Zupan I, Rakovec P, Budihna N, Brecelj A, Kozelj M
Department of Cardiology, University Medical Centre Ljubljana, Slovenia.
Int J Cardiol. 1996 Sep;56(1):75-81. doi: 10.1016/0167-5273(96)02728-3.
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.
长期的室性心动过速（VT）和室上性心动过速（SVT）可导致可逆性左心室功能障碍。心肌病的发生及心动过速后改变的严重程度至少取决于心动过速的三个参数，包括其类型（室性或室上性）、心率和持续时间。十只比格犬以每分钟180次的频率起搏3周。每只犬采用两种起搏方式，即室上性和室性起搏。其中一半犬从室性起搏开始研究，另一半从室上性快速起搏开始。在左心室功能完全恢复后应用交替起搏方式。通过放射性核素心室造影、超声心动图和 Swan - Ganz 导管检查评估心室功能和形态。在起搏停止后的窦性心律中研究心动过速后的改变。与基线值（69.5±2.3%）相比，两种类型的心动过速（室上性心动过速：53±5%，室性心动过速：48±7%，P<0.05）后左心室射血分数（LVEF）均显著下降。收缩末期（室上性心动过速：2.1±0.3 cm，室性心动过速：2.4±0.2 cm，对比基线值1.6±0.3 cm）和舒张末期内径（室上性心动过速：3.0±0.3 cm，室性心动过速：3.3±0.4 cm，对比基线值2.7±0.3 cm）显著增加（P<0.05），表明起搏动物存在心室扩张。与基线值相比，两种类型的心动过速后左心室肺毛细血管楔压均显著升高（室上性心动过速：7.5±1.2 mmHg，室性心动过速：8.4±1.1 mmHg，对比基线值1.9±1.5 mmHg，P<0.05）；两种心动过速之间的差异不显著。本研究表明，慢性室上性心动过速和室性心动过速即使心率不是很高，也会在相对较短的时间内导致左心室功能障碍。慢性室性心动过速比慢性室上性心动过速更明显地导致左心室射血分数恶化和左心室扩张。
