Abstract
BackgroundHeart failure from adverse ventricular remodeling follows myocardial infarction, but the contribution of periinfarct and remote myocardium to the development of cardiomyopathy remains poorly defined. 2D strain echocardiography (2DSE) is a novel and sensitive tool to measure regional myocardial mechanics. The aim is to quantify radial strain in infarcted (I), periinfarct (PI) and remote (R) myocardial regions acutely and chronically following anterior infarction in rats.MethodsThe left anterior coronary artery of male Sprague-Dawley rats (270–370 g) were occluded for 20–30 minutes and 2DSE was performed in the acute setting (n = 10; baseline and 60 minutes post-reperfusion) and in the chronic setting (n = 14; baseline, 1, 3 and 6 weeks). Using software, radial strain was measured in the mid-ventricle in short axis view. The ventricle was divided into 3 regions: I (anteroseptum, anterior and anterolateral), PI – (inferoseptum and inferolateral) and R – (inferior). Infarct size was measured using triphenyl tetrazolium chloride in the acute group.ResultsFollowing infarct, adverse remodeling occurred with progressive increase in left ventricular size, mass and reduced fractional shortening within 6 weeks. Radial strain decreased not only in the infarct but also in the periinfarct and remote regions acutely and chronically (I, PI, R, change vs. baseline, 60 minutes -32.7 ± 8.7, -17.4 ± 9.4, -13.5 ± 11.6%; 6 weeks -24.4 ± 8.2, -17.7 ± 8.3, -15.2 ± 8.4% respectively, all p < 0.05). Reduced radial strain in periinfarct and remote regions occurred despite minimal or absent necrosis (area of necrosis I, PI, R: 48.8 ± 23, 5.1 ± 6.6, 0 ± 0%, p < 0.001 vs. I).ConclusionFollowing left anterior coronary occlusion, radial strain decreased at 60 minutes and up to 6 weeks in the periinfarct and remote regions, similar to the reduction in the infarct region. This demonstrates early and chronic myopathic process in periinfarct and remote regions following myocardial infarction that may be an under recognized but important contributor to adverse left ventricular remodeling and progression to ischemic cardiomyopathy.
Highlights
Heart failure from adverse ventricular remodeling follows myocardial infarction, but the contribution of periinfarct and remote myocardium to the development of cardiomyopathy remains poorly defined. 2D strain echocardiography (2DSE) is a novel and sensitive tool to measure regional myocardial mechanics
It has recently been shown that myocardial strain measured by 2-dimensional strain echocardiography (2DSE) is more sensitive in detecting regional myocardial dysfunction compared with conventional means of functional assessment such as thickening or fractional shortening in both ischemic [12] and doxorubicin-induced cardiomyopathy animal models [13]
The 2DSE method relies on motion estimation based on tracking of unique ultrasound speckle patterns within the tissue to calculate myocardial strain [14,15,16]. 2D strain echocardiography, because it measures the deformation of a myocardial segment, is a more direct measure of myocardial mechanics compared to conventional measures of ventricular function such as ejection fraction/fractional shortening
Summary
Heart failure from adverse ventricular remodeling follows myocardial infarction, but the contribution of periinfarct and remote myocardium to the development of cardiomyopathy remains poorly defined. 2D strain echocardiography (2DSE) is a novel and sensitive tool to measure regional myocardial mechanics. Heart failure from adverse ventricular remodeling follows myocardial infarction, but the contribution of periinfarct and remote myocardium to the development of cardiomyopathy remains poorly defined. Prior studies have demonstrated reduced contractility in normally perfused myocardial regions adjacent to the infarct with preserved function in remote regions [8,9,10] The expansion of this periinfarct zone is believed to cause increased dynamic wall stress and leads to adverse remodeling [9]. The aim of this study is to utilize this sensitive technique to quantify the change and to determine the temporal course of myocardial radial strain following occlusion of the left anterior coronary artery in infarcted, periinfarct and remote regions in rats
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