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Left ventricular filling and early diastolic function at rest and during angina in patients with coronary artery
1Brompton Hospital, London.
Insights
Angina pectoris significantly impairs early left ventricular diastolic function in coronary artery disease patients. This dysfunction, characterized by an upward shift in the diastolic pressure-volume relation, is not due to increased chamber stiffness.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Diastology
Background:
- Coronary artery disease (CAD) can affect left ventricular (LV) diastolic function.
- Understanding diastolic dysfunction during angina is crucial for patient management.
Purpose of the Study:
- To investigate the impact of angina on LV diastolic function in patients with CAD.
- To elucidate the mechanisms underlying diastolic pressure-volume relation changes during angina.
Main Methods:
- Studied 11 CAD patients using simultaneous ventriculography and LV pressure monitoring.
- Analyzed LV shape, volume, and pressure decay during rest and induced angina.
- Calculated time constant (tau) of pressure fall and constructed pressure-volume loops.
Main Results:
- Angina increased end-systolic volume and decreased ejection fraction, with unchanged end-diastolic volume.
- LV minimum and end-diastolic pressures increased, shifting the diastolic pressure-volume relation upwards.
- The proportion of stroke volume entering during early diastole decreased significantly during angina.
- LV chamber stiffness (late diastole slope) remained unchanged.
Conclusions:
- Angina profoundly disturbs early LV diastolic function, evidenced by an upward shift in the diastolic pressure-volume relation.
- This shift is apparent early in diastole and not caused by increased passive chamber stiffness.
- Loss of elastic recoil and asynchronous relaxation likely contribute to early diastolic dysfunction during angina.
Abstract:
Left ventricular diastolic function was studied in 11 patients with coronary artery disease. Single plane ventriculography (30 degrees right anterior oblique projection) was performed at rest and during an episode of angina immediately after a period of rapid atrial pacing. Left ventricular pressure was recorded simultaneously by a micromanometer tipped catheter. The ventriculograms were digitised frame by frame to derive continuous plots of left ventricular shape, volume, and rate of change of volume. The time constant (tau) of the fall in left ventricular pressure was determined from the exponential portion of pressure decay during isovolumic relaxation. Ventricular pressure-volume loops were constructed to study the left ventricular diastolic pressure-volume relation. The time of minimum left ventricular pressure was used to divide diastole into an early phase and a late phase. Angina was associated with an increase in end systolic volume and a fall in ejection fraction with no significant change in end diastolic volume. Peak left ventricular pressure was unchanged but left ventricular minimum and end diastolic pressures were both increased and the diastolic pressure-volume relation was moved upwards. The time constant of left ventricular pressure fall was prolonged. At rest more than 50% of the stroke volume entered the left ventricle during the period of early diastole. This proportion was significantly reduced during angina and as a consequence a significantly greater proportion of the stroke volume entered the ventricle during late diastole. Despite this, and although the left ventricular diastolic pressure-volume relation was moved upwards with angina, the mean slope of the relation during late diastole--that is, chamber stiffness--was not significantly altered. The upward shift of the left ventricular diastolic pressure-volume relation seen during angina is thus already apparent in early diastole, and its extent does not change during the later phase of diastole, which alone shows the property of passive stiffness. A primary increase in the passive stiffness of the ventricle cannot therefore be the cause of the upward shift of the diastolic pressure-volume relation, and events occurring in early diastole have to be looked to for an explanation. The study findings show that left ventricular function in early diastole is profoundly disturbed during angina pectoris and it is suggested that loss of elastic recoil and dissipation of this restoring force by asynchronous onset of relaxation and abnormal changes in shape are important factors contributing to this disturbance of function.