Absence of detectable regression of human hypertensive left ventricular hypertrophy following drug treatment for 1 year.
1. The present study was designed to compare and contrast the effects of 1 year's treatment with angiotensin-converting enzyme inhibition (captopril 25-100 mg daily) and beta-blockade (atenolol 50-100 mg daily) on hypertensive cardiac structure and function as well as the other established cardiovascular risk factors of high blood pressure (BP), lipid profile and blood glucose. 2. This was a prospective randomized open drug trial with blinded end-point echocardiographic and cardiac Doppler assessment in 37 subjects who had primary essential hypertension and left ventricular hypertrophy of captopril (n = 20) versus atenolol (n = 17), adding hydrochlorothiazide if BP was not controlled by 1 month. Multiple time point measurements throughout the 1 year treatment period of the study were made of BP, echocardiographic parameters of cardiac structure and function, as well as lipid profile and blood glucose. 3. There were no significant between-group differences for captopril or atenolol with regard to BP (at baseline (mean +/- SD) 154.0/101.1 +/- 13.3/5.1 and 152.5/101.8 +/- 10.0/5.8 mmHg, respectively) which was normalized by 1 month (138.7/85.6 +/- 18.8/11.7 and 135.4/88.5 +/- 16.9/9.5 mmHg, respectively) in both treatment groups (both P < 0.01 vs baseline). Also, there were no between-group or within-group differences for any of the measures of left ventricular hypertrophy or systolic function throughout the 12 month treatment period; however, captopril alone significantly increased left ventricular early diastolic filling (P < 0.05 vs baseline) at most of the measured time points. Furthermore, there were no significant between- or within-group differences with regard to metabolic (lipids and glucose) profile over the 1 year treatment period of the present study. 4. Markers of cardiovascular risk, including BP, echocardiographic measures of left ventricular hypertrophy, lipid profile and blood glucose were not significantly different between therapies. Despite good BP control by 1 month, neither drug regimen regressed left ventricular hypertrophy. However, captopril significantly increased left ventricular early diastolic filling after 3 months of treatment.
Laufer
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Alfred and Baker Medical Unit, Alfred Hospital and Baker Medical Research Institute, Prahran, Victoria, Australia. v.wootton@alfred.org.au
Reid
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C
Qi
X L
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Jennings
G L
GL
D000293:Adolescent; D000328:Adult; D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001262:Atenolol / Q000627:therapeutic use*; D001794:Blood Pressure; D018660:Blood Pressure Monitoring, Ambulatory; D002216:Captopril / Q000627:therapeutic use*; D004232:Diuretics; D005260:Female; D006339:Heart Rate; D006801:Humans; D006852:Hydrochlorothiazide / Q000627:therapeutic use; D006973:Hypertension / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D049993:Sodium Chloride Symporter Inhibitors / Q000627:therapeutic use; D016277:Ventricular Function, Left
D000959:Antihypertensive Agents; D004232:Diuretics; D049993:Sodium Chloride Symporter Inhibitors; D006852:Hydrochlorothiazide; D001262:Atenolol; D002216:Captopril