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Impact of regression of left ventricular hypertrophy on cardiac function in hypertension
1Department of Cardiology, Stobhill General Hospital, Glasgow.
Insights
Regression of left ventricular hypertrophy (LVH) in hypertensive patients maintains cardiac function. This regression, influenced by blood pressure reduction and medication, does not harm systolic or diastolic function, even if pressure rises post-treatment.
Area of Science:
- Cardiology
- Hypertension Research
- Cardiac Physiology
Background:
- Left ventricular hypertrophy (LVH) is a common adaptation to hypertension.
- Regression of LVH occurs with blood pressure reduction.
- The impact of LVH regression on cardiac function requires clarification.
Purpose of the Study:
- To assess the effects of LVH regression on cardiac function in hypertensive patients.
- To determine if LVH regression is detrimental to systolic and diastolic function.
- To evaluate cardiac function maintenance when blood pressure returns to pretreatment levels.
Main Methods:
- Review of current data on LVH regression and cardiac function.
- Analysis of factors influencing regression (blood pressure, drug therapy, hypertrophy degree).
- Assessment of cardiac function at rest and during exercise post-regression.
Main Results:
- Systolic function is maintained at rest and during exercise following LVH regression.
- Diastolic function shows improvement in some studies.
- Cardiac function remains stable even if blood pressure reverts to pretreatment levels.
Conclusions:
- Regression of LVH in hypertensive patients does not appear to damage cardiac function.
- Both systolic and diastolic functions are generally maintained or improved.
- Further research is needed on the impact of LVH regression on long-term morbidity and mortality.
Abstract:
It is now established that regression of left ventricular hypertrophy (LVH) occurs following reduction of arterial pressure in patients with hypertension. A number of factors contribute towards this regression, including the fall in blood pressure itself, the drug therapy given, and the pre-existing degree of hypertrophy. LVH is in some senses a beneficial adaptive response in terms of systolic function, and therefore it is important to clarify whether or not regression of hypertrophy is damaging to cardiac function. Overall assessment of these effects has been more difficult because the antihypertensive drug therapy and the changes in blood pressure also contribute to left ventricular function. Current data indicate that systolic function is maintained both at rest and following exercise but not necessarily improved. In contrast, diastolic function in some but not all studies, has been shown to have been improved. Recent information has allayed fears that regression of LVH may cause a deterioration in function if blood pressure is allowed to return to its pretreatment levels. It would appear that in this situation function is maintained both at rest and during exercise. Finally, the assessment of cardiac function following regression of hypertrophy remains a surrogate end-point. The key information required remains the influence of regression of hypertrophy and its alteration in function on morbidity and mortality in patients with hypertension.
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