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Stress-induced hemodynamic and hemostatic changes in patients with systemic hypertension: effect of verapamil

O C Gebara1, A H Jimenez, C McKenna

  • 1Institute for Prevention of Cardiovascular Disease, Deaconess Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Clinical Cardiology
|March 1, 1996
PubMed

Insights

Sustained-release verapamil reduced harmful stress responses in hypertensive patients. The medication blunted increases in blood pressure and platelet activity, potentially lowering cardiovascular event risk.

Area of Science:

  • Cardiovascular Science
  • Pharmacology
  • Hypertension Research

Background:

  • Stress can trigger acute cardiovascular events like myocardial infarction through hemodynamic and hemostatic changes.
  • Atherosclerotic plaque disruption and thrombosis are critical in stress-induced cardiac events.

Purpose of the Study:

  • To evaluate hemodynamic and hemostatic responses to three stressors (posture, mental stress, cold pressor test).
  • To determine if sustained-release verapamil modifies these stress responses in hypertensive patients.

Main Methods:

  • A randomized, double-blind, placebo-controlled crossover trial involving 13 mild-to-moderate hypertension patients.
  • Patients were assessed after 4 weeks of verapamil or placebo, undergoing postural changes, mental stress, and cold pressor tests.
  • Hemodynamic (blood pressure, heart rate) and hemostatic (platelet aggregability) parameters were measured.

Main Results:

  • Stress increased systolic pressure, heart rate, and platelet aggregability during placebo.
  • Verapamil lowered baseline and post-stress blood pressure but did not change the absolute stress-induced increase.
  • Verapamil prevented stress-induced increases in platelet reactivity and reduced responses to epinephrine and collagen.

Conclusions:

  • Once-daily sustained-release verapamil blunted potentially harmful stress-induced hemodynamic and hemostatic changes in hypertensive patients.
  • Verapamil's effects on platelet reactivity suggest a mechanism for reducing cardiovascular event risk.
  • Further research is needed to confirm if these blunted responses translate to a lower incidence of acute cardiovascular events.

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