By Betty S. Riggs
BERLIN -- June 18, 2008 -- A new analysis of data from the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) demonstrates that antihypertensive therapy with an amlodipine-based regimen reduces electrocardiographic (ECG) evidence of left ventricular hypertrophy (LVH) more effectively than atenolol-based therapy.
The finding is important because LVH is associated with cardiovascular morbidity and mortality.
T. Berglund, MD, Sahlgrenska University Hospital/Ostra, Goteborg, Sweden, and colleagues reported the results of ASCOT here on June 17 at the 18th Scientific Meeting of the European Society of Hypertension (ESH).
In the prospective, open-treatment, blinded ASCOT trial, 19,257 eligible patients 40 to 79 years old with hypertension and at least 3 other risk factors but no clinical coronary heart disease (CHD) were randomised to amlodipine 5 to 10 mg daily (adding perindopril 4-8 mg as required) or atenolol 50 to 100 mg daily (adding bendroflumethiazide 1.25-2.5 mg and potassium as required). Patients were followed for a median of 5.5 years.
The primary endpoint was nonfatal myocardial infarction (MI), including silent MI, and fatal CHD. Amlodipine-treated patients had lower blood pressure levels than atenolol-treated patients throughout the study by a mean of 2.7/1.9 mm Hg (P < .0001). Fewer patients treated with amlodipine-based therapy had a primary endpoint compared with atenolol-based therapy (429 vs 474, respectively), but the 10% reduction was not statistically significant (hazard ratio 0.90; 95% confidence interval, 0.79-1.02; P = .1052).
In the ECG LVH substudy, the severity of ECG LVH was assessed at baseline, at 2 years, and at the last visit using the Cornell Voltage Duration Product (CVDP) and Sokolow-Lyon Voltage (SLV). There were 17,420 patients with valid ECGs for CVDP and 17,565 patients with valid ECGs for SLV interpretation. All ECGs were read at a core laboratory.
In the analysis of data, results were adjusted for baseline ECG LVH, baseline and in-treatment systolic and diastolic blood pressure, and body mass index (BMI).
After a median 5.5 years of follow-up, amlodipine-based therapy was associated with greater regression of LVH than atenolol-based therapy as measured by CVDP (means -133.1 vs -73.4 mm/ms, adjusted P < .0001) and by SLV (means -3.4 vs -2.3 mm, adjusted P < .0001). These differences in regression of LVH were significant after 2 years of treatment. The findings were consistent across all subgroups, defined by age, gender, diabetes, BMI >30 kg/m2, and metabolic syndrome.
Dr. Berglund stated, "Remember that half of the patients randomised to amlodipine also received an angiotensin-converting enzyme inhibitor, perindopril. This study shows that amlodipine plus a RAAS [renin-angiotensin-aldosterone system] blocker is a good combination and is better than atenolol."
The researchers concluded that antihypertensive treatment with an amlodipine-based regimen reduces ECG LVH more effectively than an atenolol-based regimen. ECG LVH is strongly associated with cardiovascular morbidity and mortality. Therefore, the findings of this study could explain part of the differential effect of the 2 regimens on cardiovascular outcomes in ASCOT.
The results for the primary data analysis of the ASCOT-Blood Pressure Lowering Arm were previously published in 2005 (Dahlöf B, et al. Lancet. 2005;366:895-906).
Funding for this study was mainly provided by Pfizer, Inc.
[Presentation title: Differential Regression of Electrocardiographic Left Ventricular Hypertrophy by Amlodipine Versus Atenolol in the ASCOT Trial. Abstract PS17]
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