Regional left ventricular wall stress postmyocardial infarction with magnetic resonance imaging in swine.

This study presents a novel approach to measure regional left ventricular (LV) wall stress using cardiac magnetic resonance (CMR) imaging. We studied a chronic heart failure (CHF) model in Yucatan mini swine. Animals underwent 90-min balloon occlusion and reperfusion of the left anterior descending (LAD) coronary artery. LV pressures were measured using solid-state micromanometer pressure-tipped catheters. End-systolic elastance, end-diastolic pressure-volume relationships, and CMR imaging were collected at baseline and 1-mo postmyocardial infarction (MI). One month post-MI, data showed reduced LV function with increased end-systolic volume, end-diastolic volume, LV myocardial mass, and reduced ejection fraction. Hemodynamic data showed no significant changes in heart rate, LV pressures, tau, or LV dP/dt. However, end-systolic elastance decreased significantly (1.8 ± 0.2 to 1.1 ± 0.1, P < 0.05), indicating reduced LV contractility. Regional LV wall stress calculations revealed increasing trends in anterior septal (anteroseptal) and posterior lateral (posterolateral) end-systolic wall stress (ESWS). Anteroseptal ESWS increased from 10.1 ± 2.0 kPa to 20.0 ± 3.3 kPa (P < 0.05), whereas posterolateral ESWS increased from 6.8 ± 0.3 kPa to 11.7 ± 1.4 kPa (P < 0.05). This study demonstrates the benefit of a regional approach to LV wall stress assessment. Our findings revealed significant changes in both the anteroseptal (involved) and posterolateral (uninvolved) regions, suggesting a widespread impact of localized injury. Regional wall stress calculations can assess cardiac damage and provide prognosis of injury extent, potentially offering insights into global LV remodeling post-MI.NEW & NOTEWORTHY This study introduces a novel approach to assess regional left ventricular wall stress using cardiac MRI in a clinically relevant model of myocardial infarction. We demonstrate that postinfarction remodeling leads to increased wall stress not only in the infarcted region but also in remote myocardium. This regional analysis method provides mechanistic insights into the widespread mechanical impact of localized injury and could inform future investigations into the pathophysiology of adverse remodeling following myocardial infarction.