Mechanisms of prolongation of pre-ejection period in patients with left ventricular disease.
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 disease, 10 of whom were taking beta-adrenergic blocking drugs, were studied non-invasively. Recordings of carotid pulse, and apex, phono-, 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 individual patients using non-invasive methods based on echocardiography.
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D003327:Coronary Disease / Q000188:drug therapy / Q000503:physiopathology*; D004452:Echocardiography; D006333:Heart Failure / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D009200:Myocardial Contraction / Q000187:drug effects; D013599:Systole / Q000187:drug effects
D000319:Adrenergic beta-Antagonists