CARDIOTHORACIC SURGERY

 Head of Department:

Prof. Oz Shapira

Tel:  02-6776960

STAFF

Professors Emeritus:

Borman, J.B. FRCS (Eng.), FACS. (Head, Cardiac Surgery Research Center)

Merin, G., MD 

Professor:

Shapira Oz, M.D. (Head of Department)

Elami, A., M.D.  (Head, Heart Transplant Unit)

Senior Lecturers:

Milgalter, E., M.D., (Head, Pediatric Cardiac Surgery Unit)

Rudis, E., M.D.

Izhar, U., M.D.

Research Associates:           

Schwalb, H., Ph.D.

Olivson, A., Ph.D.

Physicians Participating in Research and Teaching:

Elami, A., M.D.

Rudis, E., M.D.

Izhar, U., M.D.

Deviri, U., M.D.

Levi, E., M.D.

Viola, N., M.D.

Ad, N., M.D.

Korach, A., M.D.         

Marzouka, B., M.D.

Mourar, A., M.D.         

INTRODUCTION

The research laboratory of the Cardiothoracic Surgery Department, The Joseph Lunenfeld Cardiac Surgery Research Center, was established on 1982 by Prof. Joseph B. Borman – then the Head of Department of Cardiothoracic Surgery.  This Center is involved in basic research and R & D of innovative devices for cardiac surgery.

Current research in the laboratory focuses on methods to improve the ability of the myocardium to withstand induced short ischemia (open heart surgery or acute MI) and long-term ischemia (myocardial preservation for transplantation). Ischemic preconditioning and pharmacological alternatives are investigated in the isolated rat heart model. In the same model, we study the restoration of function of frozen/thawed isolated rat hearts as means for prolonged donor heart preservation.

Postoperative arrhythmia (atrial fibrillation) is recognized as a serious complication of open-heart surgery, with an incidence of 30% or higher. Different aspects of this intriguing problem are now studied. Cellular metabolism including mitochondrial function, adrenoreceptor function and endogenous cardiac glycosides are investigated as possible contributing factors in the development of this phenomenon.

The human body is exposed daily to several potentially toxic chemicals. Such chemicals may cause myocardial damage by either loss of physiologic function or acquisition of pathologic function. Loss of physiologic function may occur due to damage to constituents (e.g., proteins, nucleic acids, metabolic pathways) of cellular structures: membranes, mitochondria, nucleus, and myofibrils. Acquisition of pathologic function may occur when there is an increased release of damaging oxygen radicals from mitochondria or release of mitochondrial Cytochrome C, a trigger for apoptosis (cell death). We study the effect of environmental pollution on myocardial morbidity and its capability to withstand challenges.

Congestive heart failure is a clinical syndrome in which heart failure is accompanied by symptoms of pulmonary or peripheral congestion. Although heart failure is most commonly associated with impaired left ventricular systolic function, as many as 40-50% of the patients with heart failure have normal systolic function. In these patients, diastolic dysfunction is implicated as a major contributor for congestive heart failure. Thus, a device to decrease the diastolic pressures, which is under research at our laboratory, is potentially of utmost importance.   

Following acute myocardial ischemia and thrombolytic peptides evolved from lysed fibrin clot are released into the blood stream,. a new line of research tests the effect of these released peptides on myocardial function.

RESEARCH AREAS