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[The role of hypertension in apical hypertrophy]
Insights
Hypertension can cause various cardiac hypertrophy types. Asymmetrical apical hypertrophy (AAH) in hypertensive patients is linked to mild hypertension and hyperkinetic states, showing preserved cardiac function.
Area of Science:
- Cardiology
- Hypertension Research
- Cardiac Imaging
Context:
- Echocardiography advances reveal hypertension's impact on cardiac hypertrophy.
- Classifying hypertensive patients by hypertrophy type is crucial for understanding cardiac function.
- Previous studies have not fully elucidated the specific cardiac functional characteristics of different hypertrophy subtypes in hypertension.
Purpose:
- To classify hypertensive patients by cardiac hypertrophy type.
- To evaluate left ventricular function and hypertension severity in these groups.
- To compare cardiac function across different hypertrophy subtypes and normotensive controls.
Summary:
- This study classified 257 hypertensive patients into four groups: no hypertrophy, concentric hypertrophy, asymmetrical septal hypertrophy (ASH), and asymmetrical apical hypertrophy (AAH).
- Patients with AAH and hypertension exhibited mild blood pressure levels and organ involvement, with cardiac function comparable to normotensive AAH patients.
- Hypertensive AAH patients showed higher cardiac index and left ventricular systolic function, with larger left ventricular dimensions and end-diastolic volume index, and lower total peripheral resistance compared to concentric hypertrophy.
Impact:
- Findings suggest that mild hypertension in AAH may stem from regulatory mechanisms in hyperkinetic states.
- Highlights the distinct cardiac functional profile of AAH in hypertensive individuals.
- Provides insights into the heterogeneity of cardiac adaptation to hypertension.
Abstract:
Recent advances in echocardiography have revealed that hypertension causes several types of cardiac hypertrophy. We classified hypertensive patients by type of cardiac hypertrophy, and evaluated left ventricular function and the severity of hypertension. The subjects consisted of 257 hypertensive patients, 13 patients with cardiac hypertrophy, and 95 normotensive controls. The hypertensives were classified in four groups: no hypertrophy, concentric hypertrophy, asymmetrical septal hypertrophy (ASH), and asymmetrical apical hypertrophy (AAH). The normotensive patients with cardiac hypertrophy included nine with ASH and four with AAH. Cardiac functions in these patients were determined by echocardiography, RI-angiocardiography and cardiac catheterization. The results were as follows: Among 257 hypertensive patients, the incidence of concentric hypertrophy, ASH, and AAH was 53%, 10%, and 4%, respectively. In patients with AAH and hypertension, the hypertensive blood pressure levels and hypertensive organ involvements were mild. The blood pressures of most of these patients fell to the normal range after admission. The cardiac index and left ventricular systolic function (FS, mVCF, and ejection fraction) were significantly higher in AAH with hypertension than in the other hypertensive groups or in the normotensive controls. The hypertensive patients showed lower E-F slopes and higher A/E ratios than the normotensive controls, as well as the normotensive patients with ASH or AAH. Cardiac function did not differ appreciably between normotensive AAH and hypertensive AAH. Left ventricular dimension and left ventricular end-diastolic volume index were larger in AAH with hypertension. The total peripheral resistance of the hypertensive AAH was significantly lower than that of the hypertensives with concentric hypertrophy (p less than 0.01), though it was higher than that of the normotensive AAH (p less than 0.01). It was, therefore, concluded that mild hypertension observed in patients with AAH may be the result of regulatory mechanisms in the hyperkinetic states.