Effect of propranolol on left atrial systole in ischaemic and hypertensive heart disease.

The sympathetic nervous system has an important effect on the strength of myocardial contraction which is mediated through beta-adrenergic receptors (Ahlquist, 1948), and the administration of a selective beta-adrenergic blocking agent such as propranolol might be expected to reduce myocardial contractility in patients who have a high sympathetic tone. There is evidence that patients in heart failure have increased activity of the sympathetic nervous system (Braunwald and Chidsey, 1965), which may act as a compensatory mechanism, increasing the strength of myocardial contraction and allowing the stroke output to be maintained at a lower diastolic pressure than would otherwise be possible. Under these circumstances beta-adrenergic blockade might be expected to have a deleterious effect on myocardial performance. In fact the development of cardiac failure is a recognized hazard of treatment with beta-adrenergic blocking drugs (Braunwald and Chidsey, 1965). These agents are now being used extensively in ischaemic and hypertensive heart disease, and reports have appeared of their value in reducing the severity of angina pectoris (Apthorp, Chamberlain, and Hayward, 1964), of their use in myocardial infarction (Snow, 1965), and of their hypotensive effect in systemic hypertension (Prichard and Gillam, 1964). The possibility that cardiac failure might be produced in patients with serious heart disease has necessarily restricted the use of beta-adrenergic blocking drugs in these conditions. In this study an attempt has been made to assess the changes in diastolic tone of the left ventricle produced by beta-adrenergic blockade, so that patients likely to suffer from left ventricular failure after propranolol can be distinguished from those who will tolerate this treatment without difficulty. The diastolic properties of the left ventricle have