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Continuous positive airway pressure (CPAP) was used to support the ventilation of infants less than 3 months of age who had undergone thoractomy for cardiovascular surgery. The functional residual capacity, which was approximately 30 per cent of predicted at zero CPAP, increased 35 per cent in cyanotic and 33 per cent in acyanotic infants with the application of 5 mm Hg pressure. Increasing airway pressure from zero to 5 mm Hg increased PaO2 4 per cent in cyanotic and 13 per cent in acyanotic infants. There was no change in heart rate, respiratory rate, mean arterial pressure, pH or PaC02 under similar circumstances, but central venous pressure increased 1.5 mm Hg in cyanotic and 0.8 mm Hg in acyanotic infants.

A review of articles published since 1979 indicates that thrombotic and bleeding complications account for about 50% of valve-related complications in patients with bioprosthetic aortic and mitral valves and for approximately 75% of the complications in patients with mechanical valves. Although compromised by lack of standard definitions and by variability in reporting and follow-up, the data suggest that the linearized rate of both thrombotic and bleeding complications in patients with aortic bioprostheses is approximately half that for aortic mechanical prostheses (2% versus 4%), but is approximately equal for both bioprostheses and mechanical valves in the mitral position (approximately 4%), and for mechanical and bioprosthetic aortic and mitral valves in combination. However, linearized rates for fatal thrombotic and bleeding events are two to four times higher in patients with mechanical prostheses. The adequacy of warfarin anticoagulation is the most important factor affecting thrombotic and bleeding complications in patients with mechanical valves and over shadows the dubious importance of other phenomena such as atrial fibrillation and left atrial thrombus. Short-term warfarin anticoagulation or the use of long-term platelet inhibitors, or both, do not appear to reduce the incidence of thrombotic complications in patients with aortic bioprostheses but increase bleeding. For mitral bioprostheses, the postoperative use of warfarin for three months or aspirin indefinitely is as effective in preventing thromboembolism as long-term warfarin. Acute prosthetic valve endocarditis is associated with a 13 to 40% incidence of thrombotic complications. Likewise, the recurrence rate of cerebral emboli is high (20-30%) in patients with prosthetic valves who are not anticoagulated. Bioprostheses are strongly preferred for women who wish to bear children; fetal wastage occurs in 25 to 30% of pregnant women with mechanical heart valves who receive either warfarin or heparin, or a combination of the two. Heparin, however, greatly increases the risk of maternal bleeding. In children, the efficacy of platelet inhibitors without warfarin anticoagulation is unproven; nearly all serious strokes occur when warfarin is omitted; and permanent disability from warfarin-related bleeding is rare. All prosthetic cardiac valves initiate coagulation and affect the dynamic equilibrium between activated procoagulants and endogenous anticoagulants. Warfarin is the only available oral exogenous anticoagulant.(ABSTRACT TRUNCATED AT 400 WORDS)

Since January, 1977, 64 patients (3%) out of 2,112 who underwent open cardiac operation had 74 emergency thoracotomies in the surgical intensive care unit 10 minutes to 12 days after operation. In all instances thoracotomy was performed for inadequate circulation. Patients were divided into two groups. In Group 1, 44 patients suddenly and unexpectedly became hypotensive due to an arrhythmia (13 patients), sudden massive bleeding (15), suspected tamponade (6), or unexplained reasons (10). In Group 2 (20 patients), circulatory insufficiency was progressive despite maximum pharmacological and intraaortic balloon support. Circulation was restored after 37 of the 74 thoracotomies (50%), including 8 in Group 2. Nineteen patients (30%) were ultimately discharged; however, no patient in Group 2 survived hospitalization. Of the 19 survivors in Group 1, only 2 of the 13 with a sudden arrhythmia and 3 of the 10 with unexplained hypotension survived. However, 5 of the 6 with tamponade and 9 of the 15 with sudden massive bleeding survived. Overall, 43% of Group 1 patients survived. We conclude that emergency thoracotomy in the surgical intensive care unit after open-heart operation may be lifesaving if performed promptly in patients with sudden, unexpected hypotension. The incidence of wound infection in survivors in 5% whether or not the chest is closed in the operating room.

Forty-four infants, 2 to 90 days of age, with severe obstructive lesions of the aortic arch, underwent emergency surgical correction between Jan. 1, 1966, and April 1, 1975. The typical clinical presentation was severe congestive heart failure and acidemia. Resection of an aortic coarctation with end-to-end anastomosis was performed in 31 patients. Eight (26 per cent) died after the operation. Since 1969, the mortality rate has been reduced to 14 per cent (3 of 22 patients) even though the incidence of major associated cardiac lesions has remained essentially constant (56 per cent from 1966 through 1969, 64 per cent from 1970 through March, 1975). This suggests that the higher survival rate has resulted from improved surgical techniques and postoperative care. The mortality rate in the infants operated upon during the second and third months of life was twice as high as that in those operated upon before the age of 1 month. Eight patients with Type A interrupted aortic arch were operated upon and 5 survived. Five patients with Type B aortic arch were operated upon and 3 survived.

In 10 patients, cardiopulmonary bypass decreased the number of fibrinogen binding sites from 31,730 +/- 12,802 per platelet to 18,590 +/- 9,644 per platelet. Bypass also decreased the amount of the platelet membrane glycoprotein IIIa, which is part of the fibrinogen receptor complex, from 17.1 +/- 3.6 ng/10(9) platelets to 12.9 +/- 4.7. The fibrinogen binding constant did not change. Platelet sensitivity to adenosine diphosphate did not change; however, template bleeding times increased from 5.2 +/- 1.5 minutes before bypass to 8.5 +/- 2.3 minutes after bypass. Analysis of detergent washings from the perfusion circuit after bypass in five patients indicated that platelet material remains attached to the surface as membrane fragments and degranulated platelets. These data further elucidate the mechanism of platelet loss and dysfunction during cardiopulmonary bypass and highlight the importance of platelet membrane fibrinogen receptors and surface adsorbed fibrinogen in this process.

The role of platelet fibrinogen receptors and platelet-protein interaction in platelet consumption during simulated cardiopulmonary bypass was investigated. In five recirculation experiments, with whole blood, the platelet count fell to 13% of initial values and in two experiments, with blood from patients with Bernard-Soulier syndrome, to 3% of normal values. However, in three experiments with blood from the patients with Glanzmann's thrombasthenia, the platelet count decreased to 69% of initial values. The extent of platelet consumption in normal blood was diminished to only 72% by addition of 0.5 microM prostaglandin E1 (PGE1) (5 experiments) and to 80% by precoating surfaces of the circuit with 2.5% human albumin (5 experiments). beta-Thromboglobulin antigen (beta TG) loss from platelets was associated with thrombocytopenia. The extent of beta TG loss was significantly reduced by the addition of PGE1 to blood or precoating surfaces with albumin. Proteins adsorbed on the surface of the circuit exposed to normal blood were removed with 0.5% Triton X-100. Some of these proteins were identified to be glycoprotein IIIa (GPIIIa) (3.4-4.3 micrograms/ml), beta TG (1.0-1.6 micrograms/ml), and fibrinogen (1.9-3.7 micrograms/ml). The amount of GPIIIa recovered in the Triton X-100 eluates correlated with the number of platelets lost during recirculation. These studies indicate that exposure of fibrinogen receptors associated with GPIIb-GPIIIa complex contributes to platelet consumption during cardiopulmonary bypass.

Since January 1980, 92 consecutive patients received St. Jude Medical aortic and mitral prostheses simultaneously. Mean age was 57.6 years (standard deviation 12.4); 14 were 70 years or older. Twenty-three had a previous cardiac operation and 22 had additional procedures performed at the time of double valve replacement. Before the operation 62% of the patients were in New York Heart Association functional class III and 29% were in class IV or required emergency operation. There were six (6.5%) deaths within 30 days. None of the hospital deaths were valve related; all occurred in patients who had additional risk concerns. Follow-up is 100% complete and ranges from 2 to 80 months, totaling 242 patient-years (mean 33.8 months). All except four hospital survivors reached class I or II and 40 patients (47%) remain asymptomatic. The actuarial survival rates are 82% at 1 year, 70% at 3 years, and 60% at 5 years. Causes of late death include heart failure (10), sudden, unexplained death (five), reoperation for coronary artery disease (one), noncardiac (four), and valve related (five). The linearized rate of fatal valve-related events is 2.1% pt-yr. A total of 22 valve-related complications (including five fatal) occurred is 18 patients, for a linearized rate or incidence of 9.1%/pt-yr. Eleven thromboembolic episodes (rate 4.6%/pt-yr) occurred in nine patients; three of these (1.2%/pt-yr) were fatal. Thromboembolic and bleeding complications represented 64% of all valve-related complications. Four patients had six episodes of prosthetic valve endocarditis (incidence 2.5%/pt-yr), of which one (incidence 0.4%/pt-yr) was fatal. Paravalvular leak contributed to the fifth valve-related death. At 5 years, 83% of patients were free of thromboembolic complications; 94% were free of anticoagulant-related hemorrhage; and 71% were free of all valve-related complications. There are few comparable data for patients who have had simultaneous replacement of aortic and mitral valves with other mechanical prostheses. The total incidence of valve-related complications for patients with bioprostheses ranges between 3.9%/pt-yr and 10.4%/pt-yr and is similar to the 9.1%/pt-yr observed in the present series. The type of valve-related complication (thromboemboli and bleeding versus valve deterioration) is the principal difference between St. Jude Medical and bioprosthetic valves in patients who require simultaneous replacement of aortic and mitral valves.

The effect of end-expiratory airway pressure on the accumulation of extravascular lung water during lobar venous occlusion for 2 h was studied in closed-chest artifically ventilated dogs. Dogs were divided into two groups by end-expiratory airway pressures of 0 or 10 cmH2O. High-pressure lobar pulmonary edema was produced by lobar venous occlusion, which elevated microvascular hydrostatic pressure. After occlusion of the lobar pulmonary vein, lobar venous pressure (and microvascular hydrostatic pressure) rapidly became identical to pulmonary arterial pressure. We measured extravascular lung water (post mortem) and pulmonary arterial pressure and calculated plasma colloid osmotic pressure to determine the relationship between the accumulation of lung water and the difference between pulmonary microvascular pressure and plasma colloid osmotic pressure (net intravascular filtration pressure). At comparable net intravascular filtration pressures, dogs ventilated at the higher end-expiratory airway pressure accumulated more extravascular lung water. This study indicates that increasing end-expiratory airway pressure from zero to 10 cmH2O increases the accumulation of extravascular lung water when microvascular hydrostatic pressure is raised.

Long-term clinical and laboratory findings in three children who required mitral valve replacement below age four years are reported. In each instance a second valve replacement was necessary approximately 8 1/2 years after the initial one, following a two and one-half fold increase in body weight. Inadequate mitral valve orifice size was found in each instance, producing a hemodynamic picture equivalent to mitral stenosis: congestive heart failure, pulmonary hypertension and atrial fibrillation. A second valve was placed without mortality in each instance and relieved the mitral valve obstruction. Pulmonary vascular resistance increased postoperatively in two patients and failed to decrease in the third. Pulmonary arterial hypertension and left ventricular hypertrophy persisted as long as 13 to 37 months after the second valve placement in all patients. The consequences of increasing body size and the long-term interposition of a rigid prosthesis in a growing heart introduce additional complications to mitral valve replacement in childhood. Frequent hemodynamic observations and the use of a prosthesis other than the ball-cage variety is recommended for improved management.

In 12 months since March, 1975, 25 of 27 patients with tetralogy of Fallot have had corrective operations without ventriculotomy. Infundibular obstructions were excised and ventricular septal defects were closed through a right artiotomy with retraction of the anterior leaflet of the tricuspid valve. Pulmonary valve stenosis was relieved through a pulmonary arteriotomy. In five patients the pulmonary annulus was patched 0.5 to 1.5 cm. into the right ventricle. Immediately after repair peak right ventricular-pulmonary arterial systolic pressure difference averaged 17 mm. Hg and ranged between zero and 40 mm. Hg. Cardiac indices averaged 2.85 L. per square meter per minute 4 hours after operation. All but two patients developed right bundle branch block. One patient with severe pulmonary hypertension died. Fourteen patients have been recatheterized. Right ventricular-pulmonary peak systolic pressure differences ranged between zero and 45 mm. Hg (mean, 22). Cineangiograms show contraction of the free right ventricular wall during systole. Transatrial repair of tetralogy of Fallot is feasible technically in many patients, avoids muscle necrosis and coronary arterial injury, and improves cardiac output in the immediate postoperative period.

A pedicled diaphragmatic skeletal muscle graft was used to replace a portion of resected right ventricle in 35 dogs. The graft contracted when electrically stimulated directly or via the phrenic nerve before and after insertion. The electrical pacing threshold was lower for phrenic nerve stimulation (0.9 +/- 0.20 mamp) than for direct graft stimulation (2.3 +/- 1.19 mamp). The heart could be captured and paced by stimulating the muscle graft with higher current (16.2 +/- 4.49 mamp). The delay from pacing stimulus to muscle graft contraction when the graft was paced directly was 10 msec. The epicardial activation time delay when the heart was paced through the muscle graft was 27.0 +/- 9.08 msec. When the muscle graft pedicle was transected, the graft lost its ability to contract. The heart, however, could still be captured electrically through the graft for up to 4 hours. Strain gauge studies of the nonstimulated muscle graft showed tension development during pre-ejection ventricular contraction identical to that of the right ventricle. In the ejection phase, muscle graft tension slowly declined. The stimulated muscle graft developed active tension and echographically demonstrated muscle thickening during contraction. This study demonstrates that a vascularized, neurally innervated diaphragmatic muscle graft can be placed into the right ventricle. The graft retains its ability to contract in response to direct or phrenic nerve stimulation. It can be made to contract during any phase of the cardiac cycle. Thus diaphragmatic muscle grafts may provide a method to augment ventricular cavity size with synchronously contracting muscle.

The accumulation of extravascular lung water was related to changes in plasma colloid osmotic pressure and pulmonary hydrostatic pressures in 12 normal dogs and 13 dogs that had venovenous perfusion for 2 hours at 45 to 70 ml. per kilogram per minute. The venovenous perfusion system included a membrane oxygenator and a roller pump. Net intravascular filtration pressure was calculated from plasma colloid osmotic pressure and pulmonary hydrostic pressures. Rapid accumulation of extravascular lung water occurred in control and bypass animals when net intravascular filtration pressure exceeded zero. At lower filtration pressures, venovenous perfusion did not affect accumulation of extravascular lung water.

The electrocardiographic pattern of right bundle branch block (RBBB) is routinely observed after transatrial repair of tetralogy of Fallot even though no ventriculotomy has been performed. The mechanism of this conduction disturbance was studied in 16 patients with tetralogy of Fallot and one patient with infundibular pulmonic stenosis. Preoperative ECGs and vectorcardiograms showed right ventricular hypertrophy and no RBBB. Epicardial activation maps were obtained before and after total surgical repair in all patients and after infundibular resection but before closure of ventricular septal defect (VSD) in four of these patients. After infundibular resection, RBBB appeared and activation was markedly delayed (greater than 30 msec) over the pulmonary outflow tract, but was unchanged over the body of the right ventricle. No further changes in ventricular activation occurred after closure of the VSD. This study shows that RBBB after transatrial repair of tetralogy of Fallot is usually produced by infundibular resection, but not by VSD closure, and is associated with delayed activation of the pulmonary outflow tract and base of the right ventricle which results from damage to portions of the right ventricular conduction system.

A 5-year-old boy with acute lymphoblastic leukemia in complete continuous remission developed life-threatening varicella pneumonia and acute respiratory insufficiency (ARI). The child recovered after 92 hours of partial venoarterial perfusion with a membrane oxygenator. Functional asplenia developed. Serial pulmonary function tests after perfusion indicate moderately severe restrictive lung disease which has slightly improved during an 18 month period.

A cohort of 61 consecutive patients 24 months of age of younger had palliative shunts for symptoms of tetralogy of Fallot during a 12-year period. Thirty-six of these patients have been followed through definitive intracardiac repair or to death. For analysis palliative operations were separated into two six-year periods, 1965--1970. During the first period seven of 30 infants operated on died; all 31 infants operated on during the second period survived. The Waterston anastomosis was performed most frequently (67%) during the first period; the Blalock-Taussig anastomosis was performed in 68% of infants during the second period. Of 54 hospital survivors, three died before definitive intracardiac repair. Two of the three interim deaths were related to heart disease. Twenty-six of the remaining 51 patients have had definitive intracardiac repair with two deaths (8%). Twenty-four in this group had intracardiac repair since 1973 with one hospital death (4%). The cumulative mortality for the entire cohort is 25%, but more recent experience (1971--77) indicates a cumulative mortality near 5%. The recent mortality rate for staged management is less than the 14% rate reported by others for primary intracardiac repair of tetralogy of Fallot in 205 infants. We conclude that primary intracardiac repair has important advantages for infants with tetralogy of Fallot who have favorable anatomic features and no other associated cardiac lesions or medical problems. Staged management of tetralogy of Fallot is still recommended for infants with unfavorable anatomy, additional lesions or associated medical problems.

Since 1973, 11 patients have had emergency valve replacement for severe mitral insufficiency and cardiogenic shock within 1 month (mean 10.0 days) of acute myocardial infarction. Mean age was 60 years (range 44 to 71 years). Nine infarcts affected the inferior wall, one patient had a prior myocardial infarction, and only two patients had a history of cardiac symptoms. Ten patients had pulmonary edema, five were oliguric (less than 0.5 ml/kg/hr for 12 hours), four required endotracheal intubation, nine required preoperative intra-aortic balloon support, and three had had a cardiac arrest. Preoperative cardiac index averaged 1.7 L/m2/min even with pharmacologic and circulatory support. Eight patients had cardiac catheterization and nine had echocardiograms. Left ventricular ejection fraction varied from 23% to 83% (mean 51%) and was not prognostic. Five patients had papillary muscle rupture and six patients had papillary muscle dysfunction. The mitral valve was replaced with a mechanical prosthesis in all patients. Five had simultaneous coronary artery bypass grafts. Three of five patients with papillary muscle rupture and two of six with papillary muscle dysfunction survived hospitalization. Two patients could not be weaned from cardiopulmonary bypass, two patients died within 24 hours of low cardiac output, and two patients died 3 weeks postoperatively of acute tubular necrosis and sepsis following prolonged preoperative cardiogenic shock. The interval from onset of shock to operative therapy averaged 1.7 days for survivors versus 9.3 days for nonsurvivors. Although the amount of viable left ventricular mass cannot be measured preoperatively, we recommend early operation, before other organ systems fail, for patients having severe mitral insufficiency and cardiogenic shock within 30 days of acute myocardial infarction.

A 7 and one-half yr-old girl developed bacteremia from S. marcescens following debanding of the pulmonary artery and closure of multiple ventricular septal defects with a Dacron patch and multiple Teflon pledgets. The site of entry was probably a radial arterial catheter left in place for 8 days. Infection was eradicated by a combination of gentamicin and carbenicillin over a 4-wk period. Of 12 cases of postoperative Serratia bacteremia in adults following valve replacement, only four survived. Antibiotics of proven effectiveness against the specific isolated Serratia strain, prompt therapy sustained for 6 wk offers the prospect for cure of this serious complication of cardiac surgery.

Cardiopulmonary bypass prolongs bleeding time and increases postoperative blood loss. During in vitro recirculation in an extracorporeal circuit containing a membrane oxygenator and primed with fresh heparinized human blood, we previously observed thrombocytopenia, impaired platelet aggregation, and depletion of granular contents, all of which were prevented with prostaglandin E1 (PGE1). To investigate these changes further, we studied the number and affinity of platelet alpha 2-adrenergic receptors by measuring the binding of 3H-yohimbine. Before recirculation, we found 235 +/- 28 alpha 2-adrenergic receptors per platelet, a Kd of 3.37 +/- 0.78 nmol/L, complete aggregation with 1.04 mumol/L epinephrine, and a platelet count of 281,000 +/- 33,000 microliters-1. After 2 minutes of recirculation, 9.44 mumol/L epinephrine was required to produce complete aggregation, and the platelet count was 104,000 +/- 22,000 microliters-1 (44% of control). The number of binding sites significantly decreased to 139 +/- 16 per platelet, but the affinity did not change (Kd = 3.78 +/- 0.44 nmol/L). After 2 hours of recirculation, the platelet count had increased to 123,000 +/- 21,000 microliters-1. However, epinephrine did not induce platelet aggregation even at 100 mumol/L. Moreover, alpha 2-adrenergic binding sites were not detectable, and affinity for yohimbine could not be calculated. Two minutes after PGE1 0.3 mumol/L was added to the circuit, platelet numbers, response to epinephrine, alpha 2-adrenergic binding sites per platelet, and affinity for yohimbine were not significantly different from control values. At 2 hours, the number of alpha 2-adrenergic sites was not significantly changed from control, but the affinity of yohimbine for platelets was significantly decreased 2.5-fold.(ABSTRACT TRUNCATED AT 250 WORDS)

Between 1975 and 1981, late infection of the prosthesis developed in 4 out of 207 patients (1.9%) who had prosthetic grafts placed in the chest or mediastinum. Organisms were Staphylococcus epidermidis (2 patients), Enterococcus, and Aspergillus. Infection occurred 4 to 57 months after initially clean operations for thoracoabdominal aneurysm, aortic angioplasty with valve replacement, ruptured postcoarctation aneurysm, and type A dissecting aortic aneurysm. All 4 patients were managed successfully and remain free from infection 11 to 42 months later. Based on this experience, several guidelines useful in the management of these infections have evolved: (1) prompt reoperation with complete debridement of infected and necrotic tissue, (2) removal of infected prosthetic material if suture lines are involved, (3) local antiseptic irrigation and appropriate, specific systemic antibiotics, (4) rerouting of blood flow through clean operative fields, and (5) use of pedicle flaps.

Eight children were recognized to have Turner's syndrome, among 353 patients over 1 year of age who had undergone surgical treatment for coarctation of the aorta. Of these eight children, three developed a significant perioperative hemorrhage from aortic rupture, resulting in one death and one instance of paraparesis related to a period of prolonged hypotension. In two of the other five patients with Turner's syndrome, a decision was made to perform an angioplasty rather than a resection of the coarctation because of apparent friability of the aortic wall. In contrast, only one of the 345 patients without Turner's syndrome died as a result of surgical treatment, and none developed spontaneous perioperative aortic rupture or neurologic deficit. This experience suggests that the operative risk for coarctation of the aorta in this subgroup of patients is considerably greater than that in patients without Turner's syndrome (p < 0.001). Special precautions should include use of rubber-jaw vascular clamps, choice of technique to avoid tension at the anastomotic suture line, and careful control of systemic blood pressure intraoperatively and postoperatively. Indications for surgical treatment of coarctation as well as the type of operative procedure must be individualized cautiously in patients with Turner's syndrome.

Eighty-one patients with resectable primary peripheral lung carcinomas were studied to determine the effect of associated scarring on prognosis. Twelve tumors (15%) originated from bronchi. 24 (30%) were associated with scars, and 45 (55%) were not associated with either bronchus or scar (non-scar). Scar carcinomas differed significantly in cell type from bronchogenic and non-scar tumors in that 21 (88%) scar carcinomas were either adenocarcinomas or bronchioloalveolar carcinomas (p less than 0.001). Origin (bronchogenic, scar, non-scar) independent of cell type and tumor stage did not significantly influence survival. Stage of disease independent of cell type or origin affected survival (p less than 0.0001), as did cell type independent of tumor stage or origin (p less than 0.0001). Stage I disease and bronchioloalveolar carcinoma were associated with longer survival, while Stage II or III disease, small cell anaplastic carcinoma, and adenocarcinoma were associated with reduced survival. We conclude that associated scar influences cell type of peripheral lung carcinoma but does not influence patient survival, even among patients with similar cell type and stage of disease.

The spiral coil membrane oxygenator was used without an arterial line filter during short term total cardiopulmonary bypass in 50 infants and children. The compact oxygenator proved to be efficient and reliable, was easy to operate in a simple perfusion circuit, has a high flow rate to priming volume ratio and eliminated gaseous emboli. During perfusion, platelet counts and fibrinogen concentrations descreased 51 and 31% respectively. Coagulation studies in eight infants less than 15 kilograms perfused with the membrane oxygenator system did not differ from those in 7 infants perfused by a bubble oxygenator system.

This study included 89 patients, 70-82 years (mean 72.8 years), who had procedures using cardiopulmonary bypass since 1955. Twenty-six patients had elective aortic valve replacement (AVR), with two hospital deaths. One patient who underwent emergency AVR for bacterial endocarditis died of septic shock. Ten patients had AVR and coronary artery bypass surgery (CABG), with one hospital death (10%). Fourteen patients had mitral valve replacement (MVR), with eight hospital deaths (57%). Two died of left ventricular rupture after leaving the operating room, and the remainder died of low cardiac output. Twenty-five patients had CABG with no early deaths. Seven patients had aneurysms of the thoracic aorta, with two early deaths. Six patients had other procedures with one death, making a total of 16 operative deaths in the 89 patients. Eighty-four of the patients (94%) were New York Heart Association (NYHA) Functional Class III or IV for congestive heart failure and/or angina, preoperatively. Of these, 12 were in extremis immediately before surgery, and six survived. There were 10 late deaths. The actuarial survival rates for one, two and five years for all patients were 69% (40 patients), 47% (20 patients) and 21% (seven patients), respectively. At recent follow-up (mean 20 months) 84% of the hospital survivors were symptomatically improved at least one NYHA Functional Class. We conclude that CABG and/or AVR can be performed in elderly patients with a low hospital mortality and with symptomatic improvement. However, MVR in the elderly carries an unusually high mortality (7.3 times greater than patients less than 70, in our experience), and this risk must be weighed when considering MVR in these patients.

One hundred eighteen consecutive patients undergoing valve replacement for aortic stenosis were analyzed to determine the incidence of and predisposing factors to postoperative atrial tachyarrhythmias. Univariate and multivariate analyses were performed on 70 clinical, hemodynamic, radiographic, electrocardiographic, operative, and postoperative variables. Forty-seven patients (40%) experienced atrial tachyarrhythmias at a median of 3 days after surgery (70% atrial fibrillation, 22% atrial flutter, and 6% junctional tachycardia). Preoperative descriptors associated with an increased prevalence of atrial tachyarrhythmias were age 70 years or older (p less than .02), mitral regurgitation (p less than .002), history of paroxysmal atrial fibrillation (p less than .03), or antiarrhythmic therapy (p less than .006), diabetes mellitus (p less than .01), and elevated pulmonary systolic, mean, and capillary wedge pressures (p less than .02, p less than .007, p less than .005). Postoperative descriptors were prolonged respirator therapy (p less than .001), use of catecholamines (p less than .01) or vasodilators (p less than .05), and prolonged stay in the intensive care unit (p less than .04). Multivariate analysis of these 12 variables showed advanced age, diabetes mellitus, and prolonged respirator use to be independently associated with atrial tachycardias and to predict them with a sensitivity of 62% and a specificity of 77%. Anticipation of atrial arrhythmias in patients with specific clinical descriptors may be used to guide prophylactic therapy.

The occupation of cardiovascular perfusion has evolved from a technical to a professional status during the past 25 years. The national thoracic surgical organizations, The American Association for Thoracic Surgery and the Society of Thoracic Surgeons, have supported this process of development through participation on various boards and committees of the perfusionist organizations. The rapid growth of cardiac surgical services in the past decade produced concern about the availability of perfusionist manpower. This concern was exacerbated by creation of formal processes for the certification of perfusionists and the accreditation of perfusion educational programs. Today, these issues are largely resolved and cardiovascular perfusion is recognized as an allied health profession.

Massive pulmonary hemorrhage secondary to an acquired arteriovenous fistula is a rare event associated with high mortality. Cotton wads mounted on steel coils were inserted by percutaneous catheter and successfully occluded a pulmonary arteriovenous fistula in a patient who had massive hemoptysis and contraindications to thoracotomy.

In vitro recirculation of fresh human heparinized blood in an extracorporeal circuit with a membrane oxygenator decreased fibrinogen-induced platelet aggregation and diminished the number of fibrinogen receptors and glycoprotein IIb/IIIa (GPIIb/GPIIIa) antigenic sites on the platelet surface. In seven experiments, the mean +/- SD Km value for fibrinogen (i.e., molar concentration of fibrinogen required to cause 50% of the maximal rate of aggregation) was 1.58 X 10(-7) mol/L +/- 0.68 X 10(-7) mol/L. After recirculation, this value increased to 3.8 X 10(-7) mol/L +/- 1.94 X 10(-7) mol/L (P less than or equal to 0.025). The maximal aggregation rate of chymotrypsin-treated platelets decreased by 40% after 2 hours of recirculation (P less than or equal to 0.025). The number of fibrinogen receptors on platelets, which were treated with chymotrypsin after a recirculation, decreased from 41,370 +/- 24,000 to 13,230 +/- 10,230/platelet under the same conditions (P less than or equal to 0.025). The number of antigenic sites for monoclonal antibody reacting with GPIIb/GPIIIa complex of adenosine diphosphate-stimulated platelets decreased from 34,200 +/- 5,940 to 19,500 +/- 9,680/platelet after recirculation (P less than or equal to 0.025). Prostaglandin E1 (0.3 mumol/L) in the perfusion circuit preserved the ability of platelets to react with fibrinogen. In conclusion, the loss of fibrinogen receptors from the surface of platelet membranes results from the interaction of platelets with the surfaces of perfusion circuits.

Prolonged extracorporeal circulation (ECC) using heparin as anticoagulant may be associated with pronounced thrombocytopenia and excessive bleeding. We, therefore, tested the hypothesis that reversible inhibition of platelet function, in lieu of heparinization, might preserve platelets and prevent coagulation in a perfusion circuit. When 500 ml of fresh heparinized (one U/ml) human blood was recirculated in a perfusion circuit constructed of standard silicone rubber components and a membrane oxygenator (0.95 M2), platelet counts declined to 9 +/- 2 (SEM) % of initial levels within 15 mins; plasma levels of the platelet specific protein LA-PF4 rose to 15 +/- 2 micrograms/ml within one hour indicating extensive release of platelet granule contents, and leukocyte counts declined to 91 +/- 4% within 15 mins. Prostacyclin (PGI2, greater than or equal to 25 eta M) or prostaglandin E1 (20 microM) and theophylline (12 mM) prevented platelet loss and release of granule contents. When heparin was reversed with protamine, however, immediate coagulation ensured. This occurred despite the absence of detectable activation of Hageman factor as evidenced by stability of plasma concentrations of prekallikrein in systems anticoagulated with heparin or citrate and despite our inability to detect thromboplastin-like properties in isolated leukocytes. Thus, coagulation in the presence of platelet inhibition suggests that alternative pathways, independent of platelet activation may exist. Platelet inhibition does preserve platelets preventing contact initiated release, but cannot serve by itself for anticoagulation.

Pure sarcomas of the esophagus are exceedingly rare. We report a case of esophageal synovial sarcoma which occurred in an adolescent. The tumor was locally resected, sparing the patient esophagectomy. After postoperative radiation therapy, the patient remains alive and well without evidence of disease 28 mo after operation. The unique nature of polypoid sarcoma of the esophagus, and the potential for cure without esophagectomy, is discussed.

Extracorporeal membrane oxygenation uses peripherally placed cannulas and a streamlined circuit without a venous reservoir. This study tests the flow dynamics of venous catheters connected without a reservoir directly to a centrifugal pump. During in vitro testing, a 30 cm segment of collapsible tubing interposed between the reservoir and pump simulates the vein. In five sheep, flow was measured between catheters placed in the right atrium and inferior vena cava from peripheral sites. Catheter tip design (four types) does not affect flow within a simulated vein in vitro. Maximum pump flow is independent of filling pressures (6 to 21 mm Hg) in vitro and in vivo when the catheter tip is in a tank reservoir or the right atrium. However, when the catheter tip is within a collapsible segment or in the inferior vena cava, maximal flow is significantly influenced by filling pressure (6 to 18 mm Hg) and by the ratio of catheter outer diameter to venous diameter. At all filling pressures, maximal flow in vivo is significantly reduced when this ratio is greater than 0.5. During extracorporeal membrane oxygenation, central venous pressure and catheter/vein ratio, not catheter size alone, control flow through peripheral venous catheters.

A simple, inexpensive, accurate method of measuring the amount of blood returned by the cardiotomy suction system was devised and calibrated. Preoperative and postoperative platelet counts were obtained in 76 patients with congenital heart disease in whom the amount of cardiotomy suction return was measured. The mean percentage of total perfusate returned by the cardiotomy suction system was 8.9%. Both postoperative platelet count and the percentage change between preoperative and postoperative platelet counts correlated with the amount of blood returned by the cardiotomy suction system, time on bypass, and the percentage of total perfusate aspirated by the system.

Since 1971 we have seen 15 children with the diagnosis of purulent pericarditis. The causative organism was Hemophilus influenzae in seven, Staphylococcus aureus in three, and five were due to other organisms. In one child the diagnosis was unsuspected until autopsy. The other 14 patients were all treated with intravenous antibiotics to which the organism was sensitive. One child had an immediate pericardiectomy because of tamponade. The other 13 patients had pericardiocentesis for diagnosis and initial therapy. Pericardiocentesis alone resulted in recovery of four patients and failed in nine, including all seven patients with H. influenzae. These nine had recurrent tamponade or a persistent picture of sepsis that was unresponsive to repeated pericardiocenteses and necessitated operative intervention. The procedure used was subxiphoid tube drainage in two patients. One recovered and the other required further operation. The remaining seven patients were treated with pericardiectomy. All pericardiectomy patients recovered without complications or recurrent symptoms. Survivors are asymptomatic with no evidence of pericardial constriction. We recommend immediate pericardiocentesis for diagnosis and initial therapy. Early pericardiectomy should be performed if the causative organism is H. influenzae, if tamponade occurs after initial pericardiocentesis, or if fever persists despite appropriate antibiotics.

We evaluated the ability of the calcium antagonist, verapamil, to alter human platelet function. With the concentrations tested (20 ng to 0.1 mg/ml of whole blood), verapamil inhibited epinephrine-induced aggregation and release of 14C-serotonin; produced a dose-dependent inhibition of 14C-serotonin uptake and prevented aggregation dependent release of thromboxane B2. The action of verapamil could be overcome by higher concentrations of both epinephrine and calcium. Furthermore, verapamil-induced inhibition could be reversed by gel-filtering platelets suggesting that verapamil's anti-platelet activity does not outlast its presence in plasma. Verapamil was relatively ineffective as an inhibitor of ADP-induced aggregation. As with epinephrine-induced platelet activation, the effects of verapamil on ADP-induced 14C-serotonin and thromboxane release correlated with its effects on secondary aggregation. Finally, verapamil failed to alter calcium ionophore-induced platelet aggregation. Thus, verapamil at the concentrations tested, appears to be functioning as a reversible, relatively specific inhibitor of epinephrine-induced platelet activation. Our findings suggest that the actions of verapamil in this regard are complex; there may be competitive inhibition of epinephrine binding as well as a blockade of epinephrine-induced calcium flux.

The effects of heparin, protamine, and the heparin-protamine complex on the abilities of platelets to aggregate in vitro in response to adenosine diphosphate (ADP) and epinephrine were determined. Citrated blood was obtained from normal volunteers and portions were treated with heparin, protamine, and three different ratios of heparin and protamine. The threshold concentrations of ADP and epinephrine required to produce complete platelet aggregation were then determined. Compared with control citrated plasma, the geometric mean of the threshold concentration for ADP in the heparinized sample was decreased twofold, from 1.88 to 0.94 micrometer; and that for epinephrine more than threefold, from 0.5 to 0.14 micrometer. In contrast, the threshold concentration for ADP was increased to 3.68 micrometer in the neutralized and to 2.78 micrometer in the overneutralized samples and that for epinephrine to 1.62 micrometer in the neutralized and 1.82 micrometer in the overneutralized samples. These data indicate that heparin increases the sensitivity of platelets to ADP and epinephrine as determined by platelet aggregation, and protamine added to heparinized blood not only reverses this effect, but decreases platelet sensitivity when it is added in concentration that neutralize heparin. Additional protamine has no further effect, and protamine alone has no effect on platelet aggregation.

Extracorporeal membrane oxygenation (ECMO) reduces the systolic stress integral (SSI) in the normal left ventricle. We tested the hypothesis that the SSI does not decrease in poorly contracting, dilated, ejecting hearts during ECMO. In 14 sheep, four pairs of ultrasonic crystals measured changes in left ventricular (LV) wall thickness and three LV diameters. Volume calculations were validated by balloon distention of the ventricles after death (slope = 0.85; r = 0.85). SSI was measured during ECMO flows of 20 to 100 ml/kg/min in both normal and dilated, poorly contracting hearts produced by 30 minutes of warm ischemia. After warm ischemia, end-systolic elastance, an index of contractility, decreased from 8.3 +/- 0.6 mm Hg/ml to 2.9 +/- 0.4 mm Hg/ml (p = 0.001) and peak systolic pressure decreased from 47.4 +/- 0.7 mm Hg to 37.5 +/- 0.08 mm Hg (p = 0.01). In normal hearts, as ECMO flow increased, SSI decreased from 10.5 +/- 2.2 mm Hg.sec to 7.7 +/- 0.8 mm Hg.sec at 60 ml/kg/min (p = 0.001). However, in postischemic hearts, SSI progressively increased from 6.6 +/- 0.3 mm Hg.sec before ECMO to 12.4 +/- 1.8 mm Hg.sec at ECMO = 100 ml/kg/min. These studies indicate that the initial effect of ECMO on the poorly contracting, dilated heart increases LV wall stress and that the increase in stress is proportional to ECMO flow. The increase in stress is primarily due to an increase in afterload, which more than offsets decreases in systolic and diastolic volumes.

Between Jan. 1, 1979, and Jan. 1, 1986, 72 septuagenarians had open heart operations for disease of the mitral valve. Thirty-two (44%) had additional operative procedures. Overall seven patients (9.7%) died within 30 days of operation. Eleven patients had bar calcification of the posterior mitral annulus as defined by three criteria and 61 did not. No differences between these two groups were present except for hospital mortality. Three of the 11 patients (27.3%) died at or soon after operation of complications resulting from the calcified annular bar. Only four of 61 patients (6.6%) without bar calcification died early. The difference in early mortality between the two groups is significant (p less than 0.05) and identifies the presence of bar calcification of the posterior mitral annulus as an independent risk factor of mitral valve operations in elderly patients.