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Assessment of left ventricular systolic function in man from simultaneous echocardiographic and pressure measurements
Insights
This study investigated impaired left ventricular systolic function in heart disease patients using echocardiography and micromanometry. Findings reveal diverse disturbances, including abnormal contraction patterns and reduced myocardial power, impacting overall cardiac efficiency.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Echocardiography
Background:
- Left ventricular systolic function is crucial for effective cardiac output.
- Understanding the mechanisms of systolic dysfunction in heart disease is clinically important.
- Echocardiography and micromanometry offer simultaneous insights into ventricular mechanics and hemodynamics.
Purpose of the Study:
- To investigate the mechanisms underlying impaired left ventricular systolic function in patients with heart disease.
- To correlate echocardiographic measurements with pressure data for a comprehensive assessment of ventricular performance.
- To identify and differentiate various types of disturbances contributing to clinical left ventricular disease.
Main Methods:
- Simultaneous echocardiography (left ventricular dimension, wall thickness) and micromanometry (pressure) during cardiac catheterization.
- Digitization of echocardiograms and pressure traces for continuous analysis of dimensional and thickness changes.
- Estimation of ejection fraction from digitized cineangiograms; calculation of myocardial power and construction of pressure-dimension loops.
Main Results:
- Strong correlation (r=0.92) observed between peak left ventricular dP/dt and peak rate of dimension reduction (excluding severe mitral regurgitation).
- Peak myocardial power in normal function ranged from 30 to 60 mW cm-3 myocardium.
- Incoordinate contraction led to pressure-dimension loop distortion and reduced cycle efficiency (<75% of maximum).
Conclusions:
- Patients with left ventricular disease showed reduced ejection fraction, peak power, and cycle efficiency, individually or combined.
- No single pattern emerged, suggesting diverse underlying disturbances in clinical left ventricular disease.
- Disturbances include structural abnormalities, reduced myocardial shortening/power rates, and incoordinate contraction, which can be studied individually.
Abstract:
Simultaneous measurements of left ventricular dimension and wall thickness by echocardiography, and of pressure by micromanometer, were made at cardiac catheterization in 30 patients with heart disease, in order to study mechanisms of impairment of left ventricular systolic function. Echocardiograms and pressure traces were digitized so that continuous measurements of left ventricular wall thickness and dimensions with their rates of change could be obtained. Ejection fraction was estimated from digitized cineangiograms. In all patients, except those with severe mitral regurgitation, there was close correlation (r=0.92) between peak left ventricular dP/dt and peak rate of reduction of dimension. Myocardial power values, calculated as the product of circumferential shortening rates and wall stress were plotted throughout the cardiac cycle, and peak values in patients with normal left ventricular function were in the range 30 to 60 mW cm-3 myocardium. Pressure-dimension loops were constructed, which reflected the relation between the function of a localized region of cavity studied by echocardiography and that of the ventricle as a whole in the pressure wave form. Incoordinate contraction was associated with distortion of the loop and a reduction in its area to less than 75% that of the maximum for the cycle in question (cycle efficiency). In patients with left ventricular disease, ejection fraction, peak power, and cycle efficiency were all reduced, either singly or in combination. There was no consistent pattern, however, suggesting that clinical left ventricular disease may be the resultant of a number of different types of disturbance. These include structural abnormalities, reduction in peak rates of myocardial shortening or power development, and incoordinate contraction. The present investigation suggests ways in which these may be separated and studied in individual patients.