Tachycardia induced cardiomyopathy in dogs; relation between chronic supraventricular and chronic ventricular tachycardia.

Long-standing ventricular tachycardia (VT) and supraventricular tachycardia (SVT) can produce a reversible left ventricular dysfunction. The onset of cardiomyopathy and the severity of posttachycardic changes depend at least on three parameters of tachycardia, including its type (VT or SVT), rate and duration. Ten dogs (beagles) were paced at 180 beats/min for 3 weeks. Two pacing modalities, supraventricular and ventricular, were used in each dog. In half of them, the study was started by ventricular, and in the other half by supraventricular high-rate pacing. The alternate pacing modality was applied after complete recovery of left ventricular function. Ventricular function and morphology were evaluated by radionuclide ventriculography, echocardiography and Swan-Ganz catheterisation. Posttachycardic changes were studied in sinus rhythm after cessation of pacing. Left ventricular ejection fraction (LVEF) fell significantly after either type of tachycardia (SVT: 53 +/- 5%, VT: 48 +/- 7%, P < 0.05) compared with baseline values (69.5 +/- 2.3%). Significant increases (P < 0.05) in end-systolic (SVT: 2.1 +/- 0.3 cm, VT: 2.4 +/- 0.2 cm vs. 1.6 +/- 0.3 cm) and end-diastolic dimensions (SVT: 3.0 +/- 0.3 cm, VT: 3.3 +/- 0.4 cm vs. 2.7 +/- 0.3 cm) indicated ventricular dilation in paced animals. Left ventricular pulmonary capillary wedge pressure increased significantly after either type of tachycardia as compared with baseline values (SVT: 7.5 +/- 1.2 mmHg, VT: 8.4 +/- 1.1 mmHg vs. 1.9 +/- 1.5 mmHg, P < 0.05); the difference between tachycardias was not significant. The present study demonstrates that chronic SVT and VT result in left ventricular dysfunction in a relatively short time, even if the heart rate is not very high. Deterioration of left ventricular ejection fraction and dilation of the left ventricle are more marked in chronic VT than in chronic SVT.