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Objectives: The mechanisms of cardiac allograft vasculopathy and its predisposing factors are multifactorial and as yet not well established. To determine the influence of endothelial dysfunction on the development of intimal thickening, we prospectively analyzed the vasomotor response to acetylcholine and nitroglycerin, as well as other donor and recipient variables. Findings were correlated with the coronary intimal thickness, which was evaluated by means of intravascular ultrasonography., Methods: Nineteen patients who had undergone heart transplantation 4.89 +/- 2.35 years previously and who had angiographically normal coronary arteries were included. Endothelial function was analyzed by quantitative coronary analysis of the vasomotor response of the left anterior descending artery to acetylcholine. An intimal thickness index, reflecting the percentage of intima obstructing the coronary lumen, was calculated., Results: Nine (47%) patients showed endothelial dysfunction, and the remaining 10 (53%) patients had a normal response. Four (44%) of 9 patients with a weight gain of greater than 20% after the operation showed endothelial dysfunction compared with none of the 10 patients with normal responses (P <.04). The severity of the intimal thickness correlated with the years after transplant (r = 0.45, P <.05). Patients with endothelial dysfunction had more intimal thickening than those without (32% +/- 17% vs 17% +/- 12%, respectively; P <.05). Furthermore, the degree of intimal thickening correlated with the magnitude of the vasomotor response to acetylcholine (r = -0.60, P =.006). No relationship was found between intimal thickness and the vasodilatory response to nitroglycerin. As independent variables for intimal thickness, multivariate analysis detected the magnitude of the response to acetylcholine (P =.0005), years after transplant (P =.01), and ischemic time (P =.03)., Conclusions: Cardiac allograft vasculopathy is a multifactorial disease the severity of which increases over time. Endothelial dysfunction is a predictive factor of intimal thickening severity. Predisposing factors that provoke endothelial injury, such as perioperative ischemic time and obesity, may contribute to the development of allograft vasculopathy.

Background: Aprotinin reduces blood loss in operations done with cardiopulmonary bypass, whereas the use of desmopressin remains controversial. We compared aprotinin, desmopressin, and placebo in a double-blind, randomized trial to evaluate bleeding and transfusion requirements., Methods and Results: One hundred forty-nine patients (48 received aprotinin, 50 desmopressin, 51 placebo) were included. Blood loss and transfusion requirements were recorded and levels of Factor VIII coagulant activity, von Willebrand's factor, thrombin-antithrombin complexes, and D-dimer were measured. Overall blood loss was 195 +/- 146 ml/m2 in the aprotinin group, 400 +/- 192 ml/m2 in the desmopressin group, and 489 +/- 361 ml/m2 in the placebo group (95% confidence intervals: difference between desmopressin and aprotinin 98 to 312 ml/m2, p < 0.001; difference between placebo and aprotinin 190 to 398 ml/m2, p < 0.001). Twenty-six percent of patients treated with aprotinin, 66% of those treated with desmopressin, and 56% of those treated with placebo were given transfusion (95% confidence intervals: difference between aprotinin versus placebo plus desmopressin 51% to 71%, p < 0.001). Fibrinolytic activation throughout cardiopulmonary bypass was markedly higher with placebo or desmopressin administration. D-dimer level correlated with overall blood loss in patients receiving desmopressin or placebo, but not in those receiving aprotinin., Conclusion: Aprotinin administration reduces blood loss and transfusion requirements in cardiopulmonary bypass. This benefit may be explained by a lower activation of fibrinolysis.

The results of cardiac valve replacement with the Monostrut Björk-Shiley prosthesis (Shiley, Inc., Irvine, Calif.) during a 7-year period are presented. A total of 984 valves were implanted in 820 patients from May 1983 to April 1990. Aortic valve replacement was performed in 378 patients, mitral replacement in 294, and multiple replacement in 148. In addition, 180 patients (22%) underwent associated procedures. Mean age was 52.6 +/- 11 years. Operative (30 days) mortality was 5.9% (49 patients): 3.9% (15 patients) for aortic, 7.8% (23 patients) for mitral, and 7.4% (11 patients) for multiple valve replacement. All patients were given long-term anticoagulation therapy. Follow-up was 99% complete (eight patients were lost to follow-up), with a closing interval of 3 months, and totaled 2422 patient-years. Valve-related complications, expressed as percentage event-free (+/- standard error) at seven years were as follows: structural deterioration, 100%; nonstructural dysfunction, 98.3% +/- 0.6%; thromboembolism, 90.2% +/- 1.7%; anticoagulant-related hemorrhage, 88.7% +/- 2.8%; and prosthetic valve endocarditis, 98.1% +/- 0.8%. There were no cases of valve thrombosis. Actuarial survival (free from operative, valve-related, and sudden death) was 88.4% +/- 1.2% at 7 years. Freedom from reoperation was 96.8% +/- 0.1%. Probability of being free from all valve-related morbidity and mortality was 70% +/- 3%, and 708 (93%) of the survivors were in New York Heart Association class I or II. Serial Doppler echocardiograms were done prospectively in 243 patients (with 154 aortic and 120 mitral prostheses), both postoperatively and at regular intervals up to 3 years. Mean prosthetic gradients ranged from an average of 20.9 to 7 mm Hg in the aortic prostheses (21 to 29 mm) and from 6.1 to 4.8 mm Hg in the mitral prostheses (25 to 31 mm). The gradients in each patient did not change significantly during the follow-up period. Our 7 year's experience with the Monostrut valve shows a low rate of valve-related complications, a durable design, and good hemodynamic and functional results.

Patients with mitral stenosis and some degree of right ventricular failure may benefit from inotropic or pulmonary vasodilator drugs in the early postoperative period. Thirty patients undergoing an operation for mitral stenosis were randomized into three groups. In group I (n = 10), isoproterenol (5 micrograms/kg/min) was started in the immediate postoperative period. In group P (n = 10), prostaglandin E1 (0.08 microgram/kg/min) was given, and in group C, the control group (n = 10), no drugs were used. After the operation and before drug therapy was begun, basal measurements of cardiac index, mean pulmonary arterial and mean arterial pressures, and pulmonary vascular resistance were taken. Measurements were repeated at 6, 12, and 24 hours. Mean measurements of cardiac index (basal up to 24 hours) were as follows: 1.39 +/- 0.3, 1.92 +/- 0.4, 2.4 +/- 0.5, and 2.34 +/- 0.3 L/min/m2 for group C; 1.54 +/- 0.5, 2.64 +/- 0.4, 2.68 +/- 0.7, and 2.2 +/- 0.6 L/min/m2 for group I, and 1.57 +/- 0.3, 2.2 +/- 0.6, 2.72 +/- 0.7, and 2.27 +/- 0.4 L/min/m2 for group P (p less than 0.05 between groups C and I at 6 and 12 hours). Mean pulmonary artery pressures were as follows: 19.5 +/- 3.2, 24.8 +/- 7, 27.7 +/- 7.3 and 28.8 +/- 5.7 mm Hg in group C; 21.4 +/- 8.7, 25.7 +/- 7.2, 26.4 +/- 7, and 29.4 +/- 8.6 mm Hg in group I, and 19.1 +/- 4, 19.2 +/- 3, 20.4 +/- 6, and 20.7 +/- 5 mm Hg in group P (p less than 0.05, group P versus groups C and I at 6, 12, and 24 hours). Mean pulmonary vascular resistances were as follows: 3.9 +/- 2.4, 3.9 +/- 1, 3.36 +/- 2, and 3.2 +/- 1.4 Wood units in group C; 4.84 +/- 4, 3.37 +/- 2.2, 3.69 +/- 3, and 4.69 +/- 4.1 Wood units in group I, and 3.29 +/- 1.3, 1.71 +/- 0.5, 1.61 +/- 0.5, and 1.96 +/- 0.8 Wood units in group P (p less than 0.05, group P versus groups C and I at 6, 12, and 24 hours). There was no difference in mean systemic arterial pressure among the three groups. Our results indicate that patients subjected to mitral valve operations have a low cardiac index. Isoproterenol increases cardiac index but has little effect on pulmonary resistance. At low doses, prostaglandin E1 effectively decreases pulmonary vascular resistance without altering systemic arterial pressure or heart rate.

Iatrogenic coronary artery stenosis as a serious complication of aortic valve procedures is a difficult condition to solve. We present a case in which both ostia were involved. As the patient refused reoperation, percutaneous transluminal coronary angioplasty (PTCA) was used.

One hundred patients who underwent elective cardiac operations were randomized into two groups. Group 1 had a 20 micron nylon screen filter in the arterial line. In Group 2 no filter was used in the arterial line. Neurologic and neuropsychologic examination of the patients was performed with seven psychometric tests of the Wechsler Memory Scale and the Wechsler Adult Intelligence Scale. These tests were conducted before and a mean of 10 days after the operation. Platelet counts and hemoglobin and total protein levels were measured at the onset and at the end of cardiopulmonary bypass. Two patients died during their hospital stay. Neurologic damage with focal signs was found in the postoperative examination in six patients (three in each group). Twenty-eight patients (28.5%) exhibited signs of mild cerebral dysfunction as assessed by the presence of archaic (primitive) reflexes. Fifteen were in Group 1 and 13 in Group 2 (no significant difference). Sixty patients (61%) had decrements greater than one standard deviation in at least one of the three tests that showed most decreased postoperative scores. There were 32 in Group 1 and 28 in Group 2 (no significant difference). When each test was analyzed individually, there were no significant differences between the two groups. Platelet counts decreased, during cardiopulmonary bypass, a mean of 33% in Group 1 and 34.5% in Group 2 (no significant difference). Both hemoglobin and total protein levels remained virtually unchanged. These results indicate that the addition of a small-pore filter in the arterial line does not prevent the neurologic and neuropsychologic disturbances frequently encountered after cardiopulmonary bypass. The filter itself does not appear to have a direct effect on the blood components. Routine use of an arterial line filter remains questionable.

Between May 1983 and April 1986, 318 patients underwent cardiac valve replacement with the Monostrut Björk-Shiley prosthesis. There were 136 aortic valve replacements, 128 mitral valve replacements, and 54 multiple replacements. A total of 373 valves were implanted. Associated procedures were done in 79 (25%) of the patients. Hospital (30-day) mortality rate was 5.6% (18 patients): 2.9% (n = 4) after aortic, 7.8% (n = 10) after mitrals and 7.4% (n = 4) after multiple valve replacement. Follow-up was obtained in all 300 operative survivors, for a total of 500 patient-years (mean 18 months). Actuarial survival rate, excluding operative deaths, at 4 years was 94.7% +/- 1.5% (mean +/- standard error of the mean). There were 16 thromboembolic episodes (3.2/100 patient-years). Freedom from all valve-related complications was 87% +/- 2.4% at 3 1/2 years. Neither valve thrombosis nor structural failure has been observed. Eighty percent of the patients are in New York Heart Association functional class I. Forty-two patients (26 with aortic and 16 with mitral valve replacement) underwent cardiac catheterization a mean of 6 1/2 months after the operation. In the aortic position, peak gradients were an average of 6.9 +/- 1.2 mm Hg. Mean systolic gradients were 12.4 +/- 6.3 mm Hg and did not increase with exercise. In the mitral position, end-diastolic gradients were an average of 2.1 +/- 2 mm Hg and mean gradients, 5.9 +/- 2 mm Hg. Discharge coefficient (estimated orifice area/geometric area) was 0.63 +/- 0.2 for the aortic and 0.53 +/- 0.2 for the mitral prostheses. Disc opening was maximal in most patients. These results indicate that the Monostrut prosthesis has a low rate of thromboembolic events, no structural failures or thrombotic obstructions and excellent hemodynamic performance, especially in the small aortic sizes (discharge coefficient for 19 and 21 mm valves, 0.77).