Clinical evidence for an association between left ventricular geometric adaptation and extracardiac target organ damage in essential hypertension
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Y Shigematsu1, M Hamada, M Mukai
1Second Department of Internal Medicine, Ehime University School of Medicine, Japan.
Insights
Left ventricular geometry in hypertension predicts organ damage better than blood pressure alone. Concentric hypertrophy indicates more severe retinal and kidney damage, influenced by the renin-angiotensin-aldosterone system.
Area of Science:
- Cardiology
- Nephrology
- Ophthalmology
Background:
- Essential hypertension is a major risk factor for cardiovascular and extracardiac target organ damage.
- Left ventricular geometric adaptation is a key response to sustained hypertension.
- Preclinical organ damage assessment is crucial for risk stratification in hypertensive patients.
Purpose of the Study:
- To investigate the association between left ventricular geometry and preclinical extracardiac target organ damage in essential hypertension.
- To evaluate the role of neurohumoral factors in hypertension-related cardiovascular and organ damage.
- To determine if left ventricular adaptation provides better risk stratification than office blood pressure.
Main Methods:
- 140 essential hypertension patients were categorized by left ventricular mass index and relative wall thickness.
- Extracardiac damage assessed via funduscopic grading of retinal changes and serum creatinine levels.
- Plasma renin activity and aldosterone concentration were measured.
Main Results:
- Concentric left ventricular hypertrophy was present in 14% of patients.
- Concentric hypertrophy correlated with more severe retinopathy and renal damage.
- Left ventricular mass index strongly correlated with organ damage, independent of office blood pressure.
- Elevated plasma renin activity and aldosterone were observed in patients with concentric hypertrophy.
Conclusions:
- Echocardiographically determined left ventricular mass and geometry effectively stratify extracardiac target organ damage in hypertension.
- The renin-angiotensin-aldosterone system plays a significant role in myocardial hypertrophy and vascular damage in hypertension.
- Left ventricular adaptation is a more sensitive marker of hypertensive organ damage than office blood pressure.
Objectives:
To elucidate an association between left ventricular geometric adaptation to sustained hypertension and preclinical extracardiac target organ damage in essential hypertension. We also studied the clinical significance of neurohumoral factors for cardiovascular structural changes.
Design:
One hundred and forty patients with essential hypertension were divided into four subgroups, based on left ventricular mass index and relative wall thickness. With respect to extracardiac target organ damage, we measured the funduscopic grade of retinal changes and serum creatinine levels.
Results:
Among the hypertensive patients, only 19 (14%) had a typical concentric hypertrophy (increase in left ventricular mass index and relative wall thickness). Hypertensive patients with concentric hypertrophy had the most advanced funduscopic abnormalities and the greatest renal involvement, and hypertensive patients without left ventricular hypertrophy had the least extracardiac target organ damage. Plasma renin activity and plasma aldosterone concentration were higher in hypertensive patients with than in those without concentric hypertrophy. In a multiple regression model there was a strongly significant correlation between the degree of left ventricular mass index and the severity of hypertensive retinopathy and renal involvement, independent of office blood pressure.
Conclusions:
These results clearly demonstrate that echocardiographically determined left ventricular mass and geometry stratify extracardiac target organ damage in patients with essential hypertension more closely than office blood pressure. The present study also suggests that, in addition to blood pressure load, the renin-angiotensin-aldosterone system appears to play an important role in myocardial hypertrophy and peripheral vascular damage in hypertension.