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Regression of hypertensive myocardial hypertrophy does not affect ultrasonic myocardial reflectivity: a tissue
A R Lucarini1, G Gigli, F Lattanzi
1Institute of Clinical Physiology, CNR, Pisa, Italy.
Insights
Antihypertensive therapy with enalapril effectively reduces left ventricular hypertrophy in essential hypertensives. This treatment does not alter myocardial reflectivity, suggesting proportionate regression of heart muscle and connective tissue.
Area of Science:
- Cardiology
- Hypertension Research
- Medical Imaging
Background:
- Ultrasonic backscatter correlates with myocardial collagen content.
- Hypertensive patients with left ventricular hypertrophy show normal ultrasonic backscatter.
- The effect of antihypertensive therapy on myocardial connective tissue is unknown.
Purpose of the Study:
- To assess the impact of left ventricular hypertrophy regression on myocardial reflectivity in essential hypertensives.
- To investigate changes in quantitative ultrasonic backscatter after antihypertensive treatment.
Main Methods:
- 19 mild-to-moderate essential hypertensives with left ventricular hypertrophy were treated with enalapril for 8 months.
- Echocardiography assessed left ventricular hypertrophy.
- Quantitative operator-independent measurements of integrated backscatter index (IBI) were obtained using a modified echo machine.
Main Results:
- Antihypertensive therapy significantly reduced blood pressure, left ventricular mass index, and wall thickness.
- Integrated backscatter index values remained unchanged in the septum and posterior wall post-therapy.
Conclusions:
- Enalapril induces regression of left ventricular hypertrophy without increasing myocardial reflectivity.
- This suggests that enalapril promotes proportionate regression of myocytes and connective tissue in the myocardium.
Objective:
Ultrasonic backscatter from the myocardial walls is directly related to the morphometrically or biochemically evaluated collagen content in man, and shows a normal pattern of quantitatively assessed ultrasonic backscatter in hypertensive patients, even in the presence of left ventricular hypertrophy. Whether the pharmacologically induced regression of left ventricular hypertrophy in hypertensive patients is accompanied by a disproportionate increase in relative connective tissue content is not yet known. The objective of the present study was to assess the effects of regression of left ventricular hypertrophy on the quantitatively evaluated myocardial reflectivity in essential hypertensives.
Design:
We evaluated 19 mild-to-moderate essential hypertensives with echocardiographically assessed left ventricular hypertrophy, before and after 8 months' effective antihypertensive therapy with 20-40 mg enalapril once a day, associated with diuretics or calcium antagonists, or both, in six patients to achieve optimal blood pressure control. Using a modified echo machine developed in the Institute of Clinical Physiology, Pisa, an on-line radio-frequency analysis was performed to obtain quantitative operator-independent measurements of the integrated backscatter signal of the ventricular septum and the posterior wall. The integrated values of the radio-frequency signal from the myocardial walls were normalized for those from the pericardial interface and were expressed as percentages (integrated backscatter index).
Results:
In comparison with baseline, the treated hypertensives showed significant decreases in mean blood pressure, left ventricular mass index, and septal and posterior wall thickness. However, integrated backscatter index values were similar at baseline and after therapy for both the septum and the posterior wall.
Conclusion:
Antihypertensive therapy with enalapril does not increase myocardial reflectivity, although it does induce regression of left ventricular hypertrophy. This suggests that, in accord with experimental data, regression of hypertrophy is achieved by enalapril through a proportionate regression of the myocyte and connective tissue components of the myocardium.