Stress‐induced hemodynamic and hemostatic changes in patients with systemic hypertension: Effect of verapamil

Stress‐induced hemodynamic and hemostatic responses may acutely trigger atherosclerotic plaque disruption and thrombosis leading to myocardial infarction. This study was designed to evaluate the responses to three stressors and to determine if once‐daily sustained release verapamil (Verelan®) modified these responses. We studied 13 patients with mild to moderate hypertension in a randomized, double‐blind, placebo‐controlled crossover trial. After 4 weeks of therapy, patients were evaluated following assumption of the upright posture, mental stress, and cold pressor test. During placebo, the stressors produced an increase in systolic pressure (144 ± 2 to 167 ± 3 mmHg, p < 0.001), heart rate (70 ± 2 to 77 ± 2 beats/ min, p< 0.001), and platelet aggregability to adenosine diphosphate (threshold concentration fell from 2.8 ± 0.4 to 1.9 ± 0.1 μM, p = 0.05)and epinephrine (3.4±0.9 to 1.6 ±0.6 μM, p < 0.001). Verapamil lowered systolic pressure at baseline (144 ± 2 to 134 ± 2 mmHg, p < 0.001), and after stress (167 ± 3 to 154 < 3 mmHg, p < 0.001), but did not alter the absolute increase with stress. During verapamil, platelet reactivity did not increase with stress, and the post‐stress response to epinephrine was reduced (higher threshold concentration) compared with placebo (3.9 ± 1.3 vs. 1.5 ± 0.3 μM, p = 0.05). Verapamil also reduced the response to collagen (increased lag time) at baseline and after stress (111 ± 9 vs. 91 ± 3 s, p < 0.01). We conclude that verapamil blunted potentially harmful stress‐induced hemodynamic and hemostatic changes. Further studies are required to determine whether these effects translate into a lower incidence of acute cardiovascular events.