Douglas L. Mann

Dialysis-Induced Alterations in Left Ventricular Filling: Mechanisms and Clinical Significance

Quantitative two-dimensional (2-D) and Doppler echocardiography were used to determine whether hemodialysis results in alterations in left ventricular (LV) diastolic filling that might contribute to dialysis-induced hypotension, as well as to assess whether any hemodynamic variables or indices of diastolic filling might be used to identify which patients were at the greatest risk of becoming hemodynamically unstable during dialysis. Sixteen male patients undergoing routine maintenance hemodialysis for end-stage renal disease were prospectively studied before and after hemodialysis. Following hemodialysis there was a significant prolongation (P less than 0.05) in LV isovolumetric relaxation time (IVRT), as well as a significant reduction in the rate and extent of early rapid ventricular filling (P less than 0.005); in contrast, late atrial-assisted filling did not change significantly. A multiple stepwise linear regression analysis of predialysis hemodynamic parameters and noninvasive indices of LV filling showed that there was a significant independent inverse relationship between the frequency of dialysis-related hypotensive episodes and the duration of early LV filling (r = -0.81; P less than 0.001). These results suggest that hemodialysis results in discrete alterations in early LV filling, with no significant compensatory increase in late atrial-assisted ventricular filling. Further, patients with the shortest early LV filling times appeared to have the greatest predilection for becoming hemodynamically unstable during dialysis.

Relationship of functional recovery to scar contraction after myocardial infarction in the canine left ventricle

We have previously reported that regional wall motion abnormalities in a canine model of acute myocardial infarction may show substantial improvement in the first 6 weeks after infarction. To determine whether the mechanism of this improvement in function is the result of scar contraction within the infarct, we studied the relationship between changes in regional wall motion defined by cross-sectional echocardiography and the regional concentration of radioactive microspheres injected immediately before coronary occlusion and sampled 6 weeks after occlusion. Eight dogs underwent serial echocardiographic and microsphere blood flow measurements immediately before and 30 minutes, 48 hours, 1 week, 3 weeks, and 6 weeks after ligation of the left anterior descending or the left circumflex coronary artery. Wall motion and blood flow were measured in the short-axis section of the left ventricle at the level of the midpapillary muscle in each 10-degree radial segment around the circumference of the ventricle. Infarct histology was assessed at 6 weeks by means of the same radial coordinate system. Control data were collected in a similar manner from four dogs that underwent sham operations and had no histologic evidence of infarction. In all of the animals with infarcts, but not in the sham animals, the calculated preocclusion endocardial and epicardial blood flow values in the histologic infarct zone (252 +/- 44 and 168 +/- 17 ml/min/100 gm, respectively, mean +/- SEM) were significantly higher than those in the normal opposite wall (endocardial: 106 +/- 3 ml/min/100 gm, p less than 0.01); epicardial: 108 +/- 3 ml/min/100 gm, p less than 0.01. The location and circumferential extent of myocardium showing this elevation of preocclusion blood flow correlated well (r = 0.93, p less than 0.001) with the location and circumferential extent of the histologic infarct. The amount of wall motion abnormality, measured from the correlation plot area, decreased significantly from its maximum value of 39 +/- 3 degrees at 48 hours after coronary occlusion to 3 +/- 1 degrees (p less than 0.001) at 6 weeks after occlusion. The ratio of the preocclusion transmural blood flow in the infarct zone to that in the noninfarct zone, a measure of the condensation of the microspheres injected before coronary occlusion, and therefore of the degree of scar contraction at 6 weeks, correlated well (r = 0.83, p less than 0.01) with the recovery of wall motion 6 weeks after infarction.(ABSTRACT TRUNCATED AT 400 WORDS)

Functional relation between infarct thickness and regional systolic function in the acutely and subacutely infarcted canine left ventricle

Specific information regarding the relation between infarct thickness and regional systolic function is important to the overall understanding of both the pathophysiology of acute and subacute myocardial infarction and the functional benefits of myocardial salvage interventions designed to limit the transmural extent of infarction and thereby preserve left ventricular function. In the present study, quantitative computer-assisted two-dimensional echocardiography was used to define the relation between infarct thickness and systolic function in the acutely and subacutely infarcted canine left ventricle. Echocardiograms were obtained at the mid-papillary muscle level at baseline and 6 h after occlusion (acute infarction) in eight animals and at baseline and 72 h after occlusion (subacute infarction) in nine animals. Systolic function was assessed by measuring the extent of fractional radial shortening along each of 36 evenly spaced endocardial targets from end-diastole to end-systole; the transmural extent of infarction was determined from the triphenyltetrazolium chloride-staining deficit at 6 and 72 h. The relation between systolic function and transmural extent of infarction was analyzed in two ways. First, the extent of fractional radial shortening in each group was examined as a function of quartile (25%) increments in transmural infarct thickness. This analysis revealed 1) a significant overall loss of fractional radial shortening with increasing transmural extent of infarction in both groups; and 2) significant differences in the extent of systolic dysfunction between successive quartile increments of infarction. Second, the relation between infarct thickness and systolic dysfunction was modeled mathematically by fitting the data from each infarct series to linear, logarithmic and exponential functions.(ABSTRACT TRUNCATED AT 250 WORDS)

Early natural history of regional left ventricular dysfunction after experimental myocardial infarction

Existing studies provide conflicting information concerning the natural history of regional dysfunction after subacute myocardial infarction. The purpose of this study was to use quantitative computer-assisted two-dimensional echocardiography to define the natural history of abnormal wall motion in a subacute canine infarct model within individual short-axis echocardiographic planes, and in the entire ventricle as well. Serial short-axis echocardiograms were obtained from 10 closed-chest dogs before occlusion and at 0.5, 6, 24, 48, and 72 hours after ligation of the circumflex (six dogs) or left anterior descending (four dogs) coronary artery. The circumferential extent of abnormal wall motion was quantified by two different computer-assisted methods: the first, a derived correlation method, examined wall motion throughout the systolic contraction sequence; the second method examined the fractional radial change in endocardial ray length from end-diastole to end-systole. The study shows that for individual planes there is a slight but not statistically significant increase in the circumferential extent of abnormal wall motion from 0.5 to 72 hours after coronary artery occlusion; however, when the total extent of left ventricular asynergy was used to define a global functional infarct size, we observed a small (3.6% to 5.4%) but significant increase in the circumferential extent of abnormal wall motion.