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J Am Coll Cardiol, 1994; 24:663-670
© 1994 by the American College of Cardiology Foundation
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Intracavitary filling pattern in the failing left ventricle assessed by color M-mode Doppler echocardiography

M Stugaard, C Risoe, H Ihlen, and OA Smiseth

Institute for Surgical Research, National Hospital, Oslo, Norway.

OBJECTIVES. The present study aimed to investigate the mechanism of intracavitary changes in filling pattern during acute ischemic left ventricular failure and during beta-adrenergic blockade. BACKGROUND. Recent clinical studies with color M-mode Doppler imaging have shown abnormal intracavitary filling patterns in the diseased ventricle. METHODS. In open chest anesthetized dogs with intracardiac micromanometers and myocardial segment-length crystals, global ischemic left ventricular failure was induced (n = 8) by coronary microembolization. In nonischemic ventricles inotropy was decreased (n = 6) by intravenous propranolol and increased (n = 6) by intravenous isoproterenol. From color M-mode Doppler images we calculated the time difference between peak early diastolic filling velocity at the mitral tip and apex using computer analysis. The time difference of peak velocity was used as an index of the timing of apical filling. RESULTS. There was marked retardation of apical filling with microembolization and propranolol. Time difference of peak velocity increased from 20 +/- 6 (mean +/- SEM) to 101 +/- 17 ms (p < 0.05) and from 21 +/- 8 to 80 +/- 18 ms (p < 0.05), respectively. Time constant of isovolumic relaxation increased from 34 +/- 3 to 43 +/- 5 ms (p < 0.05) and from 31 +/- 1 to 39 +/- 3 ms (p < 0.05) during microembolization and beta-blockade, respectively. Isoproterenol tended to cause the opposite changes. Time difference of peak velocity showed a positive correlation with time constant of isovolumic relaxation (r = 0.89, p < 0.01) and a negative correlation with peak early transmitral pressure gradient (r = 0.88, p < 0.01). In the intact left ventricle, peak apical filling velocity coincided with peak early transmitral pressure gradient. During ischemic failure however, peak apical filling velocity occurred 53 +/- 14 ms after peak early transmitral pressure gradient had decreased to zero and at a time when transmitral flow had ceased, suggesting a change in intraventricular flow distribution. CONCLUSIONS. Color M-mode Doppler imaging revealed retarded apical filling during depression of myocardial function by global myocardial ischemia or beta-blockade. The abnormal filling pattern may be a sign of impaired left ventricular relaxation.


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