Why the study?
Does elevated heart rate increase the risk of mortality and cardiovascular disease in patients with known or suspected coronary heart disease, prior myocardial infarction, or hypertension?
Does elevated heart rate increase the risk of mortality and cardiovascular disease in patients with known or suspected coronary heart disease, prior myocardial infarction, or hypertension?
Elevated heart rate is a significant risk factor for mortality and cardiovascular events, providing a strong rationale for heart rate-lowering therapies in susceptible patients.
Supports heart rate as mortality marker in CHD/hypertension; leaves open whether lowering improves outcomes in RCTs.
Heart rate is a major determinant of oxygen consumption in patients with ischaemic heart disease. Its pharmacological modulation is increasingly the focus of therapeutic approaches to alleviate symptoms and prolong survival. It is the simplest cardiovascular variable to measure accurately and reproducibly. Many long-term follow-up studies suggest that elevated heart rate increases all-cause mortality, cardiovascular disease and sudden death in patients with known or suspected coronary heart disease, survivors of myocardial infarction and patients with hypertension. These links hold for men and women, and are unrelated to ethnic origin. The effect on sudden death or total mortality increases as a function of heart rate such that an increase in heart rate by more than 40 beats/min doubles total mortality. Conversely, low heart rate reduces risk for coronary artery disease and sudden death. Primary and secondary prevention studies in myocardial infarction indicated that elevated heart rate in susceptible patients predicts risk for developing myocardial infarction and death. Prophylactic beta-blockers attenuate risks for reinfarction, sudden death and total mortality; these effects correlate with reduced heart rate, thus providing a compelling basis for developing agents that reduce heart rate exclusively as antianginal agents for the therapy of myocardial ischaemia with broader therapeutic implications.
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Bhupinder Singh (2003) studied this question.
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