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Hypertension and left-ventricular hypertrophy
F H Messerli1, F C Aepfelbacher
1Department of Internal Medicine, Ochsner Clinic, New Orleans, Louisiana, USA.
Insights
Left-ventricular hypertrophy (LVH) is a major risk factor for cardiovascular events. Antihypertensive therapy can reduce LVH, but further studies are needed to confirm clinical benefits.
Area of Science:
- Cardiology
- Hypertension Research
Background:
- Left-ventricular hypertrophy (LVH) is the primary cardiac manifestation of hypertension.
- LVH is a significant risk factor for cardiovascular events, including myocardial infarction and heart failure.
- Increased myocardial mass in LVH impairs cardiac function and oxygen supply.
Purpose of the Study:
- To review the causes and consequences of left-ventricular hypertrophy.
- To discuss the role of antihypertensive therapy in managing LVH.
- To highlight the need for further research on the clinical benefits of LVH reduction.
Main Methods:
- Literature review of studies on hypertension and left-ventricular hypertrophy.
- Analysis of risk factors contributing to LVH, both hemodynamic and nonhemodynamic.
- Evaluation of the impact of antihypertensive therapy on LVH.
Main Results:
- Hypertension is the leading cause of LVH, a potent predictor of cardiovascular events.
- Obesity, age, and valvular disease also contribute to LVH.
- Dietary factors like salt intake and alcohol, along with neurohormones, influence left-ventricular mass.
- Antihypertensive therapies show potential in reducing LVH and its associated risks.
Conclusions:
- LVH significantly increases cardiovascular morbidity and mortality.
- While antihypertensive therapy can reduce LVH, further epidemiological studies are required to validate its clinical benefits.
- Understanding and managing LVH is crucial for preventing cardiovascular events.
Abstract:
Left-ventricular hypertrophy (LVH), the primary cardiac manifestation of hypertension, has been identified as the most powerful risk factor for future cardiovascular events causing morbidity and mortality, such as myocardial infarction, congestive heart failure, sudden death, and so forth. The increase in myocardial mass lowers coronary reserve and enhances cardiac oxygen requirements, gives rise to ventricular ectopy, and impairs left-ventricular filling and contractility. Besides hypertension, other risk factors such as obesity, advanced age, valvular heart disease, and other pathologic disorders can cause an increase in the hemodynamic burden and lead to LVH. Nonhemodynamic determinants of left-ventricular mass include dietary salt intake, alcohol, and neurohormones. LVH and its sequelae can be reduced by specific antihypertensive therapy, but despite these promising findings, future epidemiologic studies are necessary to document the clinical benefits of a reduction in LVH.