Abstract

To the Editor: The intriguing observations by Goser et al1 on autoimmunity to segregated myocardial autoantigens open new areas for understanding “cardiovascular inflammatory disease.” At the same time, the authors do not fully use the opportunity to discuss the implications of their finding on acute development of atherothrombosis. A previous contact with troponin I—a largely used, sensitive marker of even small myocardial damage—is shown to induce an autoimmune reaction that, after left anterior descending coronary artery ligation, leads to increased …

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