Association of tachycardia with morbidity and mortality: pathophysiological considerations.

An increased rate of cardiovascular and all-cause mortality has been documented in subjects with tachycardia. Hypertensive subjects with tachycardia often also exhibit overweight, higher haematocrit, plasma insulin, cholesterol, and triglyceride levels whereas high density lipoprotein (HDL) is decreased. Sympathetic overactivity seems to be responsible both for the increase in heart rate and blood pressure (BP), and for metabolic abnormalities. Excessive stimulation of beta-adrenergic receptors in the skeletal muscles can cause insulin resistance and chronic beta-adrenergic stimulation which leads to a greater proportion of fast twitch insulin-resistant fibres. Also alpha-adrenergic stimulation can cause insulin resistance through vasoconstriction and the consequent decrease in the delivery of glucose and insulin to the muscles. Experimental studies in monkeys have shown that tachycardia can also produce atherosclerotic lesions via haemodynamic disturbances, by elevating the pulsatile nature of the arterial blood flow. Conversely, a reduction of heart rate could retard the development of vascular lesions. If tachycardia in hypertension is a marker of an abnormality of the autonomic control of circulation, a centrally acting antihypertensive agent which decreases the sympathetic outflow should be preferred. Drugs with agonistic properties of the I1-imidazoline receptors of the rostral ventrolateral medulla appear particularly suitable in this respect.