doi: 10.1161/01.CIR.0000152480.72638.C1
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(Circulation. 2005;111:e17.)
© 2005 American Heart Association, Inc.
Correspondence |
Letter Regarding Article by Abbate et al, "Widespread Myocardial Inflammation and Infarct-Related Artery Patency"
Cardiothoracic and Vascular Department, Vita e Salute University, Milan, Italy
Cardiology Department, Catholic University, Rome, Italy
Abbate et al1 recently reported the presence of activated T cells in the peri-infarcted region and in the unaffected remote myocardium of patients who died from acute myocardial infarction. Because these cells were associated with persistent infarct-related occlusion, the authors suggested that an antigenic stimulus also present in the myocardium triggers an immune response that can be critical to precipitate artery occlusion.
The authors, however, failed to clarify whether the presence of activated inflammatory cells was associated with necrosis of the adjacent myocytes, which would meet the Dallas criteria for myocarditis.2 This clarification could be particularly important in explaining the presence in the remote myocardium of inflammatory cells, which are not affected by the ischemic process, indicating an additional factor in cardiac death.
With regard to the mechanism of myocarditis, several options can be considered, including infectious agents and hypersensitivity to segregated antigens released by the infarcted myocardium. Concerning the latter mechanism, we have demonstrated that a myocarditis that involves both the left and right ventricles can cause global biventricular dysfunction and heart failure in patients with severe coronary artery disease.3 Importantly, antiheart autoantibodies were detected, by indirect immunofluorescence, in 30% of our cases. These improved remarkably, in terms of cardiac dimension and contractility, after the administration of immunosuppressive therapy.
In conclusion, a Dressler-like myocarditis could explain the activated T lymphocytes that were observed distantly from the infarcted area and may have contributed to cardiac deaths that occurred some weeks after an acute ischemic event.
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1. Abbate A, Bonanno E, Mauriello A, Bussani R, Biondi-Zoccai GG, Liuzzo G, Leone AM, Silvestri F, Dobrina A, Baldi F, Pandolfi F, Biasucci LM, Baldi A, Spagnoli LG, Crea F. Widespread myocardial inflammation and infarct-related artery patency. Circulation. 2004; 110: 46–50.
2. Aretz HT, Billingham ME, Edwards WD, Factor SM, Fallon JT, Fenoglio JJ Jr, Olsen EG, Schoen FJ. Myocarditis. A histopathologic definition and classification. Am J Cardiovasc Pathol. 1987; 1: 3–14.[Medline] [Order article via Infotrieve]
3. Frustaci A, Chimenti C, Maseri A. Global biventricular dysfunction in patients with asymptomatic coronary artery disease may be caused by myocarditis. Circulation. 1999; 99: 1295–1299.
Response
Department of Internal Medicine, Virginia Commonwealth University, Richmond, Va, abbatea{at}yahoo.com
Department of Internal Medicine, Catholic University, Rome, Italy
Institute of Cardiology, Catholic University, Rome, Italy
We appreciate the interest of Dr Chimenti and colleagues in our article. The search for the cause of myocardial inflammation and, eventually, for acute myocardial infarction is ongoing. Myocardial lymphocyte infiltrate may be related to the events that are primarily associated with the causes of coronary occlusion or, as Chimenti et al suggest, that are secondary to myocardial necrosis as a Dressler-like myocarditis. In a Dressler-like myocarditis, not only would the phenomenon have pathophysiological implications, but it may also have been a determining factor in the patients’ deaths. The authors quote their excellent 1999 Circulation article in which myocarditis was the cause of ventricular dysfunction in patients with coronary artery disease, and cardiac autoantibodies were found in 30% of cases.1 The main difference between the cases reported by Chimenti and associates and our cases is the lack of evidence of myocyte injury secondary to lymphocyte activation in our samples. As described in our article,2 in none of the 16 cases was the presence of lymphocytes associated with evidence of recent necrosis that would suggest lymphocyte-dependent myocyte injury.
The interpretation of these findings is still far from complete. The reason T lymphocytes infiltrate the myocardium and the coronary arteries in patients with acute myocardial infarction without eliciting cell-mediated damage is unknown, and further studies are required.
To hypothesize that lymphocytic activation is secondary to an unrecognized antigen stimulus also present in the myocardium that ultimately triggers an acute coronary syndrome is tempting but still unproven.
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TopReferencesReferences |
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1. Frustaci A, Chimenti C, Maseri A. Global biventricular dysfunction in patients with asymptomatic coronary artery disease may be caused by myocarditis. Circulation. 1999; 99: 1295–1299.
2. Abbate A, Bonanno E, Mauriello A, Bussani R, Biondi-Zoccai GG, Liuzzo G, Leone AM, Silvestri F, Dobrina A, Baldi F, Pandolfi F, Biasucci LM, Baldi A, Spagnoli LG, Crea F. Widespread myocardial inflammation and infarct-related artery patency. Circulation. 2004; 110: 46–50.
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