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End-systolic pressure-volume and end-systolic stress-volume relationships in patients with aortic stenosis and with
Insights
Left ventricular hypertrophy in aortic stenosis patients alters the end-systolic pressure-volume relationship, making it steeper. However, the end-systolic stress-volume relationship remains unchanged, proving useful for evaluating hypertrophied ventricles.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- Left ventricular hypertrophy (LVH) is a common adaptation to pressure overload.
- The end-systolic pressure-volume relationship (ESPVR) is a key index of systolic function.
- Understanding how LVH affects ESPVR is crucial for assessing cardiac performance.
Purpose of the Study:
- To investigate the impact of left ventricular hypertrophy on the end-systolic pressure-volume relationship.
- To compare ESPVR in patients with and without aortic stenosis.
Main Methods:
- Left ventricular angiograms were performed in two groups: normal function (group 1) and aortic stenosis (group 2).
- Measurements were taken at rest and under altered afterload conditions (isosorbide-dinitrate, methoxamine).
- Drugs were used to manipulate afterload, and heart rate was controlled via atrial pacing.
Main Results:
- In group 1 (normal function), ESPVR slope (k) correlated with ejection fraction (EF): k = 0.024 * e^(0.072 * EF).
- In group 2 (aortic stenosis, higher LV mass), the ESPVR was shifted left (steeper): k = 0.135 * e^(0.057 * EF).
- The end-systolic stress-volume relationship showed no significant difference between groups.
Conclusions:
- Patients with aortic stenosis exhibit a steeper end-systolic pressure-volume relationship compared to those without valvular dysfunction.
- The end-systolic stress-volume relationship is preserved in aortic stenosis and is valuable for evaluating pressure-overload-induced left ventricular hypertrophy.
Abstract:
In order to study the effect of left ventricular hypertrophy on the endsystolic pressure-volume relationship, three left ventricular angiograms were performed in ten patients with normal valvular function but with varying left ventricular function (group 1) after 0.15 mg/kg propranolol and 1 mg atropine: at rest, after isosorbide-dinitrate at a decreased afterload and after methoxamine at an enhanced afterload. In eight patients with aortic stenosis (group 2) two left ventricular angiograms were performed: at rest and after isosorbide-dinitrate. Heart rate was kept constant by atrial pacing. Left ventricular mass in group 1 was 89 g/m2 and in group 2 180 g/m2. In group 1 the slope k of the end-systolic pressure-volume relation was related to the ejection fraction (EF) at rest: k = 0.024 . e0.072 EF; r = 0.93. In group 2 this relation was shifted to the left (P less than 0.001): k = 0.135 . e0.057 EF; r = 0.81. The relations, however, between the slope k of the end-systolic stress-volume relation and the ejection fraction were close together in group 1 and in group 2 and crossed at an ejection fraction of 67%. It is concluded: 1. In patients with aortic stenosis the end-systolic pressure-volume relation is steeper than in patients without valvular dysfunction at a given ejection fraction, so the relation between the slope k and the ejection fraction is shifted to the left. 2. The end-systolic stress-volume relationship is not altered in patients with aortic stenosis and seems to be advantageous for the evaluation of left ventricles with substantial hypertrophy due to pressure load.