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Antihypertensive therapy and cardiovascular reactivity during isometric stress
G E Garavaglia1, F H Messerli, R E Schmieder
1Department of Internal Medicine, Ochsner Clinic, New Orleans, Louisiana 70121.
Insights
Antihypertensive therapy impacts cardiovascular response to isometric stress. Calcium entry blockers preserve normal hemodynamic reactivity, unlike beta-blockers which worsen it.
Area of Science:
- Cardiology
- Pharmacology
- Hypertension Research
Background:
- Essential hypertension is characterized by elevated peripheral resistance.
- Cardiovascular reactivity to stress is a key factor in hypertension management.
- Understanding drug effects on hemodynamic responses is crucial for effective treatment.
Purpose of the Study:
- To evaluate the cardiovascular reactivity to isometric stress before and after antihypertensive therapy.
- To compare the effects of beta-blockers versus calcium entry blockers on hemodynamic responses during isometric stress.
Main Methods:
- Invasive hemodynamic techniques were used in 23 patients with essential hypertension.
- Patients received either atenolol (beta-blocker) or diltiazem/verapamil (calcium entry blockers).
- Cardiovascular responses to isometric stress were assessed before and after treatment.
Main Results:
- Before therapy, isometric stress increased arterial pressure mainly via cardiac output.
- Beta-blocker treatment exaggerated total peripheral resistance and attenuated cardiac output during stress.
- Calcium entry blockers preserved the baseline hemodynamic reactivity pattern during isometric stress.
Conclusions:
- Calcium entry blockers maintain physiological hemodynamic responses to stress in hypertensive patients.
- Beta-blockers alter normal cardiovascular reactivity, potentially making them less attractive for hypertension treatment.
- Preserving normal hemodynamic responses to stress is important in managing essential hypertension.
Abstract:
The cardiovascular reactivity to isometric stress test before and after antihypertensive therapy was evaluated by invasive haemodynamic techniques in 23 patients with mild to moderate essential hypertension. A beta-blocking agent (atenolol 50 to 100 mg daily) was given to 11 patients; 12 patients received calcium entry blockers (diltiazem 240 to 360 mg daily or verapamil 240 to 480 mg per day). The pressor response to isometric stress before therapy consisted of an increase in systolic, diastolic, and mean arterial pressure (all P less than 0.01) that was similar in both treatment groups. The rise in arterial pressure was mainly due to an increase in cardiac output (P less than 0.01), as total peripheral resistance did not change significantly. After treatment with the beta-blocker, the increase in total peripheral resistance during isometric stress was exaggerated (P less than 0.01), and, conversely, the increase in cardiac output was attenuated (P less than 0.01). In contrast, treatment with calcium entry blockers preserved the haemodynamic reactivity pattern of the untreated state: arterial pressure increased during isometric stress through an increase in cardiac output, while total peripheral resistance remained unchanged. Since the haemodynamic culprit of essential hypertension is an elevated peripheral resistance, a drug that numerically increases this culprit under conditions of resting and isometric stress becomes less attractive than one that lowers peripheral resistance and preserves the physiologic response pattern.