Characterization of Regional Changes in Myocardial Strain and Stiffness after Myocardial Infarction using Speckle‐Tracking Echocardiography in Swine

Abstract

ObjectiveLeft ventricular (LV) remodeling following myocardial infarction (MI) is characterized by dynamic changes in myocardial structure and function in infarcted as well as remote, non‐infarcted myocardium. Speckle‐Tracking Echocardiography (STE) offers a sensitive, non‐invasive approach to assess myocardial mechanical properties and may be useful for evaluating regional changes in tissue mechanics after MI. In the present study, STE‐derived strain analysis was combined with measurements of LV pressure to quantify regional alterations in myocardial stiffness in a porcine model of reperfused MI.MethodsPropofol‐anesthetized swine (n=8) were subjected to a 90 minute balloon occlusion of the distal left anterior descending coronary artery to produce MI. Peak strain values were acquired in radial, circumferential, and longitudinal directions via STE (Vivid 7; GE) at baseline and 1 month post‐MI. Circumferential diastolic stiffness was derived in vivo from stress‐strain relationships obtained via pressure catheter measurements of LV minimum and end‐diastolic pressure. Myocardial tissue samples were subsequently collected from corresponding infarcted and remote regions of the left ventricle for direct assessment of passive stiffness via post‐mortem uniaxial tensile testing.ResultsMeasurements of LV end‐diastolic volume (from 75±5 mL at baseline to 105±7 mL 1 month post‐MI, p<0.001) and LV ejection fraction (from 68±1 % to 53±2 %, p<0.001) were consistent with expected changes in LV structure and function associated with post‐infarction remodeling (infarct size: 6.7±0.7 % of LV). Serial STE revealed significant reductions in radial, circumferential, and longitudinal strain 1 month after MI that were comparable between infarct and remote segments (Table). In concordance with reductions in strain, infarct and remote segments each exhibited a significant increase in circumferential stiffness. However, the magnitude of this increase in stiffness was lower than that derived from post‐mortem measurements of passive stiffness, particularly in the infarct region (infarct scar: 584±156 kPa; remote myocardium: 96±16 kPa).ConclusionsThese results demonstrate the ability of STE to detect regional alterations in myocardial function after MI and highlight the importance of evaluating mechanical properties of remote non‐infarcted areas of the left ventricle that exhibit comparable changes in strain to that observed in the infarct segment. The addition of direct LV pressure measurements allows assessment of regional changes in myocardial stiffness, although further studies are necessary to understand the discrepancy in stiffness derived from STE vs. post‐mortem tensile testing, particularly in infarcted segments of the left ventricle.Support or Funding InformationThe National Heart Lung and Blood Institute (HL‐061610), the American Heart Association (17SDG33660200), the National Center for Advancing Translational Sciences (UL1TR001412), the Department of Veterans Affairs (1IO1BX002659), and the Albert and Elizabeth Rekate Fund in Cardiovascular Medicine.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.