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Left ventricular flow from apex to base during systole and isovolumic relaxation in a patient with hypertrophic cardiomyopathy and midventricular obstruction


Sütsch, G; Jenni, R; Krayenbühl, H P (1991). Left ventricular flow from apex to base during systole and isovolumic relaxation in a patient with hypertrophic cardiomyopathy and midventricular obstruction. European Heart Journal, 12(10):1132-1139.

Abstract

The occurrence of a left ventricular anterograde flow velocity (maximal: 3·9m . s−1) is demonstrated in a 32-year-old patient with hypertrophic cardioinyopathy and midveniricular obstruction, beginning at early systole and persisting throughout the isovolumic relaxation. Cardiac catheterization with simultaneous dual high fidelity pressure measurements in the apical and basal chambers confirmed the presence of the Doppler maximal instantaneous pressure gradient of 60 mmHg. Contrast left ventricular angiography excluded apical dyskinesia. In the two intracavity compartments, isovolumic relaxation time and the time constant of pressure decay (τ) were abnormal whereby τ was more delayed in the apical than in the basal portion. The presence of an apical high pressure zone during systole with impeded and delayed emptying through the midventricular obstacle and the late onset and prolongation of relaxation are thought to be the cause of the intraventricular flow from apex to base lasting from early systole throughout isovolumic relaxation

Abstract

The occurrence of a left ventricular anterograde flow velocity (maximal: 3·9m . s−1) is demonstrated in a 32-year-old patient with hypertrophic cardioinyopathy and midveniricular obstruction, beginning at early systole and persisting throughout the isovolumic relaxation. Cardiac catheterization with simultaneous dual high fidelity pressure measurements in the apical and basal chambers confirmed the presence of the Doppler maximal instantaneous pressure gradient of 60 mmHg. Contrast left ventricular angiography excluded apical dyskinesia. In the two intracavity compartments, isovolumic relaxation time and the time constant of pressure decay (τ) were abnormal whereby τ was more delayed in the apical than in the basal portion. The presence of an apical high pressure zone during systole with impeded and delayed emptying through the midventricular obstacle and the late onset and prolongation of relaxation are thought to be the cause of the intraventricular flow from apex to base lasting from early systole throughout isovolumic relaxation

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Item Type:Journal Article, refereed, original work
Communities & Collections:National licences > 142-005
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Scopus Subject Areas:Health Sciences > Cardiology and Cardiovascular Medicine
Language:English
Date:1 September 1991
Deposited On:16 Oct 2018 15:12
Last Modified:15 Apr 2021 14:49
Publisher:Oxford University Press
ISSN:0195-668X
OA Status:Green
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1093/oxfordjournals.eurheartj.a059847

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