Complement (C3, C4) and C-reactive protein responses to cardiopulmonary bypass and protamine administration.

Complement activation has been deemed responsible for the damaging effects of cardiopulmonary bypass (CPB) in patients undergoing open heart surgery. We studied C3, C4 and C-reactive protein (CRP) in 22 patients undergoing CPB. In Group 1 (11 patients), protamine was given intravenously and in Group 2 (11 patients), via the aortic root after CPB. Significant decreases were observed in C3 and C4 during CPB in both groups indicating complement activation primarily by the classic pathway. Protamine did not lead to further activation of the complement system. In both groups, C3 levels gradually returned toward baseline within 24 hours but C4 levels were still lower than baseline 24 hours postoperatively. CPB and protamine administration did not cause any significant changes in CRP levels, but CRP increased abruptly 24 hours after operation. Although activation of complement system during CPB is expected to invoke an acute phase response, we conclude that this period is not long enough to induce an increased production of CRP in response to tissue injury or inflammation.

A case of multiple pericardial hydatid cysts.

Pericardial cysts are rare developmental benign intrathoracic lesions and constitute 7% of all mediastinal tumors. As many as 70% of the cysts are found in the right cardiophrenic angle. Unusual locations include the left costophrenic angle, the hilum and the superior mediastinum at the level of the aortic arch. Cysts arising inside the pericardial cavity and attached to the heart are exceedingly rare. We describe a case of multiple pericardial hydatid cysts.

Clinical evaluation of the Omniscience cardiac valve prosthesis. Follow-up of up to 6 years.

From January 1984 to June 1989, 259 Omniscience valve prostheses were implanted in 225 patients. Of the 225 patients; 143 (63.6%) received mitral, 48 (21.3%) aortic, and 34 (15.1%) double valve replacements. The early mortality rate was 8.9%; 97.6% of the patients were included in this study. These patients represent a cumulative follow-up of 407.9 patient-years, with a mean follow-up of 2.03 +/- 0.1 (standard error) years. The late mortality rate was 4.03% overall, which corresponds to 2.0% +/- 0.7%/pt-yr (SE). The annual rate of valve endocarditis was 1.0% +/- 0.5%/pt-yr (SE). The linearized rate of thromboembolism was 1.2% +/- 0.5%/pt-yr (SE). Anticoagulant-related hemorrhage occurred in 15 patients with an annual rate of 3.7% +/- 0.9%/pt-yr (SE). The linearized rate of valve thrombosis was 0.2% +/- 0.2%/pt-yr (SE). By echocardiography the mean mitral valve opening was 75.9 +/- 3.1 degrees (standard deviation) for 27 patients. During follow-up study, 136 (70.8%) patients were in New York Heart Association class I, 44 (22.9%) were in class II, and 12 (6.3%) were in class III; there were 25 (11.1%) patients in class II, 166 (73.8%) in class III, and 34 (15.1%) in class IV preoperatively. Actuarial freedom from thromboembolism was 94.5% +/- 3.6% (SE); freedom from endocarditis, 97.8% +/- 1.0% (SE); freedom from anticoagulant-related hemorrhage, 91.5% +/- 2.0% (SE); freedom from valve thrombosis 99.1% +/- 0.8% (SE); and freedom from hemolysis 98.5% +/- 1.2% (SE). Actuarial survival at 6 years is 94.0% + 2.3% (SE) overall. In conclusion, the overall rate of valve-related complications with this valve is low.

Successful nonsurgical therapy of mural thrombosis of the left atrium after mitral valve replacement.

Mural thrombosis of the left atrium is a complication of mitral valve replacement. In this report we present a case of mural thrombosis of the left atrium after mitral valve replacement treated successfully without surgical intervention.

The triad of persistent left superior vena cava connected to the coronary sinus, right superior vena cava draining into the left atrium, and atrial septal defect: report of a successful operation for a rare anomaly.

The triad of right superior vena cava connecting to the left atrium, persistent left superior vena cava draining into the right atrium (coronary sinus), and atrial septal defect is a rare malformation. Recently, we successfully corrected this anomaly in a 47-year-old man.