Coronary bypass graft fate: long-term angiographic study.

In 222 patients, 741 venous coronary bypass grafts were studied angiographically early, at 1 year and at a late examination at greater than 6.5 years (mean 9.6) after operation; 565 of these grafts were also examined 5 years postoperatively. Grafts were graded for patency and disease considered to be atherosclerotic and for both extent and profile of lesions. Graft occlusion rates increased steadily from 8% early to 20% at 5, 41% at 10 and 45% at greater than 11.5 years after operation. All grafts were considered free of atherosclerosis early, but disease appeared in 8% at 1 year, increasing to 38% at 5 and 75% at 10 years postoperatively. Increasing involvement of vessel wall area was associated with greater protrusion of lesions into the graft lumen. Diseased grafts became more so at subsequent examinations, with occlusion occurring in many. However, absence of disease had little prognostic significance because diseased and abruptly occluded grafts were generated in those with healthy appearance at earlier examinations. For instance, 82% of very diseased grafts at the 5 year study originated from normal grafts at 1 year and 73% of occluded grafts at 1 year had appeared normal early postoperatively. Of 590 patent grafts free of disease at 1 year, 30% were occluded at the late examination, 76% of those patent were diseased, 55% of these were diffusely diseased and 35% were greater than 50% narrowed. Only 17% of the original 590 patent grafts were healthy at this time. Bypass graft atherosclerosis severely limits the long-term utility of these grafts. It is suggested that the solution may lie in some powerful drug regimen.

Coronary artery disease and coronary bypass grafting in young men: experience with 138 subjects 39 years of age and younger.

One hundred thirty-eight men aged less than or equal to 39 years had coronary bypass grafting during a 13 year period. Angina was the presenting symptom in 77% and of these patients, one-third had unstable angina. More than half of the patients had experienced at least one myocardial infarct. There was a high incidence of coronary risk factors, especially smoking. Nineteen patients (13.8%) had left main coronary artery stenosis (it was isolated in two); 13.8, 24.6 and 60.2% had single, double and triple vessel disease, respectively. Left ventriculograms showed serious functional impairment in 42%. A total of 461 coronary bypass grafts, 3.34 per patient, were placed; almost all were vein grafts. There were no operative deaths. Transmural myocardial infarction occurred in 4.3% of patients. All bypass grafts were opacified angiographically early after operation, 95% at 1 year, 56% at 5 years and 26% at 10 years after operation. Some patients also had coronary angiograms, dictated by clinical events, between 1 and 5 and between 5 and 10 years postoperatively. Patency rates for bypass grafts were comparable with those previously reported and were acceptable, although they decreased with time. However, increasing evidence of atherosclerosis of bypass grafts was seen beyond 1 year, particularly beyond 5 years. Of 23 subjects with a coronary bypass reoperation, 2 died and 44% had perioperative transmural myocardial infarction. During follow-up, 13.8% of the patients died, survival being 95, 84 and 76% at 5, 10 and 12 years, respectively. It is considered that the patients were advantageously treated with coronary bypass grafting especially in the short-term. However, bypass graft patency steadily decreased with the passage of time and graft atherosclerosis became an increasingly important problem.

Coronary bypass graft fate and patient outcome: angiographic follow-up of 5,065 grafts related to survival and reoperation in 1,388 patients during 25 years.

OBJECTIVES: We sought to examine, angiographically, the longterm fate of a large number of mainly venous coronary bypass grafts and to correlate graft patency and disease with patient survival and reoperation. BACKGROUND: Much is known about bypass graft patency and disease, but the precise relation between graft fate and patient outcome has not been substantiated and documented. METHODS: A total of 1,388 patients underwent a first coronary artery bypass graft procedure at a mean age of 48.9 years, 234 had a second bypass procedure at a mean age of 53.3 years, and 15 had a third bypass procedure at a mean age of 58.2 years during the 25-year period from 1969 to 1994. Most were male military personnel or veterans; 12% were < or = 39 years old. Of 5,284 grafts placed, 91% were venous and 9% arterial. Angiograms were performed on 5,065 (98% of surviving) grafts early, on 3,993 grafts at 1 year and on 1,978 grafts at 5 years after operation; other examinations were also performed up to 22.5 years after operation, and 353 grafts were examined after > or = 15 years. Grafts were graded for patency and disease. The status of all patients was known at the study's end. RESULTS: The perioperative mortality rate was 1.4% for an isolated first coronary bypass procedure, 6.6% for reoperation. Vein graft patency was 88% early, 81% at 1 year, 75% at 5 years and 50% at > or = 15 years; when suboptimal grafts, graded B, were excluded from calculation, the proportion of excellent grafts, graded A, decreased to 40% after > or = 12.5 years. After the early study, the vein graft occlusion rate was 2.1%/year. Internal mammary artery graft patency was significantly better but decreased with time. Vein graft disease appeared by 1 year and the rate accelerated by > or = 2.5 years, involving 48% of grafts at 5 years and 81% at > or = 15 years; 44% of the latter grafts were narrowed > 50%. Survival of all patients was 93.6% at 5 years. 81.1% at 10 years, 62.1% at 15 years, 46.7% (150 patients) at 20 years and 38.4% (25 patients) at 23 years after operation. Survival decreased as age increased, but curves approximated "normal" life expectancy for older patients. Survival curves at all ages showed a steeper decline after 7 years. The rate of reoperation increased between 5 years and 10 to 14 years, then decreased to stable levels. Coronary atheroembolism from vein grafts was the major cause of morbidity and mortality associated with reoperation. Vein graft patency and disease were temporally and closely related to reoperation and survival. CONCLUSIONS: Coronary bypass graft disease and occlusion are common after coronary artery bypass grafting and increase with time. They are major determinants of clinical prognosis, specifically measured by reoperation rate and survival. Intraoperative graft atheroembolism was a major reoperation hazard. Reoperation is definitely worthwhile but entails identifiable risks that must be dealt with.

Endoglin is overexpressed after arterial injury and is required for transforming growth factor-beta-induced inhibition of smooth muscle cell migration.

Endoglin is a homodimeric membrane glycoprotein primarily expressed on endothelial cells. In association with transforming growth factor (TGF)-ss receptors I and II, it can bind TGF-beta1 and -beta3 and form a functional receptor complex. There is increasing evidence that endoglin can modulate the cellular response to TGF-beta, a factor implicated in vascular lesion formation in human and experimental models. The purpose of this study was to analyze the expression of endoglin in normal and balloon-injured porcine coronary arteries and in normal and atherosclerotic human coronary arteries and to determine its ability to mediate the effects of TGF-beta on the migration of vascular smooth muscle cells (SMCs). In normal porcine coronary arteries, endoglin was of low abundance and was found primarily on endothelial cells and adventitial fibroblasts, as well as on a minority of medial SMCs. On days 3, 7, and 14 after angioplasty, endoglin was present not only on endothelial cells but also on adventitial myofibroblasts and medial SMCs of porcine coronary arteries. By day 28, few or no cells expressed endoglin. In situ hybridization revealed that endoglin mRNA expression appeared to be highest in endothelial cells on days 3, 7, and 14 days after injury and absent thereafter. With a second balloon injury, a similar pattern of endoglin protein and mRNA expression was observed. In human vascular tissue, endoglin immunolabeling was higher in endarterectomy specimens removed from diseased coronary arteries than in normal internal mammary arteries. In vitro, antisense oligonucleotides to endoglin decreased its expression and antagonized the TGF-beta-mediated inhibition of human and porcine SMC migration. In summary, upregulation of endoglin occurs during arterial repair and in established atherosclerotic plaques and may be required for modulation of SMC migration by TGF-beta.

Magnesium enhances function of postischaemic human myocardial tissue.

OBJECTIVES: The effect of Mg2+ on the developed force and concentrations of high energy phosphate metabolites in isolated human atrial trabeculae has been investigated. METHODS: Human atrial trabeculae, obtained from right atrial appendages of patients undergoing cardiac surgery requiring cardiopulmonary bypass, were dissected at room temperature in modified Krebs-Henseleit buffer containing 1.2 or 16 mM Mg2+, mounted on muscle stands, and rewarmed to 34 degrees C in the same buffer. After 30 minutes, their mechanical function was assessed. At the end of the protocol, trabeculae were fast frozen for measurement of concentrations of metabolites of high energy phosphates. RESULTS: Trabeculae collected and rewarmed in 16 mM Mg2+ Krebs-Henseleit buffer showed significantly higher mean developed force (0.59(SEM 0.10) g, p < 0.01) than those rewarmed in 1.2 mM Mg2+ Krebs-Henseleit buffer (0.32(0.03) g). Trabeculae that had a developed force > or = 0.8 g, a resting force < or = 0.7 g, and a cross sectional area < or = 1 mm2 ("functional" trabeculae) were selected for further comparison. New reverse phase high performance liquid chromatography techniques developed for the analysis of small samples (0.5-5 mg dry weight) were used to measure nucleotide, nucleoside, and creatine compounds. Total adenylate (ATP+ADP+AMP) concentrations in trabeculae revived in the presence of 16 mM Mg2+ (15.4(1.1) mumol.g-1 dry weight) were significantly higher (p < 0.01) than in those revived with 1.2 mM Mg2+ (11.8(1.0) mumol.g-1), but lower (p < 0.01) than in trabeculae fast frozen immediately after removal from the patient (22.6(1.0) mumol.g-1). There were no significant differences in NAD and total creatine (phosphocreatine+creatine) concentrations between the three groups. CONCLUSIONS: The presence of high Mg2+ during the rewarming of human atrial trabecular preparations maintains a significantly higher developed force and a significantly higher total adenylate pool than does collection and rewarming with normal concentrations of Mg2+.

Changes in regional blood flow distribution induced by infusions of dopexamine hydrochloride or dobutamine in anesthetized dogs.

Systemic blood flow distribution was determined using radionuclide-labeled microspheres in anesthetized dogs during infusions of dopexamine hydrochloride or dobutamine. Three doses of the drugs were administered intravenously, in the form of 22-minute infusions (3 X 10(-9), 10(-8), 3 X 10(-8) mol/kg/min [1.3 to 12.9 micrograms/kg/min] dopexamine hydrochloride and 10(-8), 3 X 10(-8), 10(-7) mol/kg/min [3.4 to 34.0 micrograms/kg/min] dobutamine). Both drugs induced dose-dependent acceleration of the heart rate. Blood pressure was maintained during infusions of dobutamine, while dopexamine hydrochloride induced arterial hypotension. As a result, the increments in heart rate-blood pressure product were smaller with dopexamine hydrochloride than with dobutamine. Dopexamine hydrochloride induced blood flow increments in the heart, several sections of the gastrointestinal tract, kidney and skeletal muscle. Quantitatively, these changes were different from those induced by dobutamine in only 3 organs. The myocardial blood flow increments during infusions of dopexamine hydrochloride were smaller than those of dobutamine, whereas in the stomach and in skeletal muscle, the flow increments induced by dopexamine hydrochloride were significantly greater than those induced by dobutamine. The findings suggest that dopexamine hydrochloride, by virtue of its agonist activity at beta 2-adrenergic and DA1- and DA2-dopaminergic receptors, is a powerful vasodilator.

The effect of mono(2-ethylhexyl)phthalate on an isolated perfused rat heart-lung preparation.

Di(2-ethylhexyl)phthalate (DEHP), the plasticizer used in the biomedical production of blood storage bags, hemodialysis systems, cardiopulmonary bypass (CPB) circuitry, and intubation tubes, is extracted from the plastic material when it comes into contact with biological fluids and is converted to its principal metabolite, mono(2-ethylhexyl)phthalate (MEHP). We have shown that MEHP causes cardiac and respiratory arrest, as well as hypotension, when infused into anesthetized rats. Using a well-ventilated in vitro rat heart-lung preparation, we investigated the effect of MEHP on pulmonary artery pressure (PAP) and found that MEHP had a hypertensive effect on the pulmonary vasculature ending in constriction and edema. There was a significant increase of 0.58 mm Hg/min in the PAP of isolated rat lungs when perfused with MEHP dissolved in Krebs-Henseleit (K-H) buffer (p = 0.0003). The rat lungs that were perfused with K-H buffer only increased 0.094 mm Hg/min during the same perfusion time of 20 min. The water gained during this time was 0.22 g/min with MEHP in the buffer compared to 0.04 g/min with buffer alone. The pO2 in the effluent did not decrease during the perfusion time. The concentration of MEHP in the rat lungs after perfusion varied from 20 to 40 micrograms/g. Although the mechanism of action of MEHP on PAP is too complex to be fully elucidated by this model, the increase in PAP which we have demonstrated is significant and adds yet another toxic effect of this major metabolite of the ubiquitous plasticizer, DEHP.

Patterns of failure in Ionescu-Shiley bovine pericardial bioprosthetic valves.

The experience of the University of Ottawa Heart Institute with valvular replacement by Ionescu-Shiley bovine pericardial bioprostheses has been recently reviewed. The focus of the present study is to examine the patterns of valve failure in a subgroup of these prostheses, those that required explanation for valve failure caused specifically by cusp wear and tears. A total of 22 aortic and six mitral standard-profile valves failed in this way. Twenty-five of these valves were reassessed and are the subject of this paper. Twenty-eight holes and 56 cusp tears occurred in these valves in locations which, along with coexistent pathologic findings, suggested that the cusp commissural suture/alignment stitch was the point of their origin. The importance of this observation and postulation about the genesis of these cases of valve failure lies in the potential for improvement of this valve's performance by modifications of its manufacture.

Perioperative myocardial infarction caused by atheroembolism.

We have demonstrated a phenomenon occurring during coronary artery bypass grafting (CABG) which has not been previously described. Thirteen instances of fatal perioperative myocardial infarction following CABG were associated with intraoperative atheromatous embolization in the coronary microcirculation. In five cases the emboli originated from ulcerative atherosclerotic lesions in the aortic root at the site of the vein graft ostia; in two cases they likely emanated from coronary endarterectomy sites; and in two cases from mechanical disruption of plaques in the major epicardial coronary arteries during the operation. These nine cases occurred during initial revascularization procedures. We have performed 4,095 initial CABG procedures, and the nine cases represent a risk of 0.22%. A further four cases occurred during repeat CABG procedures and resulted from manipulative disruption of atheroma in old vein grafts. Our total number of repeat CABGs is 175, and the risk at reoperation is 2.29%; this represents a tenfold increase in risk for this complication at reoperation. Inadequate histologic sampling of the myocardium at autopsy will necessarily result in underestimation of the incidence of this phenomenon. Analysis of angiograms prior to repeat CABG can identify patients at increased risk who have severe graft atherosclerosis as opposed to myointimal hyperplasia. To reduce the incidence of atheroembolism at reoperation, we advocate ligation of the vein graft at the level of the distal anastomosis as early as possible during dissection on reopening the chest.

Rupture of an intra-aortic balloon. A case report.

A case of rupture of an intra-aortic balloon is reported. The rupture, noted 34 hours after insertion of the balloon, was caused by perforation by an atheromatous plaque. The patient exhibited no adverse effects from the episode.

Sequential coronary bypass grafts. Long-term follow-up.

Sequential venous coronary bypass grafts have presented problems, mainly because of commonly reported differences between patency of side-to-side and end-to-side vein-coronary anastomoses. Better to define this, we have studied sequential anastomosis grafts done during a 13 year period. We concentrated specifically on 212 "double" grafts with 100% selective angiographic follow-up early, 90% at 1-year, and 44% at 5 years after operation. Four hundred twenty-four control single grafts were studied similarly. We found that patency rates of side-to-side anastomoses were much better than those of end-to-side anastomoses, whether of sequential or control single grafts. Considering specifically diagonal coronary artery-anterior descending coronary artery sequential grafts, the combined patency of all sequential anastomoses theoretically exceeds that of a comparable number of single grafts at all times of study, but the differences are small. Furthermore, there is definite danger of preserving proximal and perhaps limited bypass runoff at the cost of losing distal and perhaps more important myocardial perfusion. On balance, we believe that single vein grafts are to be preferred over sequential grafts unless shortage of conduit material or local aortic wall conditions dictate otherwise.

Valve failure caused by cusp tears in low-profile Ionescu-Shiley bovine pericardial bioprosthetic valves.

The pathologic findings in two low-profile Ionescu-Shiley bioprostheses that failed because of cusp tears are presented. Both valves were in the mitral position, one in place 28 months and the other 40 months. Observation of the valves and their tears suggests that stress at the cusp alignment stitches may be important in the genesis of the tears.

A study of the sequential morphologic changes after manual coronary endarterectomy.

Manual coronary endarterectomies heal in the long-term by a poorly understood process of myofibrointimal proliferation. A retrospective analysis of detailed cardiovascular pathologic examinations of 51 patients dying at varying intervals after endarterectomy provides insight into the sequence of this proliferative response. Twenty-one patients died within 7 days, 6 at 8 to 30 days, 3 at 31 days to 6 months, 4 at 6 months to 5 years, and 17 at more than 5 years after endarterectomy. The observations made suggest that the denuded arterial surface heals after the fibrin-platelet mural thrombus that covers it is organized and is replaced by fibrosis and myofibroblast proliferation. In unusual cases proliferation is exuberant, resulting in significant restenosis, an outcome in which recurrent atherosclerosis contributes to only a minor degree. This is the first series in which the sequential reparative changes at varying times after manual coronary endarterectomy have been studied.

Aorta-coronary bypass in patients with coronary artery disease who do not have angina.

During an 8 year period we performed coronary bypass operations in 118 consecutive patients who were not experiencing angina when selected for surgical treatment. Their mean age was 45 years, collectively they had had 87 myocardial infarcts, and 42% had at least moderately abnormal ventriculograms. Considering 50% coronary stenosis "significant," 9% had single-, 23% double-, and 68% triple-vessel disease; 15% had left main coronary artery disease also. Operations, which involved placing a mean of 3.6 grafts per patient, included 39 endarterectomies and 11 ventricular aneurysm repairs. There were no operative deaths, but eight (6.8%) died during a mean 6.7 year follow-up. A retrospective comparison was made between these 118 patients and a consecutive series of 605 others, mean age 46 years, having angina and also treated surgically during the same period. Five (0.83%) of these latter patients died perioperatively and 42 (6.9%) during a mean follow-up of 6.4 years. The no-angina patients had significantly more prior myocardial infarcts and more abnormal ventriculograms; the angina group had a significantly higher reoperation rate. However, there were no significant differences between the two groups in age, coronary disease severity, results of treadmill testing, number of grafted vessels, endarterectomies, ventricular aneurysm repairs, perioperative infarcts, operative or late mortality, or early, 1 year, and 5 year graft patency rates. We have concluded that, with the exception of cardiac ischemia warning, our patients without angina, treated surgically, were similar in most important respects to patients in a concurrent series in which angina was one of the indications for operation. We believe that coronary bypass is safe for such individuals without angina and probably as as effective as for those with cardiac pain.

A comparison of intracellular solutions for donor heart preservation.

Numerous solutions have been advocated for the preservation of donor hearts, and there has been much interest in universal and intracellular preservation solutions. This study compared the effects of Euro-Collins, University of Wisconsin, and Bretschneider's solutions with the use of an in vitro human right atrial muscle preparation to assess recovery of function after a 24-hour period of simulated cardiac arrest. There were no statistically significant differences among groups in length, weight, cross-sectional area, initial developed force, or resting force of muscles, including those muscles that were contracted in Krebs-Henseleit solution and served as a control. After the 24-hour arrest period at either 4 degrees or 12 degrees C, the solution was changed back to Krebs-henseleit at 34 degrees C and recovery was assessed over 30 minutes. At 30 minutes, developed forces for muscles that were cooled to 4 degree C were 58.9%, 76.6%, and 60.7% of the control for Euro-Collins, University of Wisconsin, and Bretschneider's solutions, respectively (p = not significant). For those cooled to 12 degrees C, developed forces were 9.5%, 30.5%, and 95.6% of the control for Euro-Collins, University of Wisconsin, and Bretschneider's solutions (p = 0.0001). Bretscheider's solution resulted in greatly improved recovery compared with both Euro-Collins and University of Wisconsin solutions (p = 0.005), and University of Wisconsin solution was better than Euro-Collins solution (p = 0.02). Recovery of developed force was affected by temperature for Euro-Collins and University of Wisconsin solutions (p = 0.005 and p = 0.001, respectively) but not for Bretschneider's solution. Resting force was elevated in muscles that were cooled in both Euro-Collins and University of Wisconsin solutions at 12 degrees C compared with almost normal values for Bretschneider's solution at either temperature (p = 0.07). Bretschneider's solution has a very high buffering capacity, which may be beneficial for long-term preservation. In conclusion, Bretschneider's solution resulted in the best recovery of human atrial myocardial function after a 24-hour preservation period compared with Euro-Collins and University of Wisconsin solutions and should be considered for use in donor heart transportation. The variability in quality of preservation at different temperatures with either Euro-Collins or University of Wisconsin solution make them less desirable as preservation solutions because uniform temperatures are seldom obtained during donor heart transplantation.

Retrograde dissection of the left main coronary artery after endarterectomy: a rare complication.

The case of a 72-year-old woman who died after bypass grafting and endarterectomy of the left anterior descending coronary artery is described. At autopsy a large intramural dissection of the left anterior descending artery that extended proximally to the left main ostium from the endarterectomy site was found. The dissection was associated with clotting of the false lumen and of the graft, and with a myocardial infarct that precipitated this woman's intraoperative death.

Perioperative exposure to plasticizers in patients undergoing cardiopulmonary bypass.

Di(2-ethylhexyl)phthalate and its principal metabolite, mono(2-ethylhexyl)phthalate, are contaminants of blood that are extracted on contact with polyvinylchloride surfaces, such as blood collection bags and tubing used in cardiopulmonary bypass. In this study, levels of the two plasticizers were measured in patients who underwent coronary artery bypass grafting, orthotopic transplantation, implantation of the Jarvik 7-70 total artificial heart during bridge-to-transplant procedures, and in infants who underwent corrective operations for congenital defects. In all adult patients the levels of di(2-ethylhexyl)phthalate increased tenfold by the end of cardiopulmonary bypass, whereas the levels of mono(2-ethylhexyl)phthalate increased ninefold. In infants, levels of di(2-ethylhexyl)phthalate rose seven times by the end of bypass and mono(2-ethylhexyl)phthalate rose significantly as well. In most of the patients having coronary bypass, the two plasticizers declined to preoperative levels within 24 hours. However, in some of the patients having orthotopic transplantation and in those in whom the Jarvik 7-70 total artificial heart was used as a bridge to transplant, the levels were still detectable 120 hours postoperatively. Circulating levels of mono(2-ethylhexyl)phthalate are only 20- to 35-fold lower in patients undergoing cardiac operations than the level of mono(2-ethylhexyl)phthalate causing a 50% reduction in developed contractile force and arrhythmias in an in vitro human atrial trabecular preparation. This study shows that patients with multisystem failure and infants may be at risk for this acute exposure to mono(2-ethylhexyl)phthalate.

Comparative results with the St. Jude Medical and Medtronic Hall mechanical valves.

This study compared the clinical performance of the St. Jude Medical and Medtronic Hall mechanical valves in isolated aortic or mitral valve replacement. From 1984 to 1993, 349 St. Jude Medical valves (aortic 237, mitral 112) and 465 Medtronic Hall valves (aortic 272, mitral 193) were implanted in 814 patients at the University of Ottawa Heart Institute. The patients had similar preoperative characteristics. The hospital mortality rate for aortic valve replacement was 3.4% with the St. Jude Medical valve and 5.8% with the Medtronic Hall valve (p = 0.26) and the rate for mitral valve replacement was 8.9% with the St. Jude Medical valve and 11.9% with the Medtronic Hall valve (p = 0.54). Actuarial estimates of survival and freedom from complications were calculated. At 5 years the actuarial probability of survival (including hospital deaths) for aortic valve replacement was 86% +/- 3% with the St. Jude Medical valve and 68% +/- 4% with the Medtronic Hall valve (p = 0.0001) and for mitral valve replacement was 75% +/- 7% with the St. Jude Medical valve and 70% +/- 4% with the Medtronic Hall valve (p = 0.54). The most common cause of late death was cardiac failure and no deaths were caused by structural failure. The 5-year probability of freedom from bleeding after aortic valve replacement was 99% +/- 1% with the St. Jude Medical valve and 95% +/- 2% with the Medtronic Hall valve (p = 0.06) and after mitral valve replacement 99% +/- 1% with the St. Jude Medical valve and 97% +/- 2% with the Medtronic Hall valve (p = 0.37). The 5-year probability of freedom from thromboembolism after aortic valve replacement was 88% +/- 4% with the St. Jude Medical valve and 81% +/- 3% with the Medtronic Hall valve (p = 0.08) and after mitral valve replacement was 85% +/- 7% with the St. Jude Medical valve and 77% +/- 5% with the Medtronic Hall valve (p = 0.17). Reoperation was uncommon and there were no cases of structural valve failure. The 5-year actuarial estimate of freedom from reoperation therefore for aortic valve replacement was 99% +/- 1% with the St. Jude Medical valve and 96% +/- 2% with the Medtronic Hall valve (p = 0.09) and for mitral valve replacement was 98% +/- 2% with the St. Jude Medical valve and 95% +/- 3% with the Medtronic Hall valve (p = 0.40).(ABSTRACT TRUNCATED AT 400 WORDS)

Coronary bypass graft fate. Angiographic study of 1,179 vein grafts early, one year, and five years after operation.

A total of 1,179 vein grafts were studied angiographically in 353 (45%) unselected survivors (male, mean age 45.5 years) of 786 coronary bypass operations. Studies were conducted early (0.96 months), 1 year (12.8 months), and 5 years (59.7 months) postoperatively. A previously described technique was used to grade the patency of the grafts, and a new technique was used to assess intimal irregularity, presumably caused by atherosclerosis; this new technique indicated both intimal surface distribution of disease and profile (relief or elevation). Ten percent, 17%, and 26% of grafts were occluded early, at 1 year, and at 5 years, respectively. Distal anastomotic defects were the commonest cause for low grades in the patency classification. Irregularities in patent grafts increased from 9% at 1 year to 42% at 5 years, with 11% of all the 1 year lesions and 20% of all the 5 year lesions having a high profile (more than 50% graft stenosis); of the lesions categorized as showing the widest surface spread, 17% were in high relief at 1 year and 34% at 5 years. Thus, the lesions we believed to be atherosclerotic proliferated in both surface spread and elevation. All severely diseased grafts at the 1 year study had been normal in outline early; 79% at the 5 year study had been disease free at 1 year. All newly occluded grafts at the 1 year study had been normal in outline and 82% had had good patency early; 78% of newly occluded grafts at the 5 year study had been disease free at 1 year and 77% had had good patency. Normal appearance of the intima in grafts studied at 1 year had no prognostic value for 5 year findings. However, 62% of all grafts with the appearance of intimal disease at 1 year showed deterioration by 5 years, and 28% were occluded. The differences between these outcomes are highly significant (p less than 0.0005). In conclusion, the appearance of intimal irregularity compatible with atherosclerosis in a coronary bypass graft 1 year after operation carried a poor prognosis for adverse angiographic change at 5 years. On the other hand, normally appearing intima at 1 year had no predictive valve for the 5 year study despite a generally better prognosis for nondiseased grafts.

Are temperatures attained by donor hearts during transport too cold?

Excessive myocardial cooling may have detrimental effects on donor heart integrity. This study assessed the standard technique for donor myocardial preservation using hearts from seven mongrel dogs (mean weight 192.7 gm), which were arrested, excised, and placed in a cooler containing saline and ice. Temperature probes placed in both the left and right ventricular free walls and the septum revealed that, after cardioplegia, temperatures fell to 10.3 degrees, 7.5 degrees, and 7.6 degrees C, respectively. Temperature decreased to below 1 degree C after 75, 75, and 60 minutes for the left ventricle, right ventricle, and septum, respectively, independent of the size of the heart (range = 104 to 322 gm). After 4 hours of cooling, temperature was below 0 degrees C throughout the myocardium. Examination with an electron microscope showed similar serial changes over 4 hours in all hearts, including moderate-to-severe cytoplasmic and nuclear swelling and mitochondrial calcium deposits. Cell membranes remained intact, which suggests that the damage was not irreversible. We conclude that current donor heart preservation techniques may result in unacceptably low myocardial temperatures that cause reversible myocardial injury.