Dressler's syndrome: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Dressler's syndrome is believed to result from an [[autoimmune]] inflammatory reaction to myocardial neo-[[antigen]]s. It usually occurs within weeks or months of the Infarction due to antiheart antibodies, this begins with myocardial injury that releases cardiac antigens and stimulates antibody formation. The immune complexes that are generated then deposit onto the pericardium and causes the inflamation. The | Dressler's syndrome is believed to result from an [[autoimmune]] inflammatory reaction to myocardial neo-[[antigen]]s. It usually occurs within weeks or months of the Infarction due to antiheart antibodies, this begins with myocardial injury that releases cardiac antigens and stimulates antibody formation. The immune complexes that are generated then deposit onto the pericardium and causes the inflamation. The autoimmune response and syndrome may also appear after [[pulmonary embolism]] <ref name="pmid8759817">{{cite journal| author=Jerjes-Sánchez C, Ramírez-Rivera A, Ibarra-Pérez C| title=The Dressler syndrome after pulmonary embolism. | journal=Am J Cardiol | year= 1996 | volume= 78 | issue= 3 | pages= 343-5 | pmid=8759817 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8759817 }} </ref>. | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
Revision as of 01:37, 27 July 2011
Template:DiseaseDisorder infobox
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Pericarditis Microchapters |
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Dressler's syndrome On the Web |
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American Roentgen Ray Society Images of Dressler's syndrome |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor-In-Chief: Mohammed A. Sbeih, M.D.[2] Phone:617-849-2629 , Cafer Zorkun, M.D., Ph.D. [3]
Synonyms and keywords: Postmyocardial infarction syndrome, post MI pericarditis, PMIS
Overview
Dressler's syndrome or post myocardial infarction syndrome is a form of pericarditis that occurs in the setting of injury to the heart as a result of myocardial infarction[1]. Dressler's syndrome typically occurs 2 to 10 weeks after myocardial infarctionit's[2]. This differentiates Dressler's syndrome from the much more common post myocardial infarction pericarditis which occurs between days 2 and 4 after myocardial infarction.
Historical Perspective
It was first characterized by William Dressler in 1956.[3].[4][5][6]
It should not be confused with the Dressler's syndrome of haemoglobinuria named for Lucas Dressler, who characterized it in 1854.[7][8]
Risk Factors
Dressler's syndrome is associated with myocardial infarction (heart attack). It can also be observed after pulmonary embolism.
Pathophysiology
Dressler's syndrome is believed to result from an autoimmune inflammatory reaction to myocardial neo-antigens. It usually occurs within weeks or months of the Infarction due to antiheart antibodies, this begins with myocardial injury that releases cardiac antigens and stimulates antibody formation. The immune complexes that are generated then deposit onto the pericardium and causes the inflamation. The autoimmune response and syndrome may also appear after pulmonary embolism [9].
Epidemiology and Demographics
In the setting of myocardial infarction, Dressler's syndrome occurs in about 7% of cases[10]. Dressler's syndrome was more commonly seen in the era prior to reperfusion, but its incidence has markedly decreased in the reperfusion era, presumably because of smaller infarct sizes [11].
Conditions that Dressler's Syndrome should be Differentiated From
Dressler's syndrome typically occurs 2 to 10 weeks after a myocardial infarction has occurred[12]. This differentiates Dressler's syndrome from the much more common post myocardial infarction pericarditis that occurs in 17 to 25% of cases of acute myocardial infarction and occurs between days 2 and 4 after the infarction. Dressler's syndrome also needs to be differentiated from pulmonary embolism, another identifiable cause of pleuritic (and non-pleuritic) chest pain in people who have been hospitalized and/or undergone surgical procedures within the preceding weeks.
Diagnosis
Symptoms
The syndrome consists of a persistent low-grade fever, and chest pain which is usually pleuritic in nature. The symptoms tend to occur after a few weeks or even months after myocardial infarction and tend to subside in a few days.
Physical Examination
Cardiovascular Examination
A pericardial friction rub, and /or a pericardial effusion is present.
Laboratory Findings
Elevated ESR.
Treatment
Dressler's syndrome is typically treated with high dose (up to 650 mg PO q 4 to 6 hours) enteric-coated aspirin. Acetominophen can be added for pain management as this does not affect the coagulation system. Anticoagulants should be discontinued if the patient develops a pericardial effusion.
NSAIDs such as ibuprofen should be avoided in the peri-infarct period as they:
- Increase the risk of reinfarction
- Adversely impact left ventricular remodeling.
- Block the effectiveness of aspirin
ACC/AHA Treatment Guidelines (DO NOT EDIT)[13]
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Class I1. Aspirin is recommended for treatment of pericarditis after STEMI. Doses as high as 650 mg orally (entericcoated) every 4 to 6 hours may be needed. (Level of Evidence: B) 2. Anticoagulation should be immediately discontinued if pericardial effusion develops or increases. (Level of Evidence: C) Class IIa1. For episodes of pericarditis after STEMI that are not adequately controlled with aspirin, it is reasonable to administer 1 or more of the following:
Class IIb1. Corticosteroids might be considered only as a last resort in patients with pericarditis refractory to aspirin or NSAIDs. Although corticosteroids are effective for pain relief, their use is associated with an increased risk of scar thinning and myocardial rupture. (Level of Evidence: C) 2. Nonsteroidal anti-inflammatory drugs may be considered for pain relief; however, they should not be used for extended periods because of their effect on platelet function, an increased risk of myocardial scar thinning, and infarct expansion. (Level of Evidence: B) Class III1. Ibuprofen should not be used for pain relief because it blocks the antiplatelet effect of aspirin and it can cause myocardial scar thinning and infarct expansion. (Level of Evidence: B) |
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Sources
- The 2004 ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction [13]
- The 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction [14]
References
- ↑ Hutchcroft BJ (1972). "Dressler's syndrome". Br Med J. 3 (5817): 49. PMC 1788531. PMID 5039567. Unknown parameter
|month=ignored (help) - ↑ Krainin F, Flessas A, Spodick D (1984). "Infarction-associated pericarditis. Rarity of diagnostic electrocardiogram". N Engl J Med. 311 (19): 1211–4. PMID 6493274.
- ↑ DRESSLER W (1956). "A post-myocardial infarction syndrome; preliminary report of a complication resembling idiopathic, recurrent, benign pericarditis". J Am Med Assoc. 160 (16): 1379–83. PMID 13306560.
- ↑ Bendjelid K, Pugin J (2004). "Is Dressler syndrome dead?". Chest. 126 (5): 1680–2. doi:10.1378/chest.126.5.1680. PMID 15539743. Unknown parameter
|month=ignored (help) - ↑ Streifler J, Pitlik S, Dux S; et al. (1984). "Dressler's syndrome after right ventricular infarction". Postgrad Med J. 60 (702): 298–300. PMC 2417818. PMID 6728756. Unknown parameter
|month=ignored (help) - ↑ Dressler W (1959). "The post-myocardial-infarction syndrome: a report on forty-four cases". AMA Arch Intern Med. 103 (1): 28–42. PMID 13605300. Unknown parameter
|month=ignored (help) - ↑ Template:WhoNamedIt
- ↑ L. A. Dressler. Ein Fall von intermittirender Albuminurie und Chromaturie. Archiv für pathologische Anatomie und Physiologie und für klinische Medicin, 1854, 6: 264-266.
- ↑ Jerjes-Sánchez C, Ramírez-Rivera A, Ibarra-Pérez C (1996). "The Dressler syndrome after pulmonary embolism". Am J Cardiol. 78 (3): 343–5. PMID 8759817.
- ↑ Krainin F, Flessas A, Spodick D (1984). "Infarction-associated pericarditis. Rarity of diagnostic electrocardiogram". N Engl J Med. 311 (19): 1211–4. PMID 6493274.
- ↑ Tofler GH, Muller JE, Stone PH, Willich SN, Davis VG, Poole WK; et al. (1989). "Pericarditis in acute myocardial infarction: characterization and clinical significance". Am Heart J. 117 (1): 86–92. PMID 2643287.
- ↑ Krainin F, Flessas A, Spodick D (1984). "Infarction-associated pericarditis. Rarity of diagnostic electrocardiogram". N Engl J Med. 311 (19): 1211–4. PMID 6493274.
- ↑ 13.0 13.1 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: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of Patients with Acute Myocardial Infarction)". Circulation. 110 (9): e82–292. PMID 15339869. Unknown parameter
|month=ignored (help) - ↑ Antman EM, Hand M, Armstrong PW; et al. (2008). "2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: developed in collaboration With the Canadian Cardiovascular Society endorsed by the American Academy of Family Physicians: 2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee". Circulation. 117 (2): 296–329. doi:10.1161/CIRCULATIONAHA.107.188209. PMID 18071078. Unknown parameter
|month=ignored (help)