Why the study?
Does increased infarct transmurality worsen left ventricular remodeling and function after anterior myocardial infarction in dogs?
Does increased infarct transmurality worsen left ventricular remodeling and function after anterior myocardial infarction in dogs?
In a canine model of anterior myocardial infarction, greater infarct transmurality is a major determinant of adverse left ventricular remodeling and dysfunction during healing.
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Hypothesis-generating in canine anterior MI; human studies needed before clinical relevance.
To determine the impact of greater infarct transmurality on changes in left ventricular remodeling and function after acute anterior myocardial infarction, serial topographic and functional parameters (two-dimensional echocardiograms) and hemodynamics over 6 weeks, and postmortem topography (planimetry) at 6 weeks, were measured in chronically instrumented dogs randomized to standard coronary artery ligation (group 1) or a modified lower ligation plus collateral obliteration to decrease collateral inflow and increase transmurality (group 2). At 6 weeks, postmortem scar size and collagen were similar in the two groups, but group 2 had greater transmurality associated with more necrosis relative to area at risk, Q waves, infarct expansion, thinning, regional bulging, and cavity dilatation. Over the 6 weeks, group 2 showed more early expansion, late thinning and regional bulging in the short axis, larger diastolic and systolic volumes, and more apical aneurysmal bulging in the long-axis, reflecting more topographic deterioration. More important, group 2 showed greater regional and global left ventricular dysfunction over 6 weeks, lower ejection fraction at 2 days with further decrease over 6 weeks, and more left ventricular thrombus, ventricular arrhythmias, and deaths. In addition, transmurality correlated with the severity of remodeling and dysfunction. The findings indicate that transmurality is a major determinant of remodeling and left ventricular dysfunction during healing after anterior infarction.
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Jugdutt et al. (1992) studied this question.
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