SUMMARY Echocardiographic septal and posterior wall thicknesses and the percent change with systole were measured in 146 patients with the following diagnoses: acute myocardial infarction (40), chronic coronary artery disease (49), congestive cardiomyopathy (8), atrial septal defect (20), and no cardiac disease (29). Mean diastolic thicknesses for the groups of patients with coronary artery disease and congestive cardiomyopathy were not significantly different from normal although there were abnormal values for individual patients within each group. Mean diastolic thickness of the septum was greater than normal for the group with atrial septal defect (P < 0.02). Wall thinning with systole was SEGMENTAL ABNORMALITIES of left ventricular wall motion have been demonstrated echocardiographically in patients with angiographically demonstrated coronary artery obstruction" 2 and in patients with acute myocardial infarction.34 Motion in noninfarcted areas is often greater than normal.3 These studies suggest that the abnormal left ventricular echo motion in these patients is related to segmental differences in myocardial fiber shortening. Echo motion may also be affected by other factors such as 1) motion of the entire heart within the chest; 2) unloading during systole; 3) electrical conduction;5 6 4) relative diastolic volumes of the right and left ventricles;7' 8 and 5) cardiac surgery.9 On the basis of experimental data, Ross and Franklin have suggested that dynamic changes in wall thickness might be used to study regional changes in contractile function caused by ischemia.'0 Because systolic thickening may not be influenced by the variety of factors affecting wall motion, and may therefore be more specifically related to contractility, the present study was undertaken in order 1) to determine whether there are changes in echocardiographic wall thickening in humans with coronary artery disease; 2) to see if these changes might distinguish acute myocardial infarction from chronic coronary artery disease; and 3) to see if changes in systolic thickening are related to changes in wall motion.

SUMMARYEchocardiograms of ten patients with congestive cardiomyopathy were compared to those of three groups of patients: (1) 17

1 There is a growing concensus that myocardial performance in the early stages of experimental endotoxic and septic shock is relatively normal; however, recent reports have identified an intermediate phase of shock when myocardial dysfunction is clearly apparent. 2 The mechanism of dysfunction has become a subject of intense investigation. A current view is that altered myocardial responsiveness to circulating catecholamines may play an important role in the dysfunction observed after endotoxin administration. The present studies, in which an isolated working heart preparation of the dog was used, were designed to test this hypothesis. This particular experimental preparation was selected to provide an adequate interpretation of results; cardiac output, afterload, and concentrations of adrenaline reaching the coronary vascular bed were controlled in all experiments. Responses to infusions of adrenaline were recorded in the 'steady-state' condition. Control (non-shocked) heart responses to adrenaline were highly reproducible in terms of inotropic, chronotropic and coronary vascular behaviour. 3 Results from the study document myocardial dysfunction within 4-6 h following an LD70 endotoxin administration on the basis of increased left ventricular end diastolic pressure (LVEDP), decreased cardiac power and myocardial efficiency, and depressed negative and positive dP/dt parameters. 4 Findings suggest significantly altered responsiveness of the myocardium to infused adrenaline at rates of 1, 2, and 5 pg/min with concentrations between 10 and 1 ng/ml blood. LVEDP was elevated while calculated power and efficiency parameters remained significantly below control values during infusion of adrenaline in endotoxin-treated hearts. Depressions of responsiveness were interpreted to occur on the basis of failure to restore positive and negative dP/dt to normal values and depressed coronary blood flow responses during adrenaline administration. Increases in coronary flow were regularly less in experimental hearts than the controls. Heart rate responses to adrenaline in both failing and non-failing hearts were identical. 5 In conclusion, it is suggested that myocardial contractile and relaxation characteristics and coronary vascular responses to adrenaline infusion are depressed in endotoxin shock during the period of demonstrated myocardial dysfunction. No distinct causal relationships were observed between the ailtered myocardial responsiveness and pathogenesis of heart dysfunction since myocardial dysfunction and altered responsiveness to adrenaline were generally observed together. Myocardial oedema formation after endotoxin as previously reported by this laboratory may bear a relationship to the depressed negative dP/dt response to adrenaline.

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