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J Am Coll Cardiol, 1999; 34:2150-2151
© 1999 by the American College of Cardiology Foundation
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LETTERS TO THE EDITOR

Dynamic left ventricular outflow tract obstruction as a potential mechanism of myocardial rupture after acute myocardial infarction

Jozef Bartunek, MD, PhDa, Marc Vanderheyden, MDa and Bernard De Bruyne, MD, PhDa

a Cardiovascular Center, Moorselbaan 164, 9300 Aalst,, Belgium

jozef.bartunek{at}olvz.aalst.be

We read with great interest the study of Becker et al. (1), who investigated the incidence and predictive factors of fatal cardiac rupture in patients treated with thrombolysis enrolled in the Thrombolysis and Thrombin Inhibition in Myocardial Infarction (TIMI-9) study. The authors reported female gender and age as independent risk factors for fatal cardiac rupture. Of note, they did not observe a significant relation between anticoagulation therapy and cardiac rupture. In contrast, the incidence of rupture was higher in patients with anterior myocardial infarction not receiving early angiotensin-converting enzyme inhibition and beta-blockers. Although the study did not address directly pathophysiologic mechanisms of the rupture, the authors speculated that changes in collagen matrix associated with aging and, potentially, with female gender may underlie the higher risk for mortality. This sounds plausible, but nevertheless, the authors do not report some clinically relevant information such as the extent of coronary artery disease and overall or regional left ventricular (LV) function. Likewise, they do not address triggers that may precipitate the occurrence of the rupture. However, Oliva et al. (2) reported that myocardial rupture is often preceded by particular signs—namely emesis, restlessness, pericarditis, alterations of the T waves and abrupt episodes of bradycardia or hypotension. The latter signs deserve closer attention by clinicians. Hypotension or bradycardia is often present owing to the activation of LV mechanoreceptors in patients with LV outflow tract (LVOT) obstruction. We have recently reported a novel observation of a dynamic LVOT obstruction with systolic anterior motion of the mitral leaflets in patients after acute anterior myocardial infarction that preceded a cardiac rupture or intraventricular septal defect (3). The LVOT obstruction was observed in women with nonhypertrophied ventricles and calcified posterior mitral annulus and/or thickened mitral leaflets who presented with hyperdynamic contraction of the noninfarct-related artery segments. Since this publication (3), we observed a third myocardial rupture also preceded by LVOT obstruction in a 57-year-old man. Based on our observations, we postulated that the presence of the LVOT obstruction led to an increase in the end-systolic wall stress of the infarct segments, which may represent a direct mechanical insult to a weakened necrotic tissue. This observation has several potential clinical implications. First, it implies that in patients with a large anterior infarction and hyperkinetic noninfarct segments, particular attention should be paid to LVOT flow dynamics, especially in women with abnormalities of the mitral valve apparatus. Second, in such patients aggressive treatment with vasodilators should be avoided because they may precipitate or worsen the dynamic obstruction. In contrast, beta-blockers should blunt the hyperdynamic contraction and thus, in addition to the reduction of arrhythmias and work load, prevent the fatal cardiac rupture (4). We believe that discussion of these mechanisms could stimulate other investigators to look carefully at LVOT dynamics in patients with anterior myocardial infarction to determine whether compensatory hyperdynamic contractions of the basis of the heart may indeed be deleterious in these patients.


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 References
 

  1. Becker RC, Hochman JS, Cannon CP, et al. Fatal cardiac rupture among patients treated with thrombolytic agents and adjunctive thrombin antagonists: observations from the Thrombolysis and Thrombin Inhibition in Myocardial Infarction 9 study. J Am Coll Cardiol. 1999;33:479–488[Abstract/Free Full Text]
  2. Oliva PB, Hammil SC, Edwards WD. Cardiac rupture, a clinically predictive complication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations. J Am Coll Cardiol. 1993;22:720–726[Abstract]
  3. Bartunek J, Vanderheyden M, De Bruyne B. Dynamic left ventricular outflow tract obstruction after anterior myocardial infarction: a potential mechanism of myocardial rupture. Eur Heart J. 1995;16:1439–1442[Abstract/Free Full Text]
  4. International Study of Infarct Survival (ISIS-1) Collaborative Group. Randomised trial of intravenous atenolol among 16,027 cases of suspected acute myocardial infarction: ISIS-1. Lancet. 1986;2:57–66[CrossRef][Medline]



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