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Plasma catecholamine and cardiovascular responses to nifedipine in hypertensives WHO-stage II
M Lehmann1, H Dürr, I Arratibel-Imaz
1Medizinische Universitätsklinik Freiburg, Abteilung Sport, und Leistungsmedizin, Fed. Rep. of Germany.
Insights
Nifedipine (Adalat) reduces blood pressure and peripheral resistance in patients with arterial hypertension and left ventricular hypertrophy. This medication also decreases heart wall thickness, indicating a relaxation effect, not a regression of hypertrophy.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Arterial hypertension is a common condition often associated with cardiac structural changes.
- Left ventricular hypertrophy (LVH) is a significant adaptation to increased cardiac workload.
Purpose of the Study:
- To investigate the acute effects of sublingual nifedipine on hemodynamics, cardiac structure, and sympathetic activity in patients with arterial hypertension and LVH.
Main Methods:
- Echocardiography was used to assess cardiac morphology and function in 77 hypertensive patients.
- 15 patients with confirmed left ventricular hypertrophy received 10 mg of sublingual nifedipine.
- Hemodynamic parameters, plasma noradrenaline, and heart rate were measured before and after nifedipine administration.
Main Results:
- Nifedipine significantly decreased systolic and diastolic blood pressure within 5-10 minutes.
- Plasma noradrenaline and heart rate increased post-administration, suggesting sympathetic counterregulation.
- A decrease in left ventricular wall thickness, along with increased end-diastolic volume, shortening fraction, and ejection fraction, was observed in most patients.
Conclusions:
- Sublingual nifedipine acutely reduces blood pressure and peripheral resistance in hypertensive patients with LVH.
- The observed decrease in wall thickness represents a relaxation effect, not a true regression of hypertrophy.
- Nifedipine induces sympathetic counterregulation, leading to increased heart rate and improved cardiac function parameters.
Abstract:
77 patients with arterial hypertension were consecutively examined. An evaluable echocardiogram could be recorded for 75 patients. 54 (72%) had non-pathological cardiac findings, 15 (20%) showed concentric left ventricular hypertrophy of the heart (mean left ventricular muscle mass (LVM) 2.5 g/kg or 113 g/m2; mean LVM/EDV 1.6 g/ml). 6 patients had an excentric hypertrophy of the left ventricle (8%). The influence of 10 mg nifedipine (Adalat) sublingual on the heart, blood pressure and sympathetic activity was examined in 15 patients with left ventricular hypertrophy of the heart. 5-10 min after administration, a significant decrease in systolic and diastolic pressures (p less than 0.05) and an increase in plasma noradrenaline (p less than 0.05) and heart rate (p less than 0.01) could be registered. The thickness of the posterior wall and septum decreased in 8 to 10 of the 15 patients, EDV, shortening fraction and ejection fraction increased in 8 of the 15 patients. A reduction in peripheral resistance, sympathetic counterregulation accompanied by an increase in heart rate, shortening and ejection fractions with increased enddiastolic volume and decrease in wall thickness can be observed as the gross effect in the majority of the 15 patients with left ventricular concentric hypertrophy. The decrease in wall thickness as a relaxation effect should not be confused with a regression of hypertrophy, whereby the mass-volume ratio shifts toward the normal range under nifedipine.