Left Ventricular Volume, Mass, and Function During the Development and Regression of Supraventricular Tachycardia-Induced Cardiomyopathy Disparity Between Recovery of Systolic Versus Diastolic Function

Chronic supraventricular tachycardia causes a dilated cardiomyopathy in man. Terminating this tachycardia appears to result in symptomatic improvement; however, its effects on left ventricular (LV) volume, mass, and function have not been fully examined. Accordingly, hemodynamic studies using simultaneous echocardiography and catheterization were performed in three groups of pigs: 1) those subjected to rapid left atrial pacing (240 beats/min) for 3 weeks (SVT, n =8), 2) those subjected to supraventricular tachycardia for 3 weeks followed by termination of pacing and a 4-week recovery period (PSVT, n=9), and 3) sham-operated controls (CTR, n = 10). Systolic pump function was assessed using fractional shortening (FS), peak ejection rate [peak (-)dD/dt], and maximum rate of pressure development [peak (+)dP/dt]. Diastolic function was assessed using the time constant of isovolumic pressure decline (ir), peak early diastolic filling rate [peak (+)dD/dt], the chamber stiffness constant (KJ, and the myocardial stiffness constant (K.). Supraventricular tachycardia caused LV dilation (end-diastolic dimension [EDDI increased from 3.5±0.4 cm in CTR to 4.9±0.5 cm in SVT, p<0.05) but no change in LV mass (LV weight-to-body weight ratio [LV/BW]) was 2.58±0.3 g/kg in CTR and 2.66±0.4 g/kg in SVT), all indexes of systolic function became abnormal (FS fell from 30±4% in CTR to 13±5% in SVT,p<0.05), and the indexes of relaxation and filling were slowed (-r increased from 36±3 msec in CTR to 51±13 msec in SVT, p<0.05). There were no significant changes in K, or Km. After terminating the supraventricular tachycardia, LV volume fell but remained greater than that in CTR (EDD was 4.2±0.4 cm in PSVT, p<O.O5 versus CTR) and substantial LV hypertrophy developed (LV/BW was 3.48 ±0.5 g/kg in PSVT, p<0.05 versus CTR). Systolic function returned to normal (FS was 31±5% in PSVT) but diastolic function remained abnormal. In PSVT, r remained prolonged (49±12 msec, p<0.05 versus CTR), Kc increased from 3.7± 1.0 in CTR to 7.4± 1.2 (p<0.05), and Km increased from 4.4±1.5 in CTR to 13.9±9.7 (p<0.05). Thus, the improvement in systolic function that occurs after the termination of supraventricular tachycardia is associated with the development of LV hypertrophy and persistent diastolic dysfunction. (Circulation 1991;83:635-644)