Ventricular actuation improves systolic and diastolic myocardial function in the small failing heart.
BACKGROUND
Direct mechanical ventricular actuation (DMVA) provides non-blood contacting augmentation of ventricular function. The device has promise for supporting the pediatric heart. The purpose of this study was to assess DMVA's effect in a small animal model of heart failure.


METHODS
Anesthetized rabbits (n = 6) underwent sternotomy and were instrumented for hemodynamic monitoring. A 10-MHz ultrasound probe was used for transesophageal echocardiography imaging. Heart failure (cardiac output <50% baseline) was induced with esmolol. Phenylephrine was titrated to maintain baseline mean arterial pressure. Transesophageal echocardiography imaging was acquired at baseline, heart failure, and subsequent DMVA support for 2 hours. Image analysis was used to derive ejection fraction, cardiac output, and stroke work as measures of left ventricular function. Speckle tracking software was used to derive myocardial strain rates as load-independent measures of left ventricular myocardial function.


RESULTS
Mean ejection fraction was significantly increased during DMVA support (0.585 +/- 0.035) versus failure (0.215 +/- 0.014; p < 0.001). Peak global left ventricular systolic and diastolic strain rates (1/second) were significantly increased during DMVA (-2.85 +/- 0.33 and 2.92 +/- 0.37) versus failure (-1.69 +/- 0.11 and 1.99 +/- 0.14; p < 0.001 and 0.004, respectively). Peak strain rates during DMVA in the failing heart were similar to baseline.


CONCLUSIONS
Direct mechanical ventricular actuation augments both systolic and diastolic left ventricular pump function. Diastolic augmentation distinguishes the device from other direct cardiac compression methods. This study demonstrated that DMVA in the small-sized, failing heart improves both systolic and diastolic myocardial function, which has favorable implications for left ventricular recovery. Direct mechanical ventricular actuation's salutary effects can be provided to the failing pediatric heart without complications of blood contact.
Anstadt
Mark P
MP
Department of Surgery, Wright State University School of Medicine, Dayton, Ohio 45409, USA. mpanstadt@aol.com
Budharaju
Subbaraju
S
Darner
Rebecca J
RJ
Schmitt
Benjamin A
BA
Prochaska
Lawrence J
LJ
Pothoulakis
Anthony J
AJ
Portner
Peer M
PM
D000818:Animals; D001243:Assisted Circulation / Q000295:instrumentation*; D003971:Diastole; D004195:Disease Models, Animal; D004867:Equipment Design; D006333:Heart Failure / Q000503:physiopathology / Q000628:therapy*; D006352:Heart Ventricles; D006353:Heart-Assist Devices; D009200:Myocardial Contraction / Q000502:physiology*; D011817:Rabbits; D013318:Stroke Volume / Q000502:physiology*; D013599:Systole; D016896:Treatment Outcome; D016277:Ventricular Function, Left / Q000502:physiology*