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[Echocardiographic features of left ventricular hypertrophy and contractility in malignant hypertension]
Y Nakamura1, M Arita, S Fujiwara
1Department of Medicine, Wakayama Medical College.
Insights
Malignant hypertension involves inappropriate left ventricular hypertrophy and systolic dysfunction, potentially driven by increased neurohumoral factors. This impacts cardiac hemodynamics significantly.
Area of Science:
- Cardiology
- Hypertension Research
- Echocardiography
Context:
- Malignant hypertension presents unique hemodynamic challenges.
- Understanding these characteristics is crucial for effective treatment.
- Previous studies have not fully elucidated the specific echocardiographic findings in different types of malignant hypertension.
Purpose:
- To assess and compare the hemodynamic characteristics in patients with malignant essential hypertension (MH-I) and secondary malignant hypertension (MH-II).
- To evaluate left ventricular structure and function using echocardiography.
- To investigate the role of plasma noradrenaline (NA) and renin activity (PRA) in malignant hypertension.
Summary:
- Echocardiography revealed inappropriate left ventricular hypertrophy, increased end-systolic dimension, and moderate decreases in ejection fraction (EF) and mean velocity of circumferential fiber shortening (mVcf) in both MH-I and MH-II groups.
- Plasma NA and PRA were markedly elevated in both malignant hypertension groups.
- These findings suggest that increased systolic stress and neurohumoral factors contribute to cardiac dysfunction in malignant hypertension.
Impact:
- Provides detailed echocardiographic insights into the pathophysiology of malignant hypertension.
- Highlights the significant role of neurohumoral activation in cardiac impairment.
- Informs potential therapeutic strategies targeting hemodynamic abnormalities and neurohumoral pathways.
Abstract:
To assess the hemodynamic characteristics in malignant hypertension, echocardiography was performed in 18 patients with malignant essential hypertension (MH-I, n = 9) and secondary hypertension (MH-II, n = 9). Patients with benign hypertension with or without left ventricular hypertrophy (n = 8 and 7, respectively), patients with hypertensive heart failure (n = 7) and normotensive volunteers (n = 10) were subjected to controls. Plasma noradrenaline (NA) and renin activity (PRA) were also measured prior to the antihypertensive therapy. There were no significant differences in the durations of hypertension before the malignant phase, and the mean arterial pressure between MH-I and MH-II. Although posterior wall thickness (PWTd) in MH-II was similar to that in MH-I, interventricular septal thickness (IVSTd) was less marked in MH-II. The plasma NA and PRA were markedly increased in both MH-I and MH-II. End-diastolic dimension (Dd) of the left ventricle was within normal range, but end-systolic dimension (Ds) was significantly increased in MH-I, MH-II and hypertensive heart failure. The moderate decreases in ejection fraction (EF) and mean velocity of circumferential fiber shortening (mVcf) were observed in both MH-I and MH-II. Marked decreases in EF and mVcf were also observed in patients with hypertensive heart failure. The relationship between systolic blood pressure and Dd/PWTd was shifted toward the right and upper portion of the normal relation in MH-I and MH-II. The present study demonstrated that the hemodynamic characteristics in malignant hypertension are an inappropriate left ventricular hypertrophy due to a marked increase in systolic stress; dilatation of the left ventricle in systole; and a moderate decrease in ventricular systolic function. It is suggested that a decrease in left ventricular systolic function in malignant hypertension might be due in part to a marked increase in the influence of neurohumoral factors on hemodynamics.