silhouette of the left ventricle on chest x-ray is the characteristic finding for LV aneurysm. <ref name="pmid5659397">{{cite journal |vauthors=Mourdjinis A, Olsen E, Raphael MJ, Mounsey JP |title=Clinical diagnosis and prognosis of ventricular aneurysm |journal=Br Heart J |volume=30 |issue=4 |pages=497–513 |year=1968 |pmid=5659397 |pmc=487659 |doi= |url=}}</ref> | |||
==CT scan== | |||
Chest CT scan with or without contrast may reveal the size and the location of LV aneurysm also, it can show the presence of calcification on it. | |||
==MRI== | |||
Cardiac MRI is helpful to diagnose LV aneurysm and may be emerging as the preferred noninvasive technique for the preoperative assessment of LV shape, thinning, and resectability.<ref name="pmid21907357">{{cite journal |vauthors=Hüther J, Doenst T, Nitzsche S, Thiele H, Mohr FW, Gutberlet M |title=Cardiac magnetic resonance imaging for the assessment of ventricular function, geometry, and viability before and after surgical ventricular reconstruction |journal=J. Thorac. Cardiovasc. Surg. |volume=142 |issue=6 |pages=1515–22.e1 |year=2011 |pmid=21907357 |doi=10.1016/j.jtcvs.2011.04.040 |url=}}</ref> | |||
==Echocardiography== | |||
*Echocardiography is the modality of choice for diagnosis LV aneurysm. <ref name="pmid6731299">{{cite journal |vauthors=Arvan S, Varat MA |title=Persistent ST-segment elevation and left ventricular wall abnormalities: a 2-dimensional echocardiographic study |journal=Am. J. Cardiol. |volume=53 |issue=11 |pages=1542–6 |year=1984 |pmid=6731299 |doi= |url=}}</ref><ref name="pmid3159507">{{cite journal |vauthors=Matsumoto M, Watanabe F, Goto A, Hamano Y, Yasui K, Minamino T, Abe H, Kamada T |title=Left ventricular aneurysm and the prediction of left ventricular enlargement studied by two-dimensional echocardiography: quantitative assessment of aneurysm size in relation to clinical course |journal=Circulation |volume=72 |issue=2 |pages=280–6 |year=1985 |pmid=3159507 |doi= |url=}}</ref> | |||
*It can measure size and location of aneurysm however, it is helpful to distinguish true from false aneurysms based on the mouth size. | |||
*Echocardiography is useful to diagnose dyskinesia or akinesia during systole. | |||
*Echocardiography is helpful to diagnose mural thrombosis in aneurysm sac. | |||
*Color flow echocardiography is helpful to establish the diagnosis based on ''in and out'' flow in aneurysm. | |||
==Medical Therapy== | |||
Medical therapy is indicated for small and medium sized LV aneurysms. It is based on decreasing cardiac work load (afterload reduction), anti ischemic therapy for [[chest pain]] and [[Anti coagulation therapy|anti coagulation]] if [[Thrombosis|mural thrombosis]] exist.<ref name="brawn">{{cite book | last = Mann | first = Douglas | title = Braunwald's heart disease : a textbook of cardiovascular medicine | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2015 | isbn = 978-1455751341 }}</ref> | |||
*[[Afterload]] reduction: | |||
:[[ACE inhibitor|ACE inhibitors]] are the drug of choice for decreasing the [[afterload]]. | |||
*Anti ischemic therapy: | |||
:Many medications can be used to treat underlying ischemic event as well as decreasing ischemic burden including:<ref name="brawn">{{cite book | last = Mann | first = Douglas | title = Braunwald's heart disease : a textbook of cardiovascular medicine | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2015 | isbn = 978-1455751341 }}</ref> | |||
:'''[[Chronic stable angina nitrate therapy|Nitrates]] | [[Chronic stable angina beta blocker therapy|Beta Blockers]] | [[Chronic stable angina treatment calcium channel blockers|Calcium Channel Blockers]] | [[Chronic stable angina treatment potassium channel openers|Potassium Channel Openers]] | [[Chronic stable angina newer antianginal agents|Newer Anti-anginal Agents]]''' | |||
==Surgery== | |||
*Surgical aneurysmectomy is recommended for large symptomatic aneurysms that caused angina pectoris or heart failure. Appropriate CABG is indicated at the time of aneurysmectomy.<ref>{{cite book | last = Kouchoukos | first = Nicholas | title = Kirklin/Barratt-Boyes cardiac surgery : morphology, diagnostic criteria, natural history, techniques, results, and indications | publisher = Elsevier/Saunders | location = Philadelphia | year = 2013 | isbn = 978-1416063919 }}</ref> | |||
*Another indication for surgical intervention is in patients who can not tolerate long term anticoagulation therapy.<ref name="pmid15289388">{{cite journal |vauthors=Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, Hochman JS, Krumholz HM, Kushner FG, Lamas GA, Mullany CJ, Ornato JP, Pearle DL, Sloan MA, Smith SC, Alpert JS, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK |title=ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction) |journal=Circulation |volume=110 |issue=5 |pages=588–636 |year=2004 |pmid=15289388 |doi=10.1161/01.CIR.0000134791.68010.FA |url=}}</ref> | |||
==References== | ==References== | ||
Revision as of 19:24, 9 November 2016
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Left ventricular aneurysm Microchapters |
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Differentiating Left ventricular aneurysm from other Diseases |
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Diagnosis |
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Treatment |
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Case Studies |
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Left ventricular aneurysm overview On the Web |
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American Roentgen Ray Society Images of Left ventricular aneurysm overview |
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Risk calculators and risk factors for Left ventricular aneurysm overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]
Historical perspective
- John and William Hunter, Britanian vascular surgeons first described the aneurysm in 1880.
- In 1967, Gorlin and colleagues reported that a strong suspicion of aneurysm could be obtained in 75% of patients with myocardial infarction.[1]
Classification
Based on the wall nature and its components, left ventricular aneurysms are classified as true or false aneurysms.[2]
True Left Ventricular Aneurysm
A true left ventricular aneurysm has an aneurysmal sac which contains the endocardium, epicardium, and thinned fibrous tissue (scar) that is a remnant of the left ventricular muscle.
False Left Ventricular Aneurysm or Pseudoaneurysm
Unlike a true aneurysm, which contains some myocardial elements in its wall, the walls of a false aneurysm are composed of organized hematoma and pericardium and lack any element of the original myocardial wall.
Pathophysiology
Aneurysm forms when intraventricular tension stretches the noncontracting infarcted heart muscle, producing expansion of the thin layer of necrotic muscle and fibrous tissue that bulges with each cardiac contraction. The wall of a mature aneurysm is a white fibrous scar. It becomes more densely fibrotic as the time passages, but bulges outward with each cardiac contraction and causes some of the left ventricular stroke volume to be ineffective. On microscopic histopathological analysis, hyalinized fibrous tissue is the predominant finding. It usually takes 1 month for fibrous tissue to form. [1][3]
Causes
Myocardial infarction is the most common cause of Left ventricular (LV) aneurysm formation. Less common causes include HCM, trauma, and idiopathic and congenital abnormalities.[4] Other less common causes include:[5][2][6]
Differential diagnosis
True LV aneurysm must be differentiated from false aneurysms.[7] [8]
Epidemiology
It was estimated that LV aneurysm develops in 30%-35% of patients with Q wave MI. But it has been decreased significantly due to introduction of improvements in the management of patients with acute MI.[9] Currently it is estimated that true left ventricular aneurysms develop in less than 5% of all patients with STEMI.[10] According to this report, the use of thrombolytic agents has decreased the incidence of LV aneurysm from 18.8% to 7.2%.[10]
Risk Factors
The most potent risk factor for development of the LV aneurysm is ST elevation MI. Other risk factors include:[10][2][11][12]
- Hypertrophic cardiomyopathy (HCM)
- Dilated cardiomyopathy (DCM)
- Advanced age
- Hypertension
- Use of corticosteroids
Screening
Clue for diagnosis LV aneurysm after MI is, persistant ST elevation without chest pain and there is no recommendation to screen patients for LV aneurysm.
Natural History
If left untreated it may lead to heart failure and persistent anginal pain. For false aneurysms rupture and hemodynamic compromise are the outcomes if left untreated. Improvements in STEMI management, control of hypertension and avoidance of corticosteroids in STEMI have led to better prognosis and decreased mortality.[12]
Complications
Mural thrombosis, heart failure, persistent angina and arrhythmia are it's major complications.
Symptoms
Symptoms of aneurysm depend on it's size. Small and medium sized are usually asymptomatic but large size aneurysms may present as persistent chest pain and dyspnea despite the proper treatment of underlying cardiac condition.
Physical exam
Physical findings on cardiac examination in patients with LV aneurysms include diffuse displaced apical impulse, S3 and/or S4 heart sounds and mitral regurgitation murmur.
Electrocardiography
Persistent ST elevation is suggestive finding for LV aneurysm.[12]
Chest X ray
A bulge of the silhouette of the left ventricle on chest x-ray is the characteristic finding for LV aneurysm. [12]
CT scan
Chest CT scan with or without contrast may reveal the size and the location of LV aneurysm also, it can show the presence of calcification on it.
MRI
Cardiac MRI is helpful to diagnose LV aneurysm and may be emerging as the preferred noninvasive technique for the preoperative assessment of LV shape, thinning, and resectability.[13]
Echocardiography
- Echocardiography is the modality of choice for diagnosis LV aneurysm. [14][15]
- It can measure size and location of aneurysm however, it is helpful to distinguish true from false aneurysms based on the mouth size.
- Echocardiography is useful to diagnose dyskinesia or akinesia during systole.
- Echocardiography is helpful to diagnose mural thrombosis in aneurysm sac.
- Color flow echocardiography is helpful to establish the diagnosis based on in and out flow in aneurysm.
Medical Therapy
Medical therapy is indicated for small and medium sized LV aneurysms. It is based on decreasing cardiac work load (afterload reduction), anti ischemic therapy for chest pain and anti coagulation if mural thrombosis exist.[16]
- Afterload reduction:
- ACE inhibitors are the drug of choice for decreasing the afterload.
- Anti ischemic therapy:
- Many medications can be used to treat underlying ischemic event as well as decreasing ischemic burden including:[16]
- Nitrates | Beta Blockers | Calcium Channel Blockers | Potassium Channel Openers | Newer Anti-anginal Agents
Surgery
- Surgical aneurysmectomy is recommended for large symptomatic aneurysms that caused angina pectoris or heart failure. Appropriate CABG is indicated at the time of aneurysmectomy.[17]
- Another indication for surgical intervention is in patients who can not tolerate long term anticoagulation therapy.[18]
References
- ↑ 1.0 1.1 Gorlin R, Klein MD, Sullivan JM (1967). "Prospective correlative study of ventricular aneurysm. Mechanistic concept and clinical recognition". Am. J. Med. 42 (4): 512–31. PMID 6024720.
- ↑ 2.0 2.1 2.2 Maron MS, Finley JJ, Bos JM, Hauser TH, Manning WJ, Haas TS, Lesser JR, Udelson JE, Ackerman MJ, Maron BJ (2008). "Prevalence, clinical significance, and natural history of left ventricular apical aneurysms in hypertrophic cardiomyopathy". Circulation. 118 (15): 1541–9. doi:10.1161/CIRCULATIONAHA.108.781401. PMID 18809796.
- ↑ Dubnow MH, Burchell HB, Titus JL (1965). "Postinfarction ventricular aneurysm. A clinicomorphologic and electrocardiographic study of 80 cases". Am. Heart J. 70 (6): 753–60. PMID 5842520.
- ↑ Mann, Douglas (2015). Braunwald's heart disease : a textbook of cardiovascular medicine. Philadelphia, PA: Elsevier/Saunders. ISBN 978-1455751341.
- ↑ Ichida M, Nishimura Y, Kario K (2014). "Clinical significance of left ventricular apical aneurysms in hypertrophic cardiomyopathy patients: the role of diagnostic electrocardiography". J Cardiol. 64 (4): 265–72. doi:10.1016/j.jjcc.2014.02.011. PMID 24674752.
- ↑ Xia S, Wu B, Zhang X, Hu X (2009). "Left ventricular aneurysm in patients with idiopathic dilated cardiomyopathy: clinical analysis of six cases". Neth Heart J. 17 (12): 475–80. PMC 2804080. PMID 20087451.
- ↑ Cho MN, Mehta SK, Matulevicius S, Weinstein D, Wait MA, McGuire DK (2006). "Differentiating true versus pseudo left ventricular aneurysm: a case report and review of diagnostic strategies". Cardiol Rev. 14 (6): e27–30. doi:10.1097/01.crd.0000233756.66532.45. PMID 17053370.
- ↑ Makkuni P, Kotler MN, Figueredo VM (2010). "Diverticular and aneurysmal structures of the left ventricle in adults: report of a case within the context of a literature review". Tex Heart Inst J. 37 (6): 699–705. PMC 3014120. PMID 21224951.
- ↑ Mills NL, Everson CT, Hockmuth DR (1993). "Technical advances in the treatment of left ventricular aneurysm". Ann. Thorac. Surg. 55 (3): 792–800. PMID 8452458.
- ↑ 10.0 10.1 10.2 Napodano M, Tarantini G, Ramondo A, Cacciavillani L, Corbetti F, Marra MP, Fraccaro C, Peluso D, Razzolini R, Iliceto S (2009). "Myocardial abnormalities underlying persistent ST-segment elevation after anterior myocardial infarction". J Cardiovasc Med (Hagerstown). 10 (1): 44–50. doi:10.2459/JCM.0b013e32831967b2. PMID 19145116.
- ↑ Bulkley BH, Roberts WC (1974). "Steroid therapy during acute myocardial infarction. A cause of delayed healing and of ventricular aneurysm". Am. J. Med. 56 (2): 244–50. PMID 4812079.
- ↑ 12.0 12.1 12.2 12.3 Mourdjinis A, Olsen E, Raphael MJ, Mounsey JP (1968). "Clinical diagnosis and prognosis of ventricular aneurysm". Br Heart J. 30 (4): 497–513. PMC 487659. PMID 5659397.
- ↑ Hüther J, Doenst T, Nitzsche S, Thiele H, Mohr FW, Gutberlet M (2011). "Cardiac magnetic resonance imaging for the assessment of ventricular function, geometry, and viability before and after surgical ventricular reconstruction". J. Thorac. Cardiovasc. Surg. 142 (6): 1515–22.e1. doi:10.1016/j.jtcvs.2011.04.040. PMID 21907357.
- ↑ Arvan S, Varat MA (1984). "Persistent ST-segment elevation and left ventricular wall abnormalities: a 2-dimensional echocardiographic study". Am. J. Cardiol. 53 (11): 1542–6. PMID 6731299.
- ↑ Matsumoto M, Watanabe F, Goto A, Hamano Y, Yasui K, Minamino T, Abe H, Kamada T (1985). "Left ventricular aneurysm and the prediction of left ventricular enlargement studied by two-dimensional echocardiography: quantitative assessment of aneurysm size in relation to clinical course". Circulation. 72 (2): 280–6. PMID 3159507.
- ↑ 16.0 16.1 Mann, Douglas (2015). Braunwald's heart disease : a textbook of cardiovascular medicine. Philadelphia, PA: Elsevier/Saunders. ISBN 978-1455751341.
- ↑ Kouchoukos, Nicholas (2013). Kirklin/Barratt-Boyes cardiac surgery : morphology, diagnostic criteria, natural history, techniques, results, and indications. Philadelphia: Elsevier/Saunders. ISBN 978-1416063919.
- ↑ Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, Hochman JS, Krumholz HM, Kushner FG, Lamas GA, Mullany CJ, Ornato JP, Pearle DL, Sloan MA, Smith SC, Alpert JS, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK (2004). "ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction)". Circulation. 110 (5): 588–636. doi:10.1161/01.CIR.0000134791.68010.FA. PMID 15289388.