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Left ventricular contraction and relaxation in patients with coronary heart disease
Insights
Coronary heart disease impairs left ventricular relaxation and compliance, leading to elevated end-diastolic pressure during ischemia. This study reveals delayed relaxation and active diastolic tone generation in the intact ventricle.
Area of Science:
- Cardiology
- Physiology
Background:
- Left ventricular end-diastolic pressure elevation during ischemia is a critical clinical concern.
- Understanding the interplay between relaxation, compliance, and diastolic pressure is vital for managing ischemic heart disease.
Purpose of the Study:
- To investigate the mechanisms linking left ventricular (LV) relaxation and compliance to elevated LV end-diastolic pressure during ischemia.
- To compare these mechanisms in healthy individuals and patients with coronary heart disease (CHD).
Main Methods:
- Studied isovolumic LV contraction, relaxation, and diastolic pressure-volume relationships.
- Utilized ergometric exercise and pacing to induce controlled conditions in controls and CHD patients.
- Measured LV pressures and calculated peak velocities of shortening (Vpm) and lengthening (Vpmr).
Main Results:
- LV dP/dtmax increased in both groups during pacing and exercise; LV dP/dtmin increased only in controls during exercise.
- In CHD patients, Vpm increased with pacing, but Vpmr remained unchanged during pacing and exercise.
- CHD patients experiencing angina showed altered diastolic pressure-volume relationships, indicating impaired relaxation and active diastolic tone.
Conclusions:
- Ischemia in CHD patients results in an impaired contractile state.
- Delayed relaxation and the generation of active diastolic tone contribute to elevated LV end-diastolic pressure during ischemia.
- These findings highlight significant diastolic dysfunction in CHD under ischemic conditions.
Abstract:
The relationship of left ventricular relaxation and compliance to the mechanism of elevation of left ventricular enddiastolic pressure during ischemia was investigated. Isovolumic left ventricular contraction, relaxation, and diastolic pressure-volume relationship were studied in controls and in coronary heart disease patients. Patients were studied at similar heart rates during ergometric exercise and pacing. Diastolic aortic, left ventricular systolic, and incisural pressure were not significantly different in both groups at rest, pacing, and exercise. Left ventricular dP/dtmax increased during pacing and exercise in controls (P smaller than 0.05; P smaller than 0.01) and in coronary heart disease patients (P smaller than 0.01 for both); whereas left ventricular dP/dtmin increased only in controls during exercise (P smaller than 0.01). Peak measured velocity of shortening (Vpm) and of lengthening (Vpmr) of the contractile elements was calculated as (dP/dt)/p. Vpm and Vpmr increased in controls during both pacing (P smaller than 0.05; P smaller than 0.02) and exercise (P smaller than 0.01 for both). In coronary heart disease patients Vpm increased during pacing (P smaller than 0.01) while Vpmr did not differ significantly. During exercise both Vpm and Vpmr were unchanged. In patients with coronary heart disease paced to angina, diastolic logarithmic pressure-volume relationship showed change in slope (P smaller than 0.05) of the regression line and upward shift in intercept b (+0.25; P smaller than 0.001). Ischemia produced an impaired contractile state, delayed relaxation and generation of active diastolic tone in the intact ventricle.