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SUMMARY:Multi-scale modeling of cardiac excitation-contraction coupling in
  the normal and failing heart - McCulloch\, A (UC\, San Diego)
DTSTART:20090721T123000Z
DTEND:20090721T131500Z
UID:TALK19139@talks.cam.ac.uk
CONTACT:Mustapha Amrani
DESCRIPTION:The excitation-contraction coupling properties of cardiac myoc
 ytes isolated from different regions of the mammalian left ventricular wal
 l have been shown to vary considerably\, with uncertain effects on ventric
 ular function. We developed a detailed model of excitation-contraction cou
 pling model with region-dependent parameters for epicardial\, mid-myocardi
 al and endocardial myocytes\, and then embedded it within a fully coupled 
 finite element model of ventricular electromechanics coupled to a lumped p
 arameter model of the circulation. Comparing this model with one in which 
 heterogeneous myocyte parameters were assigned randomly throughout the mes
 h while preserving the total amount of each cell subtype\, we observed sim
 ilar transmural patterns of fiber and cross-fiber strains at end systole\,
  but clear differences in fiber strain distributions at earlier times duri
 ng systole. Hemodynamic function\, including peak left ventricular pressur
 e\, maximum rate of left ventricular pressure development\, and stroke vol
 ume were essentially identical in the two models. \n\nWe also modeled vent
 ricular electromechanics in the dyssynchronous failing dog heart and exami
 ned the relative roles of dilation\, negative inotropy\, negative lusitrop
 y and electrical dyssynchrony on global and regional function. The analysi
 s suggested that there is significant interactions between dilation and dy
 ssynchrony especially on regional mechanics. \n\nFinally\, we present init
 ial findings on a preliminary clinical study to test the ability of such m
 ulti-scale models of electromechanics in the failing heart to predict clin
 ical outcomes of cardiac resynchronization therapy. \n\nSupported by : NIH
 \, NSF\, UC Discovery\, Medtronic
LOCATION:Seminar Room 1\, Newton Institute
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