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Cardiac function in systemic hypertension before and after reversal of left ventricular hypertrophy
B Trimarco1, N De Luca, B Ricciardelli
1Prima Clinica Medica, Seconda Facoltà di Medicina, Università di Napoli, Italy.
Insights
Left ventricular hypertrophy (LVH) impairs the relationship between left ventricular (LV) function and stress. Reversing LVH restores normal LV function, improving the correlation between LV fractional shortening and end-systolic stress.
Area of Science:
- Cardiology
- Physiology
- Biomedical Engineering
Background:
- Hypertension can lead to left ventricular hypertrophy (LVH).
- LVH may alter the relationship between myocardial function and afterload.
- Understanding this relationship is crucial for managing hypertensive heart disease.
Purpose of the Study:
- To compare the relationship between left ventricular (LV) fractional shortening and end-systolic stress in normotensive and hypertensive individuals with and without LVH.
- To investigate the impact of LVH reversal on this relationship.
Main Methods:
- Three groups were studied: normotensives, hypertensives without LVH, and hypertensives with LVH.
- Echocardiography was used to measure LV fractional shortening and estimate end-systolic stress.
- The hypertensive group with LVH was restudied after antihypertensive treatment to induce LV mass reduction and after a washout period.
Main Results:
- A significant correlation between LV fractional shortening and end-systolic stress was observed in all groups.
- The slope of this correlation was significantly lower in hypertensives with LVH compared to normotensives and hypertensives without LVH.
- Reversal of LVH through antihypertensive treatment restored the slope to levels comparable to normotensives and hypertensives without LVH.
Conclusions:
- Left ventricular hypertrophy significantly attenuates the influence of afterload on LV function.
- Reversal of LVH normalizes the relationship between LV function and end-systolic stress.
- These findings highlight the importance of managing LVH in hypertensive patients.
Abstract:
In 3 age- and sex-matched groups of subjects--15 normotensives, 15 hypertensives without left ventricular (LV) hypertrophy and 15 hypertensives with LV hypertrophy--the slopes of the regression line obtained by plotting the individual values of LV fractional shortening against the corresponding values of echocardiographic end-systolic stress were compared. The first 2 groups were studied only in control conditions while the third group was restudied after a 20% reduction in LV mass index induced by a long-term antihypertensive treatment and after a 3-week washout period. A significant relation between fractional shortening and end-systolic stress was found in all instances. The slope of this correlation was higher in normotensives (-0.251) and in hypertensives without LV hypertrophy (-0.232) (both p less than 0.01) than in hypertensives with ventricular hypertrophy (-0.079). In this latter group, the slope increased after the reversal of LV hypertrophy (-0.230, p less than 0.01) and remained unchanged (-0.202) at the end of the washout period. No difference was detectable between the slopes obtained in these patients after reversal of LV hypertrophy, both with the antihypertensive treatment on and off, and those of normotensives and hypertensives without LV hypertrophy. Thus, LV hypertrophy attenuates the influence of changes in afterload on LV function. Reversal of LV hypertrophy restores a fractional shortening end-systolic stress relation quite comparable to that found both in normotensives and in hypertensives before the development of LV hypertrophy.