The physiological determinants and risk correlations of elevated heart rate

A number of studies have shown that faster resting heart rate is associated with higher blood pressure, and that it is prospectively related to the development of hypertension and of cardiovascular events. These relationships have been observed across the whole range of blood pressure in the general population irrespective of age, and held true in multiple linear regression analyses where also body mass index, smoking, alcohol intake, and physical activity habits were used as additional independent variables. Using the mixture analysis test in numerous western populations we showed that the heart rate-blood pressure association was mostly explained by a subpopulation of subjects with 'high' heart rate who had higher levels of blood pressure. The percentage of subjects with tachycardia varied from 8.4% to 19.3%. Subjects with tachycardia also had high values of total cholesterol and triglycerides, high fasting insulin, and increased post-load glucose, which are characteristic features of the insulin resistance syndrome. A higher blood pressure, overweight, and disturbances of the glucose metabolism are all well-known risk factors for future hypertension. The clustering of these risk factors together with dyslipidaemia, referred to as syndrome X, may explain why cardiovascular morbidity is higher in individuals with tachycardia. Sympathetic overactivity seems to be responsible for both the increase in heart rate and blood pressure, and for the metabolic abnormalities. Experimental studies in monkeys have shown that reduction of heart rate either by ablation of sinoatrial node or use of beta-blocking agents could retard the development of atherosclerotic coronary lesions. Although a reduction of heart rate appears as an additional goal of antihypertensive therapy, several drugs which lower heart rate have unfavourable effects on the patients' metabolic profile. If tachycardia in hypertension is a marker of an abnormality in the autonomic control of the circulation characterized by an increased sympathetic tone and a decreased vagal activity, a drug which decreases heart rate by reducing the sympathetic outflow should be preferred. Agents with agonistic properties at the I1-imidazoline receptors of the rostral ventrolateral medulla appear particularly suitable in this respect.