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[Regression of hypertrophy following nitrendipine: effect on systolic and diastolic function]
1Med. Klinik und Poliklinik B, Abteilung für Kardiologie, Heinrich-Heine-Universität, Düsseldorf.
Insights
Nitrendipine treatment effectively reduced hypertensive left ventricular hypertrophy and improved diastolic function by altering left ventricular geometry. Systolic function remained stable due to consistent afterload.
Area of Science:
- Cardiology
- Pharmacology
- Echocardiography
Context:
- Hypertensive left ventricular hypertrophy is a significant risk factor for cardiovascular events.
- Dihydropyridine calcium channel blockers like nitrendipine are commonly used for hypertension management.
- The impact of antihypertensive therapy on cardiac structure and function requires further elucidation.
Purpose:
- To investigate the efficacy of nitrendipine in regressing severe hypertensive left ventricular hypertrophy.
- To assess the effects of nitrendipine treatment on systolic and diastolic ventricular function.
- To determine the relationship between blood pressure reduction and changes in left ventricular mass and function.
Summary:
- Nitrendipine treatment (10-40 mg/day) for 12 months in 11 patients with hypertensive hypertrophy led to a significant reduction in systolic blood pressure and left ventricular muscle mass.
- While systolic function and wall stress remained unchanged, diastolic filling, indexed by MLVD, significantly improved.
- The regression of hypertrophy was proportional to blood pressure reduction, with improved diastolic filling attributed to favorable changes in left ventricular geometry.
Impact:
- Nitrendipine effectively regresses hypertensive left ventricular hypertrophy, improving diastolic function without compromising systolic function.
- The study highlights the importance of geometric remodeling in improving cardiac function post-antihypertensive therapy.
- Findings suggest nitrendipine is a valuable therapeutic option for managing hypertensive heart disease.
Abstract:
The purpose of the present study was to determine whether an antihypertensive treatment with the dihydropyridine nitrendipine can induce regression of severe hypertensive hypertrophy and, whether alterations in systolic and diastolic ventricular function do occur. Eleven patients (age 49 +/- 11 years) with hypertensive hypertrophy were treated with nitrendipine (10-40 mg/day) for 12 months. Before and after therapy left ventricular hypertrophy, systolic, and diastolic function were measured by M-mode, two-dimensional- and digitized M-mode echocardiography. Systolic blood pressure dropped from 185.5 +/- 19.8 to 164.1 +/- 15.6 mm Hg (p less than 0.05). Left ventricular muscle mass was reduced from 234.5 +/- 51.2 to 201.5 +/- 37.9 g/m2 (p less than 0.05). Systolic wall stress (257.2 +/- 50.5 vs 245.2 +/- 44.4 x 10(3) dyn/cm2) and fractional shortening (34.9 +/- 6.1 vs 37.1 +/- 5.4%) remained nearly unchanged. The peak rate of left ventricular internal dimension change during diastole (MLVD), as an index of rapid early diastolic filling was increased (13.1 +/- 3.0 vs 16.5 +/- 3.7 cm/s; p less than 0.01), the relaxation time index, as an index of isovolumic relaxation, remained nearly unchanged (76 +/- 35 vs 64 +/- 24 ms; n.s.). A long-term treatment with nitrendipine regressed hypertensive left ventricular hypertrophy in proportion to blood pressure reduction. While systolic function remained unchanged as a consequence of an unaltered systolic wall stress, i.e. afterload, diastolic filling was markedly improved due to changes in left ventricular geometry through reduction in mass to volume ratio. Since relaxation time index remained nearly unchanged, factors contributing to the phase of isovolumic relaxation were not essentially affected by regression of left ventricular hypertrophy.