Finite element analysis of myocardial diastolic function using three-dimensional echocardiographic reconstructions: application of a new method for study of acute ischemia in dogs.

Abstract

The effect of acute myocardial ischemia on the myocardial elastic modulus has been a matter of controversy. To evaluate this question, diastolic elastic modulus was assessed by finite element analysis of left ventricular geometry using three-dimensional echocardiographic reconstructions and right and left ventricular pressure recordings. Elastic properties were estimated before and after coronary occlusion in 6 open-chest dogs. Elastic modulus values were derived by means of a computer program that determined the global elastic modulus that best predicted the diastolic changes in left ventricular geometry. In the finite element analysis after coronary occlusion, two analyses were performed: one utilizing the control elastic modulus for all segments of the left ventricle and one in which ischemic (dyskinetic) segments were assigned a higher elastic modulus. Results showed that the control elastic modulus was a poor predictor of diastolic left ventricular expansion after coronary occlusion. The finite element analysis in which the ischemic segments were assigned a higher elastic modulus better predicted ischemic diastolic wall motion patterns. Error values (difference between predicted and actual left ventricular segmental diastolic motion) were: control, 1.9 +/- 0.3 mm (mean +/- SD), ischemia, 2.9 +/- 0.5 mm, and 2.2 +/- 0.4 mm using the stiffer elastic modulus for ischemic segments. Error values were significantly higher (p less than 0.05) under ischemic conditions when the control elastic modulus was uniformly applied compared with control and ischemia with dyskinetic segments assigned a higher elastic modulus. From these data, it is concluded that the myocardial diastolic elastic modulus is increased by ischemia and that this approach may allow clinical assessment of intrinsic muscle stiffness.

Regional wall stress predicts ventricular remodeling after anteroseptal myocardial infarction in the Healing and Early Afterload Reducing Trial (HEART): An echocardiography-based structural analysis

“…Nevertheless, approaches to assessing myocardial material properties during systole are essential to an improved understanding of the relationship between contractility and myocardial morphologic features. McPherson et al 44 have used the finite element approach to assess diastolic elastic modulus by determining the global elastic modulus that best predicted diastolic deformations in ventricular geometry after coronary occlusion. It is conceivable that this approach might be used in a systolic model.…”

Relation between longitudinal, circumferential, and oblique shortening and torsional deformation in the left ventricle of the transplanted human heart.

“…Left ventricular shortening has been measured along various axes in canine hearts using a number of measurement techniques. 10 - 33 To date, however, the anisotropy of left ventricular shortening in human hearts has not been reported, although the relative dynamics of specific left ventricular 916 Circulation Research Vol 64, No 5, May 1989 sites (as required for the measurement of such shortening) have been studied in man both during and after cardiac surgery by means of radiopaque clips attached to the epicardium, 34 -36 strain gauges sutured to the epicardium, 37 opacified coronary artery bifurcations, 3839 radiopaque myocardial markers implanted into the midwall 40 and sonomicrometers implanted at various transmural depths. 4142 We report here the results of a study investigating the anisotropy of systolic shortening in the inferior, anterior, lateral, and septal regions of the left ventricular midwall of the transplanted heart in awake man.…”

Increased Regional Systolic Myocardial Stiffness of the Left Ventricle during Coronary Artery Occlusion in a Dog: Analysis of the Finite Element Model.

“…Many researchers reported that diastolic regional stiffness of the ischemic myocardium increased (Hess et al 1980;McPherson et al 1987;Sys and Brutsaert 1989;Ross 1989). Edwards et al suggested that a sevenfold increase in passive loading would be sufficient to produce the acute elongation of the ischemic myocardium (Edwards et al 1981), which is roughly consistent with the result in this study.…”