| Stress-induced hemodynamic and hemostatic changes in patients with systemic hypertension: effect of verapamil. | |
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MedLine Citation:
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PMID: 8674257 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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 microM, p = 0.05) and epinephrine (3.4 +/- 0.9 to 1.6 +/- 0.6 microM, 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 microM, 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. |
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Authors:
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O C Gebara; A H Jimenez; C McKenna; M A Mittleman; P Xu; I Lipinska; J E Muller; G H Tofler |
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Publication Detail:
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Type: Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Clinical cardiology Volume: 19 ISSN: 0160-9289 ISO Abbreviation: Clin Cardiol Publication Date: 1996 Mar |
Date Detail:
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Created Date: 1996-08-09 Completed Date: 1996-08-09 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 7903272 Medline TA: Clin Cardiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 205-11 Citation Subset: IM |
Affiliation:
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Institute for Prevention of Cardiovascular Disease, Deaconess Hospital, Harvard Medical School, Boston, Massachusetts, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Diphosphate
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pharmacology Adult Blood Pressure / drug effects*, physiology Calcium Channel Blockers / administration & dosage, therapeutic use* Collagen / pharmacology Cross-Over Studies Delayed-Action Preparations Double-Blind Method Epinephrine / pharmacology Female Heart Rate / drug effects*, physiology Humans Hypertension / drug therapy*, physiopathology Male Middle Aged Placebos Platelet Activation / drug effects, physiology Platelet Aggregation / drug effects*, physiology Posture Stress, Physiological / physiopathology* Stress, Psychological / physiopathology Vasodilator Agents / administration & dosage, therapeutic use* Verapamil / administration & dosage, therapeutic use* |
| Chemical | |
Reg. No./Substance:
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0/Calcium Channel Blockers; 0/Delayed-Action Preparations; 0/Placebos; 0/Vasodilator Agents; 51-43-4/Epinephrine; 52-53-9/Verapamil; 58-64-0/Adenosine Diphosphate; 9007-34-5/Collagen |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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