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Background The growth of the US cardiac transplant waiting list has outpaced the increase in donors, resulting in a widening gap between the number of waiting recipients and available donors. These trends have generated concern that longer waiting times may result in more patients deteriorating to urgent status and that transplanting only patients who are in an advanced state of decompensation will reduce posttransplant survival. Furthermore, the shortage of donors may result in extending the guidelines for donor acceptability to a degree that increases graft failure and posttransplant mortality. We measured these secular trends in the Cardiac Transplant Research Database to provide current data on time-dependent changes in US cardiac transplant practice and survival. Methods and Results At the time of this analysis, the Cardiac Transplant Research Database included all 2749 patients transplanted from January 1, 1990, to June 30, 1994, in the 25 participating transplant centers. During this 4.5-year period, the median waiting time for recipients who received a transplant increased from 2.7 to 3.5 months ( P <.0001), and the proportion of recipients whose status was urgent at transplantation increased from 41% to 60% ( P <.0001). Donor ischemic time increased from 150 to 166 minutes ( P <.0001), and the proportion of donors requiring pressor support increased from 68% to 85% ( P <.0001). Despite these changes in practice, the 1-year survival rate remained constant at 84% during this 4.5-year interval. There was no significant difference in 1-year survival rate between urgent status patients (83%) and nonurgent status patients (85%) ( P =.08). Conclusions The widening gap between the number of waiting recipients and the number of donors has resulted in a continuing trend toward transplanting urgent status recipients and to a liberalization of donor acceptance criteria. Despite these changes, posttransplant survival has remained constant.

Background Aprotinin is a serine protease inhibitor that reduces blood loss and transfusion requirements when administered prophylactically to cardiac surgical patients. To examine the safety and dose-related efficacy of aprotinin, a prospective, multicenter, placebo-controlled trial was conducted in patients undergoing repeat coronary artery bypass graft (CABG) surgery. Methods and Results Two hundred eighty-seven patients were randomly assigned to receive either high-dose aprotinin, low-dose aprotinin, pump-prime-only aprotinin, or placebo. Drug efficacy was determined by the reduction in donor-blood transfusion up to postoperative day 12 and in postoperative thoracic-drainage volume. The percentage of patients requiring donor–red-blood-cell (RBC) transfusions in the high- and low-dose aprotinin groups was reduced compared with the pump-prime-only and placebo groups (high-dose aprotinin, 54%; low-dose aprotinin, 46%; pump-prime only, 72%; and placebo, 75%; overall P =.001). The number of units of donor RBCs transfused was significantly lower in the aprotinin-treated patients compared with placebo (high-dose aprotinin, 1.6±0.2 U; low-dose aprotinin, 1.6±0.3 U; pump-prime-only, 2.5±0.3 U; and placebo, 3.4±0.5 U; P =.0001). There was also a significant difference in total blood-product exposures among treatment groups (high-dose aprotinin, 2.2±0.4 U; low-dose aprotinin, 3.4±0.9 U; pump-prime-only, 5.1±0.9 U; placebo, 10.3±1.4 U). There were no differences among treatment groups for the incidence of perioperative myocardial infarction (MI). Conclusions This study demonstrates that high- and low-dose aprotinin significantly reduces the requirement for donor-blood transfusion in repeat CABG patients without increasing the risk for perioperative MI.

Depressed myocardial contractility with paradoxically increased oxygen consumption has been demonstrated in previous studies of pressure overload hypertrophy. To determine whether altered mitochondrial respiration participates in the abnormal energetics of this muscle, right ventricular hypertrophy (RVH) was produced in 12 cats by pulmonary artery banding. A polarographic muscle bath was used to study eight control and eight RVH papillary muscles, and the respiration of mitochondria isolated from these right ventricles was characterized. RVH muscles demonstrated depressed force-velocity and length-tension curves. The myocardial oxygen consumption per gram of peak active tension was increased from 0.65 ± 0.05 nliters/mg beat -1 (control) to 1.10±0.07 nliters/mg beat -1 (RVH) ( P <0.001). Abnormal mitochondrial respiration was shown by an increase in the rate of state 4 oxygen consumption from 12.5±0.8 natoms/mg min -1 (control) to 19.9±0.8 natoms/mg min -1 (RVH) ( P < 0.001). The altered oxygen cost of active isometric tension in the RVH muscles was linearly correlated with the altered rate of mitochondrial state 4 oxygen consumption ( r = 0.91). Ruthenium red, a compound that blocks mitochondrial calcium uptake, reduced the rate of RVH state 4 oxygen consumption to the control level. The present study suggests a mechanism for the abnormal myocardial oxygen consumption in pressure overload hypertrophy and relates it to nonphosphorylating mitochondrial respiration linked to calcium transport.

BACKGROUND Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are a family of structurally related peptides that participate in the integrated control of renal and cardiovascular function. Previous studies suggest a functional role for these hormonal peptides in cardiorenal regulation in congestive heart failure (CHF). METHODS AND RESULTS The present studies were performed in normal subjects (n = 6) and in patients with mild (New York Heart Association [NYHA] class I to II, n = 20) and severe (NYHA class III to IV, n = 20) CHF by use of radioimmunoassay and immunohistochemical staining (IHCS). Plasma ANP was significantly increased in both mild and severe CHF compared with normal subjects. In contrast, plasma BNP was only moderately increased in the severe CHF group, and plasma CNP concentration was unchanged in CHF compared with normal subjects. Atrial tissue concentrations of the natriuretic peptides did not parallel circulating concentrations. ANP predominated in normal atrial tissue, but BNP predominated in CHF. In ventricular tissue, IHCS staining was present for all three peptides in normal ventricular myocardium and was markedly enhanced in CHF. CONCLUSIONS These studies support a differential regulation of ANP, BNP, and CNP circulating concentrations and tissue activity in human CHF.

BACKGROUND Atrial natriuretic factor (ANF) is produced by myocardial tissue, and the plasma ANF concentration is known to be elevated in congestive heart failure (CHF). Data from animal models indicate that myocardial concentrations of ANF are depleted in CHF, and this has given rise to the hypothesis that CHF is characterized by depletion of stored ANF. To date, the molecular forms of ANF and their concentrations in atrial and ventricular myocardium remain poorly characterized in the normal and the failing human heart. METHODS AND RESULTS We measured ANF concentrations in fresh tissue from failing human hearts explanted at the time of cardiac transplantation and from organ donors whose normal hearts could not be used for transplantation. We determined total ANF and alpha, beta, and gamma ANF concentrations in the right and left atrial appendages, atrial free walls, and ventricles. In normal hearts, ANF concentration in the atrial appendages was 40-fold higher than ANF in the rest of the atrial free wall and in the ventricles. In the failing hearts, atrial appendage ANF concentrations increased 5- to 10-fold, and atrial free wall ANF concentrations increased 200-fold. Analysis of molecular forms of ANF demonstrated significant increases in the gamma and beta forms in the left atrial appendage of failing hearts. alpha, beta, and gamma ANF forms were also significantly increased in right and left atrial free wall tissue from failing hearts. In addition, failing hearts were characterized by absolute and relative increases in the precursor form gamma ANF. CONCLUSIONS These data from fresh tissues suggest that cardiac ANF stores are not decreased in severe CHF in humans; rather, chronic CHF is characterized by marked increases in atrial ANF tissue concentrations, particularly the beta and gamma ANF forms. These findings are consistent with intracellular accumulation of precursor ANF forms in severe chronic human CHF.

During pregnancy, when surgically reparable heart disease can no longer be medically manged, open- or closed-heart surgery is the procedure of choice without prior therapeutic abortion. Cyanotic congenital heart disease in a pregnant patient when completely correctable surgically may be an indication for surgery in itself. Available data suggest that pregnancy per se does not increase the maternal risk of heart surgery with use of extracorporeal circulation. Fetal mortality in our series was 33%.

The cardiovascular response to angiographic contrast medium was studied in 28 patients undergoing diagnostic angiocardiography under anesthesia. A transient phase of hypotension and tachycardia similar to that described by other authors was noted. Cardiac output was increased initially by 50 per cent and returned to the base line in 20 minutes. Peripheral blood flow increased by 100 per cent, apparently due to the direct effect of the hyperosmotic solution on the vascular smooth muscle. Hemodilution, maximal 2 to 4 minutes after injection of contrast medium, suggested a transient increase in circulating blood volume. Increased ventricular filling pressures, which were thought to be due to hypervolemia, were associated with increased left ventricular stroke work.

Clinical, hemodynamic, and angiocardiographic findings are described in seven cases of congenital mitral insufficiency. The volumes and changes in volume of the left atrium and left ventricle were calculated from the angiocardiograms and were found to be increased above the range of normal. Left ventricular stroke volumes thus obtained were compared with forward flows calculated from indicatordilution curves in order to quantitate regurgitant flow. Regurgitant flows varied between 19 and 94 per cent of the total left ventricular ejection volume, and forward flow was maintained as a result of a considerable increase in left ventricular volume. The left ventricular ejection volume was 50 to 64 per cent of the end-diastolic volume.

The syndrome of erythermalgia is characterized by a burning distress of the extremities that is accompanied by redness and increased temperature of the skin. These symptoms are initiated or exacerbated by an increase in environmental temperature and diminished by measures that cool the skin. Of 51 patients with this clinical syndrome seen at the Mayo Clinic during the years 1951 to 1960 inclusive, 30 were considered as having primary erythermalgia because of the absence of demonstrable associated conditions, and the rest were classified as having secondary erythermalgia because the condition was associated with various diseases. Particularly significant was the relation of erythermalgia to the myeloproliferative disorders as evidenced in 10 cases. In some of these cases, erythermalgia preceded other manifestations of the myeloproliferative disorder by as long as 12 years. The primary type was found to occur in younger individuals and to be more often bilateral, to produce pain of greater intensity, and to involve larger areas of the affected extremities. The pathologic physiology of this syndrome remains unknown.

In the case of idiopathic fibrous retroperitonitis presented, the only symptoms were those of arterial insufficiency of the lower limbs and testicular and inguinal pain of uncertain origin. Relief of claudication and return of normal pulsations were achieved after surgical lysis of the common iliac arteries and the terminal segment of the aorta. Numerous reports in the literature indicate that idiopathic fibrous retroperitonitis is not rare but retroperitoneal arterial obstruction by the fibrous plaque is apparently unusual, and intermittent claudication without urinary symptoms is unique. Idiopathic fibrous retroperitonitis, therefore, should be included in the differential diagnosis of the causes of intermittent claudication. Although the aortogram may not permit differentiation of arteriosclerosis obliterans from external compression of the aorta by this fibrosing process, the excretory urogram should be helpful in making or excluding the diagnosis. Treatment is primarily surgical with thorough excision of the fibrous mass and with ureteral transplantation; vascular resection or bypass grafting is not necessary. Advisability of postoperative roentgen and adrenal corticoid therapy is not clearly established.