IMPAIRED SUBENDOCARDIAL FUNCTION IN TACHYCARDIA-INDUCED CARDIAC-FAILURE

Chronic rapid ventricular pacing (CRVP) in many experimental models in duces ventricular dilatation, reduced ejection fraction, and symptomat ic congestive heart failure. We have investigated transmural mechanica l function in the left ventricular (LV) wall of five Hanford miniature swine before and after CRVP-induced failure. Three columns of radiopa que markers 1 mm in diameter were implanted in the anterior LV wall th rough a median sternotomy. A pair of LV pacing wires were sutured into the myocardium, a pneumatic cuff was placed around the inferior vena cava (IVC), and two fluid-filled Silastic catheters were implanted int o the LV apex. Two weeks after surgery, the pigs were suspended awake in a sling, and markers were tracked with biplane cineradiography. The hearts were paced for 3 wk (225-240 beats/min), and the study was rep eated with the pacemaker off. Saline infusion and IVC occlusion were u sed to vary LV end-diastolic pressure (EDP) so control-to-failure comp arisons could be made at matched LV EDPs. End-systolic strains in the circumferential (E(11)), longitudinal (E(22)), and transmural (E(33)) directions were quantified using finite element methods. There was a s ignificant reduction in E(11) and E(33) for the subendocardium: in E(1 1), from -0.27 to -0.18; in E(33), from 0.83 to 0.46. There were no si gnificant changes in subendocardial E(22) or in any of the outer wall normal strains. These results indicate that CRVP causes substantial re duction of subendocardial, but not subepicardial, function; taken toge ther with previous data indicating subendocardial hypoperfusion, these results support the contention that an imbalance between blood flow a nd oxygen demand plays a role in the etiology of heart failure in this model.