Objective: In animals and adult humans sustained supraventricular tachycardia leads to myocardial remodelling and dysfunction, persisting even after drug-induced cardioversion to sinus rhythm. This study was undertaken, to evaluate cardiac function in the human fetus by noninvasive determination of the degree of AV valve incompetence and venous blood flow, in order to enhance understanding of the pathophysiology of fetal supraventricular tachycardia. Furthermore, we wanted to determine the usefulness of these methods in the surveillance of these fetuses before and after drug-induced cardioversion.
Study design: Eleven fetuses with supraventricular tachycardia between 24 and 35 weeks of gestation were studied. AV valve regurgitation and venous Doppler waveforms of the inferior vena cava and ductus venosus were evaluated before and after conversion to sinus rhythm.
Results: Three different groups of fetuses could be distinguished. The first group consisted of four fetuses with neither signs of hydrops nor AV valve incompetence. Venous indices normalized within one to four days (median 2.5 days) after conversion to sinus rhythm. The second group contained two fetuses with hydrops, but without AV valve incompetence. Their venous indices normalized at the day of conversion and 3 days later, respectively (median 1.5 days). The last group of five fetuses consisted of four fetuses with hydrops and AV valve regurgitation during supraventricular tachycardia. In one fetus with hydrops and supraventricular tachycardia the fetal heart rate was continuously decreased to a level of 160-190 beats/min under drug treatment, but no conversion to sinus rhythm occurred. The venous indices of these fetuses normalized within 12-42 days (median 27 days) after conversion.
Conclusion: Our data suggest that in sustained fetal supraventricular tachycardia alterations of myocardial function similar to tachycardia-induced 'cardiomyopathy' occur. The severity of tachycardia-induced changes of cardiac function is reflected by the degree and persistence of AV valve incompetence, as well as by alterations of the venous blood flow pattern. Under clinical conditions, the latter can readily and well reproducibly be demonstrated by calculating the venous blood flow indices of the inferior vena cava and ductus venosus.