Document Detail


Myocardial perfusion during long-term angiotensin-converting enzyme inhibition or beta-blockade in patients with essential hypertension.
MedLine Citation:
PMID:  15326083     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hypertension is associated with reduced coronary vasodilatory capacity, possibly caused by structural changes in the coronary resistance vessels. Because vasodilatory treatment may correct abnormal structure better than nonvasodilating treatment, we compared whether long-term angiotensin-converting enzyme (ACE) inhibition has a greater effect on coronary reserve and cardiovascular structure than beta-blockade in patients with essential hypertension. Thirty previously untreated hypertensive patients were randomized in a double-blind design to treatment for 1 year with either perindopril (4 to 8 mg per day, n=15) or atenolol (50 to 100 mg per day, n=15) and furthermore compared with normotensive controls. Cardiac output and left ventricular mass were measured with echocardiography and resistance artery structure was determined in vitro. Using positron emission tomography, myocardial perfusion (MP) was determined at rest and during dipyridamole-induced hyperemia while still on medication. Perindopril reduced left ventricular mass by 14+/-4% (P<0.01), peripheral vascular resistance by 12+/-6% (P<0.01), and media thickness-to-lumen diameter ratio of resistance arteries by 16+/-4% (P<0.05), whereas atenolol had no effect. Resting MP was decreased both by perindopril (-11+/-4%, P<0.01) and by atenolol (-25+/-4%, P<0.01) in parallel to the reduction in rate pressure product. Hyperemic MP was unaltered by perindopril (+2+/-6%, P=NS), but reduced by atenolol (-32+/-5%, P<0.01). Compared with atenolol, perindopril treatment resulted in higher coronary reserve (P<0.05). We conclude that compared with beta-blockade, ACE inhibition increases coronary reserve and results in regression of hypertensive resistance artery structure and left ventricular hypertrophy. Vasodilating may thus be superior to nonvasodilating treatment in repairing the hypertensive myocardial microcirculation.
Authors:
Niels H Buus; Morten Bøttcher; Claus G Jørgensen; Kent L Christensen; Kristian Thygesen; Torsten T Nielsen; Michael J Mulvany
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Publication Detail:
Type:  Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't     Date:  2004-08-23
Journal Detail:
Title:  Hypertension     Volume:  44     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2004 Oct 
Date Detail:
Created Date:  2004-09-24     Completed Date:  2005-03-28     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  465-70     Citation Subset:  IM    
Affiliation:
Centre for Clinical Pharmacology, Aarhus University Hospital, Aarhus C, Denmark. nhb@farm.au.dk
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MeSH Terms
Descriptor/Qualifier:
Adrenergic beta-Antagonists / therapeutic use*
Angiotensin-Converting Enzyme Inhibitors / therapeutic use*
Antihypertensive Agents / therapeutic use*
Atenolol / therapeutic use
Female
Heart / drug effects*,  radionuclide imaging*
Humans
Hypertension / drug therapy*
Male
Middle Aged
Perindopril / therapeutic use
Positron-Emission Tomography
Vascular Resistance / drug effects
Vasodilator Agents / therapeutic use*
Chemical
Reg. No./Substance:
0/Adrenergic beta-Antagonists; 0/Angiotensin-Converting Enzyme Inhibitors; 0/Antihypertensive Agents; 0/Vasodilator Agents; 29122-68-7/Atenolol; 82834-16-0/Perindopril

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