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Research Article Free access | 10.1172/JCI113778

Depression of systolic and diastolic myocardial reserve during atrial pacing tachycardia in patients with dilated cardiomyopathy.

M D Feldman, J D Alderman, J M Aroesty, H D Royal, J J Ferguson, R M Owen, W Grossman, and R G McKay

Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts.

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Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts.

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Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts.

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Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts.

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Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts.

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Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts.

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Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts.

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Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts.

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Published November 1, 1988 - More info

Published in Volume 82, Issue 5 on November 1, 1988
J Clin Invest. 1988;82(5):1661–1669. https://doi.org/10.1172/JCI113778.
© 1988 The American Society for Clinical Investigation
Published November 1, 1988 - Version history
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Abstract

Previous reports have shown that increases in heart rate may result in enhanced left ventricular (LV) systolic and diastolic performance. To assess whether this phenomenon occurs in the presence of depressed LV function, the effects of pacing on LV pressure and volume were compared in seven patients with dilated cardiomyopathy (LV ejection fraction 0.19 +/- 0.11) and six patients with no or minimal coronary artery disease (LV ejection fraction 0.69 +/- 0.11). Patients with normal LV function demonstrated significant increases in LV peak-positive dP/dt, LV end-systolic pressure-volume ratio, LV peak filling rate, and a progressive leftward and downward shift of their pressure-volume diagrams, compatible with increased contractility and distensibility in response to pacing tachycardia. There was no change in LV peak-negative dP/dt or tau. Patients with dilated cardiomyopathy, in contrast, demonstrated no increase in either LV peak-positive dP/dt or the end-systolic pressure-volume ratio, and absence of a progressive leftward shift of their pressure-volume diagrams. Moreover, cardiomyopathy patients demonstrated no increase in LV peak-negative dP/dt or LV peak filling rate and a blunted downward shift of the diastolic limb of their pressure-volume diagrams. Tau, as determined from a derivative method, became abbreviated although never reaching control values. We conclude that patients with dilated cardiomyopathy may demonstrate little or no significant enhancement in systolic and diastolic function during atrial pacing tachycardia, suggesting a depression of both inotropic and lusitropic reserve.

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