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Mechanisms of reduced left ventricular filling rate in coronary artery disease
Insights
Coronary artery disease impairs left ventricular filling due to abnormal shape changes and asynchronous wall motion. These factors reduce the heart
Area of Science:
- Cardiology
- Biomedical Engineering
Background:
- Coronary artery disease (CAD) can affect left ventricular (LV) diastolic function.
- Understanding the mechanisms of impaired LV filling is crucial for managing CAD patients.
Purpose of the Study:
- To investigate the mechanisms behind slow left ventricular filling in patients with coronary artery disease.
- To analyze global and regional cardiac function in relation to LV filling dynamics.
Main Methods:
- Digitized left ventriculograms from 93 CAD patients and 18 normal subjects were analyzed frame-by-frame.
- Global and regional LV function, including filling rates, ejection fraction, and wall motion, were assessed.
- Analysis focused on identifying correlations between cardiac function parameters and LV filling abnormalities.
Main Results:
- 39 out of 93 CAD patients exhibited slow normalized peak filling rates.
- Patients with slow filling had lower ejection fraction, higher end-systolic volume, and reduced overall shape index change.
- Asynchronous wall motion during isovolumic relaxation and slow outward wall motion were significant findings, independent of CAD distribution or ECG changes.
Conclusions:
- Slow LV filling in CAD is primarily caused by failure to achieve normal end-systolic volume and incoordinate wall motion during isovolumic relaxation.
- Asynchronous wall motion dissipates energy, hindering rapid ventricular filling.
- These diastolic dysfunction mechanisms have clinical implications, particularly when filling time is limited.
Abstract:
To identify mechanisms underlying slow left ventricular filling in coronary artery disease, left ventriculograms from 93 patients and 18 normal subjects were digitised frame by frame and global and regional function analysed. In 54 patients peak normalised filling rates were above the lower 95% confidence limit of normal (2 X 9s-1) and in 39 they were below. Patients with slow filling had a lower ejection fraction, a higher end systolic volume, and less overall shape index change, although a larger percentage occurred during isovolumic relaxation owing to asynchronous relaxation. Stroke volume was not significantly different. Slow outward wall motion was associated with increased cavity volume and systolic hypokinesis. Wall motion was also appreciably asynchronous, with wide spreads in the times of peak outward velocity and termination of rapid outward movement between regions. Early outward movement usually started in the anterior region, with peak velocity occurring before mitral valve opening, and significantly earlier than that in the apex or the inferior region. Ventricular oscillations occurred during filling in 23 patients. This asynchronous wall movement was unrelated to the distribution of coronary artery disease, systolic hypokinesis, or Q waves on electrocardiograms but was similar to that occurring in mitral stenosis. The main causes of slow left ventricular filling in patients with coronary artery disease appear to be (a) failure to achieve a normal low end systolic volume, with associated loss of physiological changes in left ventricular cavity shape, and (b) incoordinate wall motion during isovolumic relaxation which dissipates energy normally coupled to rapid ventricular filling. The resulting slow and asynchronous wall motion may have clinical implications especially when the time available for left ventricular filling is short.