Aortic valve and left ventricular outflow tract replacement using allograft and autograft valves: a preliminary report.

A comparison of allograft and autograft (pulmonary) replacement of the aortic valve has, to our knowledge, not been done in America. Fifty-seven patients (age range, 2 to 70 years; mean age, 30 years) underwent 59 operations for replacement of the aortic valve (20) or entire left ventricular outflow tract (39) using autograft (35) or allograft (24) valves. Many had undergone a previous operation (25) or had concomitant procedures (13). Postoperative mortality was 8.5% (5/59). Two deaths occurred in the allograft group and three in the more complex pulmonary autograft group. One late death occurred. One autograft was replaced with an allograft 7 months postoperatively for severe aortic regurgitation. There have been no episodes of either endocarditis or thromboembolism. Forty-nine of 51 survivors are in New York Heart Association class I. Preliminary results suggest that congenital or acquired disease of the left ventricular outflow tract and aortic valve can be safely and effectively treated with either allograft or autograft valve transplantation.

Pulmonary vascular responses to hypercalcemia and hypocalcemia in the dog.

The pulmonary artery responses in the isolated whole-blood perfused canine lung to ionized calcium ([Ca++]) were quantified over a range of hypercalcemia and hypocalcemia values ([Ca++] = 0.23-1.88 mM) under conditions of controlled pulmonary blood flow and constant mean aortic and left atrial pressures. Calcium chloride, administered as bolus doses in the clinical range (5-15 mg.kg-1) at initial normocalcemia and without interventions producing vasoconstriction did not influence mean pulmonary artery pressure at constant pulmonary blood flow. Stable hypercalcemia ([Ca++] = 1.88 +/- 0.05 mM) did not influence the slope of the pulmonary artery pressure-flow plot. Because normal pulmonary vasomotor tone is low and cannot readily be lowered further, the possible vasodilator action of hypocalcemia was assessed by its ability to decrease the slope of the mean pulmonary artery pressure-flow plot, which had been first increased by alveolar hypoxia (AHX) or infusion of the prostaglandin endoperoxide analog U46619 (PG). During AHX (n = 5), a graded reduction from normocalcemia ([Ca++] = 1.08 +/- 0.02 mM) to moderate hypocalcemia ([Ca++] = 0.8 and 0.5 mM) did not alter the pulmonary artery pressure-flow plot, but severe hypocalcemia ([Ca++] = 0.26 +/- 0.01 mM) decreased the slope by 13 +/- 0.9 mmHg.l-1.min-1. The comparison of severe hypocalcemia ([Ca++] = 0.23-0.27 mM) versus a high dose of nifedipine (bolus of 10 micrograms/kg followed by continuous infusion at 40 micrograms.kg-1.h-1) on pulmonary vascular tone increased by either AHX or PG infusion indicated that both hypocalcemia and nifedipine decreased the slope of the relationship between mean pulmonary artery pressure and flow (during AHX: -16.1 +/- 1.38 and -23.3 +/- 1.73 mmHg.l-1.min-1, both P = 0.0001 vs. AHX alone, and during PG: -17.05 +/- 1.95 and -8.4 +/- 1.78 mmHg.l-1.min-1, P = 0.0001 vs. PG alone). Two principal conclusions emerge. First, the pulmonary vessels are minimally sensitive to changes in ionized calcium throughout the clinical hypercalcemia and hypocalcemia ranges; extreme hypocalcemia is required to produce vasodilation, which was reversed with calcium infusion. Second, whereas the pulmonary vasodilator effects of extreme hypocalcemia were independent of the intervention inducing pulmonary vasoconstriction (AHX vs. PG), those of nifedipine were much more pronounced with AHX.

Myocardial temperature mapping in patients with left main coronary artery disease.

Two consecutive groups of high risk patients with left main coronary disease (greater than 50% stenosis) undergoing aortocoronary bypass grafting using different cardioplegia delivery methods were compared retrospectively for perioperative myocardial infarction (MI) and mortality. Group I (July 1979 to June 30, 1982, n = 53) received an initial 1000 ml aortic root cardioplegia infusion from a pressure regulated (85-100 mmHg) delivery system. Regional mid-myocardial wall temperatures determined the distal anastomoses sequence (with the warmest region bypassed first) followed by additional 400 ml cardioplegia infusions. Group II patients (March 1976 to June 30, 1979, n = 47) had their cardioplegia administered by a hand-held syringe without regional temperature mapping. The volume injected varied and was based on cessation of electrical activity or a septal temperature less than 20 degrees C. Background data were similar except that Group I was significantly older than Group II (63.4 +/- 1.4 years vs 57.1 +/- 1.5 years, p less than 0.01). Despite this, there was only 1 (2%) perioperative MI in Group I vs 6 (13%) in Group II (p less than 0.05). There was also a marked reduction in cardiac mortality with 1 (2%) cardiac death in Group I vs 5 (11%) in Group II (p = 0.09). These data suggest that the delivery of adequate volumes of cardioplegia, in conjunction with myocardial temperature directed bypass grafting, can improve myocardial preservation in high risk patients.

Improved myocardial preservation with oxygenated cardioplegic solutions as reflected by on-line monitoring of intramyocardial pH during arrest.

To examine the relationship between intramyocardial pH during global ischemic arrest and subsequent functional and biochemical recovery, 40 canine hearts were subjected to 4 hours of arrest at 10 degrees C. Four groups, each containing 10 hearts, were differentiated by the oxygen concentration of a hyperkalemic crystalloid cardioplegic solution (CCS), which was infused every 20 minutes. In group 1 the CCS was equilibrated at 4 degrees C with nitrogen to remove oxygen. In group 2 the CCS was aerated at 4 degrees C. In group 3 the CCS was treated to achieve an oxygen tension (PO2) similar to group 2 but with a reduced nitrogen content to prevent bubble formation, which is theoretically possible during reperfusion ("myocardial bends"). In group 4 the CCS was fully oxygenated at 4 degrees C. The resulting PO2 of CCS measured at 10 degrees C was less than 20, 170, 170, and 750 mm Hg in groups 1, 2, 3, and 4, respectively. Left ventricular function (LVF) was assessed from function curves at constant mean aortic pressure and heart rate. Functional recovery, expressed as a percentage of prearrest LVF, was 38.1% +/- 10.7% in group 1 and 84.0% +/- 8.1% in group 4 (p less than 0.008). Functional recovery was 64.9% +/- 5.5% and 69.1% +/- 7.0% in groups 2 and 3, which had similar PO2. Differences in recovery between groups 2 and 3 and group 1 approached statistical significance (p less than 0.05, NS). The mean-integrated intramyocardial pH during arrest was higher (p less than 0.003) in group 4 (7.14 +/- 0.05) than in group 1 (6.84 +/- 0.06) or group 2 (6.86 +/- 0.07). The minimum intramyocardial pH during arrest was higher in group 4 than in any other group (p less than 0.002). Myocardial adenosine triphosphate concentration at the end of arrest, expressed as a percentage of its prearrest value, was highest in group 4 (75.9% +/- 8.1%) and lowest in group 1 (54.3% +/- 5.7%), a difference approaching statistical significance (p less than 0.05, NS). These data suggest that the measurement of intramyocardial pH is a useful on-line indicator of the adequacy of preservation during hypothermic arrest and that excess nitrogen in aerated CCS had little or no effect on recovery. The data confirm the hypothesis that oxygenation of CCS is associated with good myocardial preservation, which may be attributed to the provision of oxygen for the support of aerobic metabolism during arrest.

Myocardial recovery after hypothermic arrest: a comparison of oxygenated crystalloid to blood cardioplegia. The role of calcium.

We compared multidose crystalloid hyperkalemic cardioplegic solutions with and without added red cells in 24 canine hearts subjected to 5 hr of arrest at 10 degrees C. All cardioplegic solutions were fully oxygenated at 4 degrees C before delivery. Since blood cardioplegia contained Ca++ carried over with the red cells, Ca++ was added to the crystalloid solution in one group. The table below shows the hematocrit (HCT) and ionized Ca++ concentrations of the cardioplegic solutions, and coronary arteriovenous oxygen difference during infusion of cardioplegic solution (AVO2) (ml O2/100 ml). Recovery during reperfusion is shown as percent of prearrest left ventricular function (LVF) and prearrest myocardial ATP concentration.

Preoperative coronary artery bypass grafting in patients undergoing abdominal aortic reconstruction.

The effect of preoperative aortocoronary bypass grafting on the operative mortality of patients undergoing elective abdominal aortic reconstruction was examined by reviewing a series of 224 consecutive patients (1980 to 1983) (Group I) in whom selective preoperative noninvasive and invasive cardiac screening was used to identify patients with significant coronary stenoses. One patient died during cardiac catheterization. Twenty-seven patients (12 percent) underwent aortocoronary bypass grafting with one operative death (3.7 percent) and one nonfatal myocardial infarction (3.7 percent). These 26 patients subsequently underwent abdominal aortic reconstruction with no mortality and no postoperative myocardial infarction. One hundred ninety-six patients (88 percent) underwent aortic reconstruction without prior aortocoronary bypass grafting with four operative deaths (2 percent), including two fatal myocardial infarctions. The combined operative mortality for Group I patients was 2.3 percent. Three hundred twenty-six patients (Group II) who underwent abdominal aortic reconstruction at this institution from 1970 to 1976 had an 8 percent operative mortality, of which 50 percent of the deaths were due to myocardial infarctions (Group I versus Group II, p less than 0.01). Selective preoperative screening for coronary artery disease in patients undergoing elective abdominal aortic reconstruction with aortocoronary bypass grafting in selected patients is safe and may help reduce the operative mortality.