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Determinants of left ventricular hypertrophy and function in hypertensive patients. An echocardiographic study
Insights
Hypertension commonly causes left ventricular hypertrophy in patients, regardless of treatment. Cardiac performance in hypertensive individuals is significantly impacted by afterload, particularly when left ventricular hypertrophy is present.
Area of Science:
- Cardiology
- Hypertension Research
- Echocardiography
Background:
- Hypertension frequently leads to cardiac structural changes.
- Echocardiography is crucial for assessing these alterations.
Purpose of the Study:
- To investigate echocardiographic changes in hypertensive patients.
- To compare changes in treated versus untreated hypertensive individuals.
- To analyze the relationship between cardiac performance and left ventricular hypertrophy.
Main Methods:
- Review of echocardiographic data from 74 hypertensive patients (37 treated, 37 untreated).
- Classification of left ventricular hypertrophy subtypes.
- Assessment of cardiac performance using left ventricular percent shortening.
- Analysis of end-systolic stress and myocardial contractility indices.
Main Results:
- Left ventricular hypertrophy was observed in 58% of patients.
- No significant difference in hypertrophy prevalence or subtypes between treated and untreated groups.
- Asymmetric septal hypertrophy was not associated with abnormal mitral valve motion.
- Cardiac performance correlated inversely with end-systolic stress and positively with myocardial contractility.
- Left ventricular hypertrophy, especially with dilation, increased dependence on afterload.
Conclusions:
- Hypertension commonly induces left ventricular hypertrophy, irrespective of treatment status.
- Cardiac function in hypertensive patients is significantly influenced by afterload and contractility.
- Left ventricular hypertrophy and dilation exacerbate afterload dependence in hypertensive hearts.
Abstract:
Hypertensive patients present a wide spectrum of echocardiographic alterations. A review of these changes in 74 patients (37 untreated and 37 treated) revealed left ventricular hypertrophy in 43 (58 percent). There was no significant difference between treated and untreated patients in regard to either the prevalence of left ventricular hypertrophy or of its various subtypes [concentric left ventricular hypertrophy in 15 (20.3 percent), asymmetric septal hypertrophy in 16 (21.6 percent), and combined left ventricular hypertrophy and dilation in 12 (16.2 percent)]. None of the patients who showed asymmetric septal hypertrophy had abnormal motion of the mitral valve. Cardiac performance as judged by left ventricular percent shortening was related inversely to end-systolic stress (p less than 0.001) and positively to the ratio of end-systolic pressure/end-systolic volume (an index of myocardial contractility) (p less than 0.01). Multiple regression analysis showed an increased dependence on afterload (end-systolic stress), when left ventricular hypertrophy developed and especially when it was associated with left ventricular dilation.