The contrasting effects of cyclosporin-A and azathioprine on arterial blood pressure and renal function following cardiac transplantation.

The effects of cyclosporin-A and azathioprine on the postoperative development of systemic hypertension and renal dysfunction in patients undergoing cardiac transplantation were compared retrospectively in 18 patients receiving cyclosporin-A and in 12 patients receiving azathioprine. Twelve months postoperatively, the average mean blood pressure was 116 +/- 13 mm Hg and 98 +/- 7.5 mm Hg; the average preoperative serum creatinine was 1.2 +/- 0.3 mg% and 1.5 +/- 0.3 mg%; and the postoperative serum creatinine was 2.2 +/- 0.8 mg% and 1.1 +/- 0.2 mg% (P less than 0.0001) in the cyclosporin-A-and azathioprine-treated groups respectively. Hemodynamic studies were done to characterize the de novo postoperative hypertension developing in the cyclosporin-A group. The pre- and postoperative cardiac output was 3.7 and 4.91/min, respectively (P less than 0.01). The pre- and postoperative systemic vascular resistance was 1707 and 1941 dynes sec X cm-5, respectively (P greater than 0.2). Peripheral renin activity and 24-hour urinary catecholamine excretion were not elevated. The mechanism of the hypertension developing in cyclosporin-A-treated patients is unknown, but is associated with normalization of cardiac output, an abnormally elevated systemic vascular resistance, and modest impairment of renal function. These findings are in marked contrast to azathioprine-treated patients, in whom postoperative hypertension and renal dysfunction do not occur. These observations implicate cyclosporin-A as the major contributing factor in the development of hypertension and renal dysfunction.

Respiratory augmentation of left ventricular function during spontaneous ventilation in severe left ventricular failure by grunting. An auto-EPAP effect.

A patient with severe congestive cardiomyopathy demonstrated involuntary forceful expiratory grunting that was associated with an elevated intrathoracic pressure and stable hemodynamics. Face-mask administration of 20 cm H2O as continuous positive-airway pressure (CPAP) abolished the grunting without hemodynamic compromise. However, loss of CPAP by mask leak resulted in rapid hemodynamic deterioration and resumption of grunting. Endotracheal intubation with 20 cm H2O of positive end-expiratory pressure restored hemodynamic stability. This suggests that spontaneous ventilatory efforts can augment the failing myocardium.

Intermittent mitral regurgitation due to Beall valve dysfunction: analysis of 13 patients with atrial fibrillation.

A unique hemodynamic event was noted in long-term survivors of mitral valve replacement with the Beall prosthesis. The event was a result of intermittent valve dysfunction and transvalvular mitral regurgitation (MR). At cycle lengths longer than 0.9 second that were preceded by shorter cycle lengths, 8 of 13 patients with Beall valve prostheses who had chronic atrial fibrillation (AF) intermittently had a marked unexpected decrease in peak left ventricular systolic pressure and a simultaneous increase in left atrial or pulmonary artery wedge "v" wave pressure. This event, which is a result of intermittent, severe MR, occurred more frequently at longer cycle lengths. In all 8 patients with the finding, severe valve disc wear was found at operation; however, 5 of these patients had only trace or 1+ MR on left ventricular angiography. In contrast, the event did not occur in 11 patients in chronic AF with organic MR or non-Beall valve MR, despite an appropriate number of sufficiently long cycles. The absence of the event in 5 Beall valve patients with significantly faster heart rates than in those with the event may in part be a result of its dependence on cycle length. This hemodynamic event, when present in a Beall valve recipient in AF, is an indication for valve replacement, even in the absence of angiographic evidence of severe MR.