SUMMARY In order to determine the mechanism underlying prolongation of the pre-ejection period in patients with left ventricular disease, 11 patients with congestive cardiomyopathy and 29 with coronary artery disea3e, 10 of whom were taking beta-adrenergic blocking drugs, were studied non-invasively. Recordings of carotid pulse, and apex, phon-, and echocardiogram were obtained. In the absence of treatment with beta-blocking drugs, prolongation of pre-ejection period correlated closely with incoordinate left ventricular wall movement during isovolumic contraction assessed from simultaneous apex and echocardiograms. There was no correlation between pre-ejection period index (PEPI) and end-diastolic dimension and PEPI correlated poorly with fractional shortening and peak Vcf. A PEPI of greater than 140 ms was associated with incoordinate contraction in all but one case, and of less than 140 ms with normal contraction in all. Therapeutic doses of beta-blocking drugs caused prolongation of PEPI to a greater extent than would have been predicted from wall movement during isovolumic contraction. Incoordinate left ventricular contraction and a negative inotropic effect both therefore prolong PEPI, but by different mechanisms, whose effects can be separated in individua patients using non-invasive methods based on echocardiography.Prolongation of pre-ejection period is commonly used to detect the presence of left ventricular disease, though the mechanism of this prolongation of pre-ejection period is obscure. A reduction in 'contractility' is frequently invoked, but this term is not adequately defined, and means little more than the presence of clinical evidence of left ventricular disease. We have, therefore, measured pre-ejection period and other systolic time intervals in patients with ischaemic heart disease or cardiomyopathy, analysing any impairment of left ventricular function at rest in terms of abnormal cavity size, incoordinate contraction, and reduced peak systolic rate of wall movement, measured echocardiographically. These observations were compared with those made during chronic administration of beta-blocking drugs in therapeutic dosage. MethodsSystolic time intervals were measured and echocardiographic examinations were performed in 40 patients, who were divided into the following groups:Group 1: 11 patients with congestive cardiomyo-