Wall thickness changes considered as regional myocardial function in ischemic heart disease.
Dynamic changes in left ventricular wall thickness represent a function of the myocardium which can be described, in normal subjects or in disease, without reference to behavior of other parts of the wall. Abnormalities of amplitude, rate and timing of wall thickness change interact in influencing overall ventricular performance, so that even this local function cannot be expressed as a single "index". Infarcted and acutely ischemic myocardium display reduced amplitude of thickness change. The degree to which they also show delayed wall dynamics in man is uncertain. Cross-sectional echocardiography has not been used to examine this aspect of regional thickness change, mainly because of the difficulties of processing "real-time" images. In the stable state of ischemic heart disease, such as exists in patients with angina, abnormalities of timing are common, even in the absence of significant reduction in overall thickness change, and lead to impaired energy transfer from the myocardium to the circulation. The degree of organization involved in normal myocardial function is better appreciated when one considers the complex phenomena which result from its disruption. In particular, rapid wall thinning in early diastole, normally associated with rapid filling, is revealed as an inherent property of the wall when it becomes dissociated from filling because relaxation is incoordinate. This demonstration of the active processes involved in ventricular relaxation provides an example of how the study of ischemic heart disease, in its differing local effects, may provide insight into the normal physiology of the myocardium.