Predonated autologous blood use in elective cardiac surgery.

The risks of homologous blood transfusion are well documented and recently increased with the emergence of acquired immunodeficiency syndrome. Preoperative autologous donation has been suggested to reduce these risks. This is a report concerning 104 consecutive adult autologous donors (group 1) who had an elective cardiac operation. A similar group of 111 patients operated on during the same period but without autologous blood donation was used for comparison (group 2). Both groups contained similar numbers of patients with coronary artery disease, valvular disease, and mixed lesions, and both had several patients with atrial septal defects. Group 2 patients (mean age, 67.8 years) were significantly older than group 1 patients (mean age, 58.9 years) (p less than 0.05). The mean donation in group 1 was 4.1 units, but 12 (11.5%) had to discontinue donations. Increasing angina in 10 (12.2%) of the 82 patients with coronary artery disease was the most common complication, and necessitated hospitalization in two instances. In 77 (75.5%) of the 102 group 1 patients who had operation and 23 (21%) of the 110 group 2 patients, no homologous blood products were required. Group 1 patients used significantly less homologous fresh frozen plasma (0.1 unit versus 0.97 unit; p less than 0.005) and packed red blood cells (0.6 unit versus 2.1 units; p less than 0.001) than group 2 patients. Group 1 patients received 3.3 and 3.1 units of autologous packed cells and plasma, respectively. No complications of autologous transfusion were seen. Predonation of autologous blood is an effective, safe method of reducing homologous blood requirements in elective cardiac operations, but it does carry some risk, especially in patients with coronary artery disease.

Changes in myofibrillar content and Mg-ATPase activity in ventricular tissues from patients with heart failure caused by coronary artery disease, cardiomyopathy, or mitral valve insufficiency.

Force development and shortening by cardiac muscle occur as a result of the interaction between actin and myosin within the myofibrillar lattice. This interaction is dependent upon intracellular ionized calcium and is controlled by the troponin-tropomyosin regulatory proteins situated along the actin filament. In this study, we compared the myofibrillar content and myofibrillar Mg-ATPase activity of normal human ventricular muscle with that of ventricular muscle from patients in end-stage failure caused by coronary artery disease or cardiomyopathy and ventricular muscle from patients with heart failure due to mitral valve insufficiency. The results show that the amount of myofibrillar protein (mg/g wet wt ventricle) in hearts in end-stage failure (coronary artery disease and cardiomyopathy) is significantly lower compared with normal hearts and hearts in failure due to mitral valve insufficiency. However, the Mg-ATPase activity of myofibrils from hearts in both end-stage failure and failure due to mitral valve insufficiency is significantly lower compared with myofibrils from normal hearts. The data suggest that the reduction in the amount of myofibrillar protein in ventricular tissue is a pivotal event that may be responsible for the progression of heart disease to the point of end-stage failure.

Four-year follow-up on the Albany experience with intrapleural BCG in lung cancer.

One hundred sixty-nine patients were entered into randomized controlled studies of intrapleural bacille Calmette Guérin (BCG) immunotherapy after surgical resection of lung cancer. Long-term follow-up of our initial series of BCG-treated patients with Stage I disease continues to indicate that this treatment was superior to that given to control patients. The recurrence rate in the control population was high, 62% at 3 years. The recurrence rate was 33% at 3 years in the BCG-treated group. A negative preoperative tuberculin test and squamous cell histologic type were favorable prognostic factors for BCG-treated patients. The survival of patients with more advanced disease was not improved by BCG immunotherapy.