William E. Walker

The effect of coronary bypass on the outcome of peripheral vascular operations in 1093 patients

One of the greatest risks in peripheral vascular operations is the presence of significant coronary artery disease. To assess the proper timing and demonstrate a possible protective effect of coronary artery bypass (CAB), 1093 patients who underwent one or more peripheral vascular operations in addition to CAB from 1976 through 1984 were analyzed. During that same period, 24,441 patients underwent CAB procedures, and 8530 patients underwent major vascular operations. Carotid endarterectomy (493 patients), abdominal aneurysm resection (130 patients), renal artery bypass (12 patients), aortofemoral bypass (77 patients), femoral-popliteal-tibial bypass (190 patients), and combined vascular procedures (191 patients) were included. The patients were divided into three groups according to severity of disease, which determined timing of the procedure. Group I (255 patients) underwent simultaneous CAB and peripheral vascular operation because of unstable coronary artery disease and severe vascular disease. The early mortality rate for group I was 4% (10 patients). Seven of the 10 deaths were cardiac. In group II, 279 patients had CAB and peripheral vascular operation during the same hospital admission with the same operative mortality rate (4%, 10 patients). Six deaths were from cardiac causes, three from neurologic causes, and one from hemorrhage. In group III, 559 patients underwent CAB first, then peripheral vascular operation during a separate hospital admission. There were no cardiac-related deaths and only one neurologic-related death (operative mortality rate, 0.2%). These data demonstrate the protective effect of CAB in patients who undergo elective vascular surgery. The increased risk in patients undergoing simultaneous or same admission procedures was related to the severity of the vascular and coronary artery disease and not to the combined operations. Operative complications were not increased by performing simultaneous or same admission procedures.

The management of aortoduodenal fistula by in situ replacement of the infected abdominal aortic graft

Conventional surgical wisdom dictates the complete removal of infected abdominal aortic graft, oversewing of the aorta, and restoration of lower limb bloodflow by extra-anatomic bypass grafting. Dissatisfied with this approach because of the high incidence of local complications, mortality, and loss of limb, 20 patients with secondary aortoduodenal fistula had duodenal repair, excision of the old graft, and placement of a new graft in the same location. A similar technique was used in three patients with erosion of an aortic graft into the jejunum. Length of follow-up averaged 5.2 years, and was more than 1 year in each instance. Of the eighteen patients who survived the repair, three have had early recurrent rupture or false aneurysm of the proximal aortic anastomosis, with consequent death in two, but fifteen patients (83%) have had no further related problem. There was no loss of limb. Use of greater omentum as a protective barrier seemed helpful. Optimal antibiotic usage, and the idea that varying degrees of graft infection require different approaches, require further definition. In conclusion, in situ graft replacement is the correct operative strategy in this challenging group of patients.

Sustained improvement in left ventricular function and mortality by intracoronary streptokinase administration during evolving myocardial infarction.

One hundred eighty-eight patients with acute myocardial infarction were studied prospectively from August 1980 to September 1982. One hundred thirty-six of these patients were entered into a intracoronary streptokinase study after informed consent was obtained. The remaining 52 patients, who either met exclusion criteria for the study or refused to participate, served as a control group and were treated as those in the study group except that they did not undergo emergency cardiac catheterization. Left ventricular function was determined in both groups by gated radionuclide ejection fraction (EF) on admission to the hospital, at discharge, and 6 months after discharge. With successful reperfusion up to 18 hr after onset of chest pain, mean left ventricular function in the study group improved (EF 39 +/- 13% on admission and 46 +/- 12% at discharge; p less than .001). Mean EF in control patients and those not achieving reperfusion did not change from admission to discharge. Mean EF at 6 month follow-up was not significantly different than at discharge in the study group or the control group. Total cardiac mortality in the control group was 19% compared with 10% in the study group (p = .06, NS). When patients admitted in pulmonary edema or shock (Killip class III or IV) were excluded from both groups, total cardiac mortality in the study group was significantly lower (4%) compared with in the control group (12.5%, p less than .05. The administration of intracoronary streptokinase during evolving myocardial infarction up to 18 hr after onset of chest pain may result in decreased mortality and sustained improvement in left ventricular function.

Valve failure with the Ionescu-Shiley bovine pericardial bioprosthesis: Analysis of 2680 patients

Early reports on the excellent hemodynamic function and low thromboembolic rates of the Ionescu-Shiley bovine pericardial bioprosthetic valve (BPV) encouraged us to use it as our choice for valve replacement in 2680 patients from 1978 through 1983. Analysis of these patients at 5-year follow-up (mean 21.6 months) demonstrated the following important trends. Despite anticoagulation therapy in 48%, thromboembolism occurred in 88 patients for a linearized rate of 1.87% emboli per patient-year and was not time-related. The highest incidence of thromboembolism was in mitral valve replacement (MVR) (2.76% per patient-year). The actuarial freedom from reoperation resulting from valve failure at 5 years was 82% in aortic valve replacement (AVR), 87.1% in MVR, and 92.6% in AVR/MVR. The most distressing causes for reoperation were valve calcification (33 patients, 0.68% per patient-year) and leaflet disruption (11 patients, 0.23% per patient-year). Valve calcification was related to age, small valve size, and AVR position and increased with time, especially at the 4- to 5-year intervals. In patients under 30 years of age, calcification occurred in 18.7% at a mean time of 40.8 months in AVR and in 8.2% at 44 months in MVR, for an overall rate of 11.6%. Over the age of 30 years, it occurred in 14 patients (0.6%) at a mean time of 44 months. Leaflet disruption was not related to age and occurred later in AVR (50 to 58 months) than MVR (1.5 to 61 months). Events increased with time (mean range 37 to 58 months). Because of calcification and leaflet disruption, valve failure causing reoperation has increased significantly at the 4- to 5-year intervals even when valve replacement in patients under 30 years of age is excluded. If this trend continues, the valve failure rate will be exceedingly high on further follow-up. Thus we have limited the use of the BPV to a selected group of patients in whom valve longevity is less important than effective orifice size, thromboembolic rate, and freedom from anticoagulation.

Rupture of an aortocoronary saphenous vein graft aneurysm

Abstract Few cases of aortocoronary saphenous vein (SV) graft aneurysm have been reported. These have been limited primarily to pseudoaneurysms occurring at either the proximal or distal anastomosis, although at least 6 cases of true aneurysmal change of the vein conduit itself have been reported in English. 1–5 This report reviews an unusual case of acute rupture of an autogenous SV graft aneurysm, which presented initially as acute right hemothorax after a brief period of cardio-pulmonary resuscitation.

Urgent thoracotomy for pulmonary or tracheobronchial injury.

Three hundred eighty-eight of 7,283 (5.3%) admitted trauma patients underwent urgent thoracotomy. In 61 patients (15.7%), pulmonary or tracheobronchial injury prompted thoracotomy (11, blunt; 50, penetrating). Pulmonary hemorrhage necessitated thoracotomy in 54 patients (88.5%); tracheobronchial injury in five patients (8.2%). The mortality was 27.9%. Nine patients (14.8%) underwent pneumonectomy: eight died of intractable hemorrhagic shock during thoracotomy despite rapid control of pulmonary hemorrhage: one died of sepsis. Eleven patients (18.0%) underwent lobectomy: six (54.5%) died of concomitant injuries. Thirty-six patients (59.0%) underwent pneumonorrhaphy: one died of concomitant injuries. Five (8.2%) patients underwent tracheobronchial repair: one died of concomitant injuries. Pneumonectomy was uniformly fatal and should be a procedure of last resort in the treatment of pulmonary injury, as lobectomy and pneumonorraphy are better tolerated by these critically ill patients.

Failure of glycogen depletion to improve left ventricular function of the rabbit heart after hypothermic ischemic arrest.

We tested the hypothesis that depletion of glycogen prior to myocardial ischemia diminishes lactate buildup and improves functional recovery on reperfusion in the isolated rabbit heart. Cardiac glycogen was reduced either by substituting N2 for O2 in the perfusate or by perfusion with substrate-free solution, before the onset of ischemia. Hearts were subjected to either 30 minutes of normothermic (37 degrees C) or 60 minutes of hypothermic (4 degrees C) ischemia followed by 30 minutes of reperfusion with oxygenated Krebs-Henseleit buffer. Function was assessed by measuring peak left ventricular pressure at end-diastolic pressures ranging from 0 to 20 mm Hg. N2 perfusion for 15 minutes lowered myocardial glycogen by 60% and decreased ATP and phosphocreatine (p less than 0.001). Glycogen depletion did not decrease lactate accumulation during ischemia, but it impaired recovery with reperfusion (-46%, p less than 0.05). N2 perfusion for 5 minutes also reduced glycogen by 60%, but energy-rich phosphates were not reduced and functional recovery was still impaired (-40%, p less than 0.05). Perfusion with substrate-free medium diminished glycogen by 33% (p less than 0.05). Although lactate accumulation was significantly reduced (-45%, p less than 0.05), recovery following reperfusion was not improved. The results suggest that preservation of glycogen stores, but not the prevention of lactate buildup during ischemia, is beneficial for the recovery of function with reperfusion.

Apicoaortic Conduits for Complex Left Ventricular Outflow Obstruction: 10-Year Experience

We interposed valved conduits between the left ventricular apex and aorta in 38 patients over a 10-year period. Indications included tunnel subaortic stenosis, aortic annular hypoplasia, tubular supravalvular aortic hypoplasia, and severe calcification of the ascending aorta. Operative mortality was 11%, but 78% of the survivors were alive at 5 years, and 70% had had no major complication. The results were better in adolescents and adults than in young children. Although complications included calcific degeneration of the valve and disruption of the conduit at the site of insertion into the ventricular apex, we continue to believe in the utility of this procedure in a few patients with complex left ventricular outflow tract obstruction.

Beneficial effects of intracoronary thrombolysis up to eighteen hours after onset of pain in evolving myocardial infarction

Coronary arteriography and intracoronary streptokinase (STK) infusion were performed on 89 patients with evolving acute myocardial infarction (AMI). Ventricular function was followed in these patients during their hospitalization by gated radionuclide ventriculography. In 35 of these patients thallium imaging was performed on admission and 4 hours after reperfusion. An additional 30 patients with AMI who either met exclusion criteria for the STK protocol or refused study served as a control group. In patients admitted 0 to 6, 6 to 12, or 12 to 18 hours after onset of pain, there was no difference in change in left ventricular ejection fraction (LVEF) from admission to discharge, in percent of patients with total occlusion demonstrating reperfusion, or in percent of patients demonstrating a significant increase in LVEF. The average increase in LVEF from admission to discharge in patients reperfused ws 8% (40% +/- 14% to 48% +/- 13%, p less than 0.001). No change in LVEF was demonstrated in the control population or in patients in whom coronary reperfusion was unsuccessful. Reperfusion produced an increase in thallium uptake in the infarct-related myocardium that was accompanied by an improvement in regional function. Failure of reperfusion produced no change in either thallium uptake or regional function.

Patterns of infection and mortality in thoracic trauma.

Tissue infection and systemic sepsis are common causes of morbidity and late mortality after major thoracic trauma. To seek causative mechanisms, prognostic indicators, and areas of possible improvement in therapy, we reviewed 310 consecutive adults admitted with major thoracic trauma. Of these, 56 (18%) died of massive injuries in the first 5 days; the remaining 254 were considered at risk for infectious complications. There were 21 late deaths in this group, and 15 (71%) were caused by systemic sepsis. Eighty-four patients (33%) developed thoracic infections, and 15 (6%) had significant nonthoracic infections. Markers of increased risk of infection included blunt injury, shock and unconsciousness on arrival, and splenectomy. Pulmonary infection was increased significantly following prolonged endotracheal intubation, but was virtually absent following tracheostomy. The risk of infection was increased significantly if prophylactic antibiotics were not used, but no definite correlation could be made to advanced age, pre-existent disease, nor post-traumatic malnutrition. Attention to some of these factors may decrease the risk of infection in thoracic trauma.