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Contractility of the hypertrophied human left ventricle in chronic pressure and volume overload
Insights
Left ventricular contractility was similarly depressed in patients with pressure load and volume load, despite different stimuli for hypertrophy. This finding holds true when matched for left ventricular muscle mass.
Area of Science:
- Cardiology
- Physiology
Background:
- Left ventricular hypertrophy can result from pressure overload (e.g., aortic stenosis) or volume overload (e.g., aortic incompetence).
- Assessing contractility in these conditions is crucial for understanding cardiac function and disease progression.
Purpose of the Study:
- To compare left ventricular contractility in patients with pressure load versus volume load, matched for left ventricular muscle mass.
- To investigate the impact of different loading conditions on myocardial contractility.
Main Methods:
- High-fidelity left ventricular pressure measurements and cineangiography were performed on three groups: normal controls, pressure load (PL), and volume load (VL).
- Peak measured velocity of contractile elements (Vpm) was determined as an index of contractility.
- Left ventricular muscle mass index (LMMI) was calculated and groups were matched for LMMI.
Main Results:
- Left ventricular muscle mass index (LMMI) was significantly increased in both pressure load (PL) and volume load (VL) groups compared to controls.
- Peak measured velocity of contractile elements (Vpm), an index of contractility, was significantly reduced in both PL and VL groups compared to controls.
- No significant difference in Vpm was observed between the pressure load and volume load groups, indicating similar levels of depressed contractility.
Conclusions:
- Left ventricular contractility is depressed to a similar extent in patients with predominant pressure load and volume load.
- This depression in contractility occurs regardless of the specific stimulus causing left ventricular hypertrophy when left ventricular muscle mass is matched.
Abstract:
Nine patients with normal left ventricles (C), 10 patients with pressure load (PL) due to predominant aortic stenosis, and 9 patients with predominant volume load (VL) due to aortic incompetence were studied by left ventricular high-fidelity pressure measurements and cineangiography. Peak measured velocity of the contractile elements (Vpm) used as index of contractility and left ventricular muscle mass (LMMI) were determined. The patients with PL and VL were matched with respect to LMMI. In PL LMMI was 241 +/- 41 and in VL 254 +/- 42 gm. per square meter. Both were sizably increased (P smaller than 0.001) as compared to LMMI in C (89 +/- 24 gm. per square meter). Vpm was 1.41 +/- 0.20 ML per second in C. In PL and VLVpm was reduced to 1.05 +/- 0.26 (P smaller than 0.01) and to 1.07 +/- 0.33 ML per second (P smaller than 0.02). Vpm in PL was not different from Vpm in VL. Heart rate showed no major difference in the three groups. It is concluded that in two groups of patients with predominant PL and VL matched with respect to LMMI left ventricular contractility was depressed to a similar extent regardless of the stimulus to hypertrophy.