Handgrip-Induced Reduction in Left Ventricular Ejection Fraction and Contractility in Pediatric Patients with Mitral Valve Prolapse Syndrome as Evaluated by Relation of Fiber Shortening Velocity to End-Systolic Wall Stress

Publisher Website
Google Scholar
Abstract
Load-induced or latent cardiac dysfunction (LCD), in which normal left ventricular performance at rest is decreased due to afterload challenge, is an important clinical condition in children with mitral valve prolapse (MVP) who acquire significant symptoms (MVP syndrome). Asymptomatic children with MVP do not have LCD. To diagnose LCD, we have used handgrip and ejection fraction (EF) obtained from M-mode echocardiograms. In this study, we evaluated changes in EF and left ventricular contractility due to handgrip in patients with LCD by means of Colan’s principle, in which velocity-force relation is expressed. Subjects were as follows: non-MVP (n = 16), MVP + LCD (n = 16), MVP + recovered LCD after coenzyme Q(10) (CoQ) treatment (n = 16), and asymptomatic MVP (n = 25). Rate-corrected velocity of fiber shortening (V(c)f(c)) for end-systolic left ventricular wall stress (W(es)), expressed by %ΔV(c)f(c)/ΔW(es) and EF, decreased significantly due to handgrip only in patients with LCD, while in others these parameters increased. Handgrip significantly increased systolic and diastolic blood pressure values and heart rate without intergroup differences. We conclude that (1) handgrip provided a sufficient afterload challenge to detect LCD and (2) in LCD, left ventricular contractility and EF were depressed simultaneously by handgrip. The underlying abnormality in LCD must be an intrinsically depressed inotropic state caused by a molecular bioenergetic misfunction related with CoQ. Our previous catheterization studies showed that LCD hearts have abnormally high ventricular end-diastolic pressure values. Added afterload may induce an exhaustion of the preload reserve, and as a result failure of the Frank-Starling mechanism, which has maintained the contractility of the LCD heart at maximum by increasing preload as much as possible.

This publication has 0 references indexed in Scilit: