Mechanisms of prolongation of pre-ejection period in patients with left ventricular disease.

Abstract

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-

Left ventricular function in diabetes mellitus. I: Methodology, and prevalence and spectrum of abnormalities.

“…The synchronous mechanism of left ventricular contraction and relaxation is lost and this disturbs the normal relations of the isovolumic period, where aortic valve closure precedes minimal dimension by 40 to 50 ms and there is no dimension change before mitral valve opening. '2 14 In the anginal groups (both controls and diabetics) minimal dimension occurred early (around the time of aortic valve closure) and the dimension change during the isovolumic period was the result of a change of shape, not of volume, before the mitral valve opened. Sixteen asymptomatic diabetics showed incoordinate relaxation.…”

“…(ii) 25 patients with typical angina of exertion, 14 men and 11 women (mean age 52±9 years), undergoing investigation. All had significant coronary artery atherosclerosis on angiography and none had had a myocardial infarct or was taking beta-blocking agents.…”

Effect of left bundle branch block on diastolic function in dilated cardiomyopathy.

“…Results-Mean (SD) age 60 (15) v 55 (18) years, left ventricular end diastolic dimension 72 (9) v 70 (7) mm, and heart rate 88 (15) v 84 (15) beatsimin were similar in both groups. In patients with left bundle branch block the electromechanical delay, 50 (20) v 70 (20) ms, was shorter (p < 0 05) whereas the preejection contraction time, measured from the onset of mitral regurgitation to that of aortic ejection, 130 (40) v 70 (20) ms (p < 0 01), and left ventricular relaxation time, A2 to the end of mitral regurgitation, 130 (30) v 80 (30) ms (p < 0 01), were both prolonged.…”

Relation of Kinetocardiogram to Systolic Time Intervals in Patients with Old Myocardial Infarction

“…The rather frequent observation of prolonged PEP in patients with coronary artery disease [9, 54. 61] was therefore regarded by some authors as an expression of impaired contractility [2, 45,49,65], Recently, Chen and Gibson [11] have demonstrated that, in patients with ischemic heart disease who were not under treatment with ()-blocking drugs, prolongation of PEP closely correlated with incoordinate left ven tricular wall movement during isovolumic contraction, whereas the correlation was poor with peak Vcf. It is also to be mentioned that the most marked abnormalities of STI have been found in patients with transmural MI as opposed to nontransmural MI, and, among the former, in those who subsequently died [14], Moreover, a relation was found between the degree of left ventricular dys function and the number of coronary branches involved on one side and the pro longation of PEP on the other [15,48,53].…”