Pii: 0002-9149(86)90135-9

soon after cardiac transplantation, but the recipient patients seldom show a postoperative precordial murmur attributable to valve dysfunction. This is not surprising, because mild forms of valvular regurgitation detected by Doppler are often clinically inaudiblee5 Overt signs of tricuspid regurgitation and right ventricular failure were observed in 2 patients with residual postoperative pulmonary hypertension of moderate degree. This minor form of multivalvular regurgitation is usually transient; the abnormalities detected in the 4 cardiac valves tend to disappear during the first 3 months. The pathophysiology of such multivalvular regurgitation is unclear. Despite the anecdotal description of valve infiltration in severe forms of cardiac rejection leading to death,7 we found no relation between early cardiac rejection detected by endomyocardial biopsy and presence or severity of valvular regurgitation (Table I). In some patients rejection developed when valvular regurgitation had disappeared, and detection of regurgitation was not necessarily associated with the presence of rejection. It is uncertain if more severe forms of rejection can lead to valve dysfunction. Neither can changes in left ventricular function or dilatation account for transient valvular regurgitation. There was a correlation between calculated left ventricular mass and the presence of valvular regurgitation. Absolute left ventricular mass is often increased at 1 to 2 weeks after cardiac transplantation, irrespective of the presence or absence of rejection, and there is a gradual reduction of calculated left ventricular weight thereafter (Table I]. We believe that early postoperative increased left ventricular mass is due to cardiac edema related to both manipulation and transport of the donor heart, and in fact myocardial edema is systematically seen in the first few cardiac biopsies performed. Although not detectable by ultrasound, mild edema of the cardiac valves or papillary muscles may be the cause of these transient valve abnormalities, and its reabsorption would normalize valve function. The low reabsorption rate of myocardial edenia could be due to the lack of cardiac lymphatic drainage.