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Left ventricular hypertrophy and antihypertensive therapy
F H Messerli1, S Oren, E Grossman
1Department of Internal Medicine, Ochsner Clinic, New Orleans.
Insights
Left ventricular hypertrophy (LVH) increases sudden death risk and ventricular ectopic activity. Certain antihypertensive drugs can regress LVH and suppress arrhythmias, unlike diuretics.
Area of Science:
- Cardiology
- Hypertension Research
- Pharmacology
Background:
- Long-standing arterial hypertension causes left ventricular hypertrophy (LVH), increasing cardiovascular risks.
- LVH is linked to increased premature ventricular contractions and a higher risk of sudden death.
- Effective antihypertensive therapy should reduce blood pressure and reverse LVH.
Purpose of the Study:
- To evaluate the impact of different antihypertensive agents on left ventricular mass and ventricular ectopic activity.
- To determine if regression of LVH by specific drugs affects ventricular arrhythmias.
- To assess the potential of antihypertensive therapy to alter the prognosis of LVH.
Main Methods:
- Review of existing evidence on antihypertensive therapies and their effects on cardiac structure and function.
- Analysis of studies comparing the efficacy of various drug classes, including ACE inhibitors, beta-blockers, calcium antagonists, and diuretics, on LVH.
- Examination of data on ventricular ectopic activity in patients with and without LVH, and in response to different treatments.
Main Results:
- Certain antihypertensive drugs (ACE inhibitors, beta-blockers, etc.) decrease left ventricular mass, while others (diuretics, hydralazine) have minimal or detrimental effects.
- Drug-induced regression of left ventricular mass significantly suppresses ventricular ectopic activity (by 85%).
- Diuretic therapy does not alter left ventricular mass or ventricular ectopic activity, and may even increase them.
Conclusions:
- Antihypertensive medications vary significantly in their ability to induce left ventricular mass regression.
- Regression of LVH by specific drugs effectively suppresses ventricular ectopic activity.
- Further research is needed to ascertain if this LVH regression impacts sudden death risk and overall prognosis.
Abstract:
Cardiac adaptation to long-standing arterial hypertension consists of left ventricular hypertrophy (LVH), usually of the concentric type, i.e. an increase in wall thickness at the expense of chamber volume. LVH can no longer be considered only as a simple adaptive myocardial process; it drastically increases the risk of sudden death and cardiovascular morbidity and mortality, irrespective of the levels of arterial pressure. Patients with LVH have more premature ventricular contractions than patients without LVH or normotensive subjects, which indicates that LVH per se increases ventricular ectopic activity. Antihypertensive therapy should not only lower blood pressure, but also prevent or improve end-organ damage and therefore allow left ventricular mass to regress. Although they lower blood pressure, certain antihypertensive agents such as the thiazide diuretics and arteriolar dilators (hydralazine, minoxidil) have little or even a detrimental effect on LVH. In contrast, other agents such as angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, antiadrenergic drugs, and certain calcium antagonists decrease left ventricular mass in parallel with arterial pressure. Recent evidence has shown that a decrease in left ventricular mass induced by certain antihypertensive drugs suppresses ventricular ectopic activity by 85%. In contrast, left ventricular mass and ventricular ectopic activity remain unchanged or may even increase in patients treated with diuretics. It is not known whether the risk of sudden death can be decreased and the ominous prognosis of LVH altered by such specific antihypertensive therapy.