Spatial and temporal variability in the pattern of recovery of ventricular geometry and function after acute occlusion and reperfusion.

Myocardial ischemia and infarction are known to cause changes in both ventricular shape and function. Little is known about the recovery of ventricular geometry after transient myocardial ischemia and its relationship to recovery of function. To examine the pattern of recovery of ventricular geometry following transient coronary artery occlusion and to assess the relationship of this to the return of systolic function, we used echocardiography to study 13 dogs following 15-minute occlusion of the left anterior descending coronary artery. During ischemia, total endocardial surface area (ESA) increased from 32.55 +/- 1.77 to 45.36 +/- 3.18 cm2 (p = 0.001). The most striking increase was at the apex, where circumference increased from 5.04 +/- 0.24 at baseline to 7.86 +/- 0.43 cm at the end of occlusion (p = 0.0001), an increase of 58%. During reperfusion, ventricular geometry rapidly returned toward normal (baseline), with recovery of 80% of the increase in ESA evident by 15 minutes of reperfusion. Recovery of systolic function was substantially slower (p < 0.005 for all periods of observation during the 2 hours of reperfusion). During reperfusion, recovery of ventricular geometry and function was not uniform throughout the ischemic bed. The apex recovered most slowly, with the centroid of the area of abnormal contraction progressively moving along the long axis of the left ventricle toward the apex. There was also a progressive decrease in the radius of the area of dysfunction, from 2.0 +/- 0.15 at end occlusion to 0.13 +/- 0.07 cm at 120 minutes of reperfusion (p = 0.0001). There was no difference in blood flow between the apical and anterior segments during ischemia or reperfusion. Reperfusion favorably reduced the ischemic zone dilation before recovery of active systolic function and geometric recovery thus may be important in determining ultimate functional recovery. In addition, recovery of function proceeded inward towards the center of the ischemic territory and in a wavefront from the base to apex. This heterogeneous and asymmetric recovery suggests that sampling at one point within the ischemic zone may not reflect the true temporal pattern of recovery.

Combined influence of ventricular loading and relaxation on the transmitral flow velocity profile in dogs measured by Doppler echocardiography.

The relation of the Doppler transmitral flow velocity profile to left ventricular loading conditions and diastolic properties remains poorly described. We studied seven adult mongrel dogs with an open-chest right heart bypass model in which left atrial pressure, representing preload, was varied by controlling blood flow into the pulmonary artery and left ventricular systolic pressure, representing afterload, was controlled independently by pumping blood into or from the femoral arteries. Heart rate was kept constant by crushing the sinus node and pacing the right atrium. Mitral inflow velocity profiles were measured by pulsed-wave Doppler echocardiography at multiple left atrial and left ventricular systolic pressures. In individual dogs, the peak E-wave velocity increased linearly with increasing left atrial V-wave pressure at constant left ventricular systolic pressure and decreased with increasing left ventricular systolic pressure at constant left atrial pressure. Stepwise multiple linear regression analysis of data pooled from all experimental stages in all dogs identified left atrial V-wave pressure, the time constant of relaxation (TL), and left ventricular systolic pressure, in order of decreasing significance, as predictors of the peak E-wave velocity (n = 82, multiple r = 0.87, p less than 0.0001). Multivariate analysis with the same three factors in individual dogs yielded higher r values (mean r = 0.89; range, 0.85-0.97), suggesting the presence of important interdog differences that were not accounted for by these three factors alone. When the values of codeterminant hemodynamic factors were kept within narrower limits, correlations between peak E-wave velocity and left atrial V-wave pressure (n = 35, multiple r = 0.83, p less than 0.0001), TL (n = 76, multiple r = -0.54, p less than 0.0001) and left ventricular systolic pressure (n = 20, multiple r = -0.59, p less than 0.005) improved substantially. In the pooled data, the relation of the peak E-wave velocity to left atrial V-wave pressure was shifted downward by an increase in TL (reduced relaxation rate), and the relation of the peak E-wave velocity to TL was shifted upward by an increase in left atrial V-wave pressure. Multivariate analysis also selected left atrial V-wave pressure and TL as the two most significant correlates of the velocity-time integral and deceleration rate of the E wave.(ABSTRACT TRUNCATED AT 400 WORDS)