Tachycardia-Induced Cardiomyopathy

Background. Chronic supraventricular tachycardia (SVT) causes a dilated cardiomyopathy and myocyte injury. Termination of SVT improves left ventricular (LV) function but is associated with LV hypertrophy. Changes in myocardial blood flow (MBF) that may accompany the development of and recovery from SVT cardiomyopathy might have a significant effect on LV function and myocyte structure. The goal of this study was to relate changes in LV function, myocyte composition, and coronary vascular structure to changes in MBF with the development and recovery of SVT cardiomyopathy. Methods and Results. LV function and MBF were measured in three groups of conscious pigs: sham control (control; n=8), after 3 weeks of atrial pacing (SVT, 240 beats per minute; n=8), and after a 4-week recovery from SVT (post-SVT; n =8) by echocardiography catheterization and microspheres. Measurements were made under three states: 1) at rest with a basal heart rate, 2) rapid atrial pacing (240 beats per minute), and 3) during adenosine infusion (1.5 .lmolI1 kg-1 * min-') without pacing. LV myocyte, capillary, and arteriole morphometric studies were performed in five additional pigs from each group using histochemistry and electron microscopy. LV fractional shortening was lower and left atrial pressure was significantly higher in the SVT group compared with control at rest, during pacing, and with adenosine (p< 0.05). In the post-SVT group, fractional shortening returned to control values at rest and with adenosine, but fell from control values with pacing (p<0.05). Left atrial pressure fell in the post-SVT group but remained significantly higher than control (p<0.05). LV/body weight ratio was significantly increased in the post-SVT group (p <0.05). In all states, SVT LVMBF was significantly reduced from control values (rest, 0.8±0.3 versus 1.6±0.3 ml. min`. g-'; pacing, 1.2±0.2 versus 3.1±0.3 ml min-l. g-1; adenosine, 1.4±0.3 versus 4.4±0.4 ml* min`* g-', respectively, p<O.OS). In the post-SVT group, LVMBF was similar to control at rest (1.3±0.2 ml * min` . g-') but was significantly lower than control with pacing and adenosine (2.0±0.4 and 2.5±0.5 ml * min`* g-', respectively, p<0.05). Myofibrillar content fell significantly with SVT compared with control (42±5 versus 61±3%, p<0.05) and returned to control values in the post-SVT group (64±3%). Capillary density remained unchanged in the SVT and post-SVT groups, but capillary luminal diameter decreased and arteriole diameter increased in the SVT group (p<0.05). Conclusions. The LV dysfunction and myocyte injury with SVT cardiomyopathy were associated with reduced MBF. Early recovery from SVT cardiomyopathy resulted in hypertrophy with normal MBF at rest, but significantly reduced coronary reserve. (Circuion 1992;85:717-729)