Why the study?
Does betaxolol reduce ischemia-type ST-segment depressions in patients with hypertension without significant coronary artery disease?
Does betaxolol reduce ischemia-type ST-segment depressions in patients with hypertension without significant coronary artery disease?
Beta-blockade with betaxolol significantly reduces the frequency and duration of ischemic ST-segment depressions in hypertensive patients without significant coronary artery disease.
Answers are grounded in this paper and cite their sources.
Betaxolol may reduce ischemic ST depressions in hypertensives without CAD; leaves open need for randomized confirmation.
In hypertensives, a reduced coronary flow reserve is observed and may contribute to angina pectoris and silent (painless) myocardial ischemia, which frequently occur in these patients even in the absence of coronary artery disease (CAD). To assess the frequency of ischemia-type ST-segment depressions in these patients and the influence of heart rate (HR) and blood pressure (BP) as major determinants of myocardial oxygen demand and to test the effects of beta-blocker therapy (10-20 mg betaxolol/day for 4 weeks) on these variables, simultaneous 24-h Holter and 24-h ambulatory BP monitoring was performed in 19 patients with hypertension (age, 43-71 years; nine women, 10 men) without CAD (stenosis < 50% in angiography). Before treatment, 25 periods of significant ST-segment depressions with a total duration of 470 min were observed in nine patients. ST-segment depressions were significantly correlated with preceding increases in HR and the rate-pressure product. The majority (79%) of episodes with ST-segment depression were clinically painless. In this open study, beta-blockade significantly decreased the number of episodes with ST-segment depressions to six in four of 15 patients and the total duration to 38 min (p < 0.05). The data demonstrate that HR seems to be associated with the development of ischemic ST-segment deviations in patients with hypertension without CAD. Antihypertensive therapy in these patients should target not only sufficient BP control, but also reduction of ischemic events.
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Christ et al. (1996) studied this question.
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