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Complications attributed to central venous stenosis and subsequent thrombosis are increasing in frequency and are most commonly associated with neointimal fibroplasia as well as neoplastic, fibrotic, and traumatic pathologies. We present the successful venous bypass and thoracic wall reconstruction of a 58-year-old female with chronic atypical symptoms secondary to brachiocephalic vein occlusion from congenital thoracic dystrophy.

background: Multiple complications occur after repair of a thoracoabdominal aortic aneurysm, the most common of which is respiratory failure. methods: One hundred consecutive thoracoabdominal aneurysm repairs were studied retrospectively using univariate, bivariate, and multiple logarithmic regression analyses to identify factors associated with respiratory failure. results: The mean of days of intubation was 5.8 ± 0.8 (mean ± SEM), with a median of 2 days. Patients who developed respiratory failure (21%) had a 42% mortality compared with a 6% mortality in patients who did not develop respiratory failure (P

Direct graft replacement with local debridement and prolonged administration of antibiotics was used in the treatment of six patients with mycotic thoracoabdominal aneurysms. The only early death occurred in a patient with systemic sepsis related to Staphylococcus aureus mycotic suprarenal aneurysm. Long-term survival of the remaining patients has been excellent: two patients died of unrelated causes at 5 and 6 years, respectively; one patient remains alive with known persistent infection at 5 years; and the remaining patients are alive with no evidence of infection at 1 1/2 and 10 years, respectively. Percutaneous aspiration of infected perigraft fluid with local instillation of antibiotics along with administration of intravenous antibiotics may provide palliation in selected patients with recurrent infections. In view of the magnitude of the problems associated with recurrent infection, life-time administration of antibiotics is recommended after in situ graft replacement of mycotic thoracoabdominal aneurysms.

An algorithm for screening and management of abdominal aortic aneurysms was developed at the Ochsner Medical Institutions to address the considerable variation identified in clinical practice. A consensus panel of physicians whose opinions differed regarding the management of abdominal aortic aneurysms was convened to develop the algorithm. Based on a literature review and clinical experience, the panel established criteria to determine how frequently and by which methodologies patients with abdominal aortic aneurysms should be followed and when a referral to a vascular surgeon is appropriate. The algorithm developed by the consensus panel method was used to establish practice guidelines that are flexible enough to address individual patient needs yet structured enough to eliminate inappropriate care. Data are being collected and analyzed in real time to determine whether elements of the algorithm should be revised.

The records of 150 consecutive patients undergoing thoracoabdominal aortic replacement from 1980 to 1991 were retrospectively reviewed. There were 89 men and 61 women; mean age was 67.8 years (range: 33 to 88 years). Since June 1989, a multimodality prospective perioperative protocol was used to reduce the risk of spinal cord dysfunction. Ischemia is minimized by complete intercostal reimplantation whenever possible, cerebrospinal fluid drainage, and maintenance of proximal hypertension during cross-clamping. Spinal cord metabolism is reduced by moderate hypothermia, high-dose barbiturates, and avoidance of hyperglycemia. Reperfusion injury is minimized by the use of mannitol, steroids, and calcium channel blockers. Ninety-seven percent of patients survived long enough for evaluation of their neurologic function. Spinal cord dysfunction was reduced from 6 of 108 (6%) in the preprotocol group to 0 of 42 in the protocol group (0%) (p less than 0.01). The overall 30-day operative mortality was not significantly different between the groups (9% versus 12%, p = NS). A multimodality protocol appears to be effective in reducing the risk of spinal cord injury during thoracoabdominal aortic replacement.

Spontaneous atheromatous visceral embolization from diffuse aortic atherosclerotic disease is an unusual and poorly understood entity. We have reviewed our experience with 88 patients who suffered atheromatous embolization from a "shaggy" aorta. Visceral embolization was evident in 36 patients (40.9%). Nine were treated nonoperatively with three patients dying within a week of presentation and an additional five patients dying within five years due to continuing renal and intestinal embolization. Surgical correction was undertaken 28 times in 27 patients. Endarterectomy or graft replacement of the aorta did not necessarily prevent visceral infarction or renal failure. Extra-anatomic bypass with ligation of the distal external iliac arteries appears to be associated with the lowest morbidity and mortality. Anticoagulation of these patients does not prevent embolization and may be contraindicated for long-term management.

To evaluate the efficacy of venous reconstruction versus percutaneous transluminal angioplasty for the treatment of obstruction of the superior vena cava and its major tributaries, we retrospectively reviewed the clinical course of 27 patients, of whom 13 underwent operative reconstruction and 15 had angioplasty (1 had both). Three patients had obstruction of the superior vena cava, 8 had occlusion of the innominate veins, and 16 had obstruction of the subclavian or axillary veins. In both treatment groups, mean age, indications, etiology, and location of the lesion were comparable. No major surgical complications occurred; one patient who underwent angioplasty experienced stent migration to the pulmonary artery without sequelae. Primary symptomatic relief at 1 year was achieved in 88% in the surgical group versus 36% in the angioplasty group (p0.9), respectively. We conclude that the long-term success rate of operative reconstruction exceeds that of single percutaneous transluminal angioplasty. However, with repeated angioplasty, success rates approach those of operative reconstruction.

We have reviewed our experience regarding hospital costs and reimbursement for 72 patients who underwent thoracoabdominal aneurysm repair. Preoperative risk factors, postoperative complications, length of stay, and source of reimbursement were recorded for all patients. Patients covered by Medicare resulted in a mean net institutional loss of $16,472 per patient, whereas a mean net profit of $17,847 per patient resulted from patients with commercial insurance. Factors associated with institutional financial loss were: age over 75 years, preoperative coronary disease, postoperative respiratory failure, and length of stay. By multivariate analysis, however, only length of stay was independently associated with institutional loss.

The recognition of the extent of vascular disease has introduced several medical subspecialties, radiology and vascular surgery, to a multidisciplinary approach to these problems. Of particular importance is the primary care physician, who often is the first to see these patients and should be familiar with common vascular problems. Only then will initial care and disposition be appropriate.

To determine comparative rates of development and progression of peripheral occlusive arterial disease, 110 healthy nondiabetic control subjects, 112 patients with peripheral occlusive arterial disease (POAD), 240 patients with diabetes mellitus (DM), and 100 patientswith diabetes mellitus and peripheral occlusive arterialdisease (DM + POAD) were studied over 4 yr with noninvasive techniques. The presence of peripheral occlusive arterial disease was determined by postexercise ankle-brachial index (ABI) values; progression of peripheral occlusive arterial disease was determined by the rate of change in postexercise ABI. Patients who underwent peripheral arterial reconstructive surgery or amputation were also classified as having progression of their peripheral occlusive arterial disease. On this basis, follow-up revealed that peripheral occlusive arterial disease developed and therefore progressed in 1 (1%) of the control group and 22 (9%) of the DM. Peripheral occlusive arterial disease progressed in 31 (28%) of the POAD and 26 (26%) of the DM + POAD. The presence of peripheral occlusive arterial disease predisposes to progression of disease, and peripheral occlusive arterial disease is more likely to develop in diabetic patients who do not have peripheral occlusive arterial disease than in nondiabetic control subjects. However, the presence of diabetes mellitus in patients with peripheral occlusive arterial disease does not seem to increase the risk of progression.

The clinical, biochemical, and vascular laboratory measurements potentially associated with the development and/or progression of peripheral occlusive arterial disease (POAD) were assessed during a 4-year period in 110 normal control subjects, 112 patients with POAD without diabetes mellitus, 240 patients with diabetes mellitus without POAD, and 100 patients with diabetes mellitus and POAD. Age, history of hypertension or coronary heart disease, history of cigarette smoking, presence of POAD, systolic blood pressure, and β-thromboglobulin level were associated with progression of POAD. A multivariate logistic regression model indicated that the presence of diabetes mellitus or POAD or both at baseline, decreased postexercise ankle-brachial index, increased arm systolic blood pressure, and current smoking were independently associated with progression of POAD. This study suggests that cessation of smoking and control of hypertension are essential treatment modifications to decrease the risk of progression of peripheral vascular disease in diabetic patients. (Arch Intern Med.1991;151:717-721)

Recent reports in the literature have promulgated nonresective treatment of abdominal aortic aneurysm as a safer procedure than conventional aneurysmectomy with graft replacement in high-risk patients. This review of 106 high-risk patients who underwent conventional aneurysm repair between 1980 and 1985 was undertaken to compare the relative risks, perioperative morbidity, and operative mortality of these patients to that reported for patients treated by nonresective therapy. Excluded were those patients who had rupture initially or underwent a concomitant renovascular procedure. Patients were considered to be at high risk if they met one or more of the following criteria: (1) age equal to or greater than 85 years; (2) receiving oxygen at home, PO2 less than 50 torr, or forced midexpiratory flow less than 25% of predicted; (3) serum creatinine equal to or greater than 3 mg/dl; (4) biopsy-proven cirrhosis with ascites; (5) retroperitoneal fibrosis; or (6) New York Heart Association functional class III-IV angina, left ventricular ejection fraction less than 30%, recent congestive heart failure, complex ventricular ectopy, large left ventricular aneurysm, severe valvular disease, recurrent congestive heart failure or angina after coronary artery bypass grafting, or severe unreconstructed coronary artery disease confirmed by angiography. The mortality rate for conventional aneurysm repair in high-risk patients was 5.7%, compared with a reported 7% mortality rate for nonresective therapy. In those patients with severe cardiac dysfunction, intraoperative pharmacologic manipulation and the selective use of intra-aortic balloon counterpulsation appeared helpful in achieving survival. Late morbidity or mortality from vascular complications did not occur in this series (mean, 2½ year follow-up) after conventional repair but is reported to be a significant problem after nonresective therapy, from either inadequate thrombosis of the aneurysm, rupture of the thrombosed aneurysm, or thrombosis of the axillofemoral graft. This study supports the concept that conventional repair of abdominal aortic aneurysm is preferable to nonresective therapy. (J VASC SURG 1986;3:712-7.)

The incidence and prevention of systemic embolism in patients with chronic left ventricular aneurysm have been controversial. This retrospective study investigated the incidence of clinically evident embolic events and the effect of oral anticoagulation in patients with unequivocal angiographically defined left ventricular aneurysm. Between 1971 and 1979, 76 patients met the ventriculographic criteria and received initial medical management. The median interval from myocardial infarction to ventriculography was 11 months (range 1 month to 16 years) and subsequent median follow-up time was 5 years. Twenty patients receiving anticoagulant therapy were followed up for a total of 40 patient-years and 69 patients not on anticoagulant therapy were followed up for a total of 288 patient-years; 13 patients were included in both subsets. Twenty-eight patients died during follow-up and the 3 and 5 year survival rates were 75 and 61%, respectively. Only one patient not receiving anticoagulant therapy had a clinical embolic event, resulting in an incidence of 0.35 per 100 patient-years. Therefore, in the absence of other predisposing conditions, the extremely low incidence of systemic emboli in these patients with chronic (first documented at least 1 month after myocardial infarction) left ventricular aneurysm does not justify the use of long-term oral anticoagulant therapy.

Optic neuropathy has been diagnosed in several amiodarone-treated patients, including the 13 patients described in this report. The clinical severity of this drug-related optic neuropathy is milder than that characteristically described in anterior ischemic optic neuropathy. The incidence of occurrence was significantly higher than that found in an age-matched general population sample. Whether this result was due solely to amiodarone therapy, to the underlying poor health of these patients, or to a combination of these two factors is uncertain. The findings in this study prompt us to recommend that all patients who receive amiodarone undergo complete ophthalmologic examinations, including careful evaluation of the ocular fundus regularly during such therapy. Appearance of optic neuropathy is probably a relative indication for discontinuing the use of the drug, in the hopes of avoiding bilateral involvement or perhaps recovering vision. The risks of complications of amiodarone treatment must be weighed against the benefit of therapy in patients whose lives are threatened by cardiac arrhythmias. On the basis of this study, the benefits of treatment seem to outweigh the small risk of optic neuropathy. No randomized study has been undertaken to determine the true incidence of complications associated with this medication and at this time could not be justified.

Coronary artery disease is recognized as the major cause of perioperative and late death after abdominal aortic aneurysm (AAA) repair. Routine coronary angiography and prophylactic myocardial revascularization for all significant lesions, regardless of symptoms, have been recommended as a means of reducing this mortality risk. We have advocated a more selective approach in which coronary angiography and myocardial revascularization are performed on the basis of cardiac symptoms. Studies have shown that this selective approach is just as effective as the prophylactic approach in reducing perioperative deaths. To evaluate the effect on late survival of selective myocardial revascularization on the basis of symptoms, we reviewed the preoperative coronary status and course of 485 patients who successfully underwent AAA repair between 1980 and 1985. Late survival was evaluated by means of the Kaplan-Meier method and compared with life expectancy of an age- and sex-matched population. Late survival of the entire group of patients was no different from that of the matched population. Patients with no preoperative evidence of coronary artery disease did significantly better than expected (p = 0.05), whereas those patients with uncorrected or previously bypassed coronary disease had survival no different from that expected. When age was considered as a variable, patients in their 50s and 60s had survival significantly worse than the matched population (p

A 40-year-old man who presented with exertional angina had had two myocardial infarctions within the same myocardial distribution several years earlier. Coronary arteriography revealed a large intramural thrombus in the right coronary artery and minimal atherosclerotic disease. Special coagulation studies detected a circulating lupus anticoagulant. The association of repeated episodes of thrombosis and lupus anticoagulant is important. In patients with repeated thrombotic events, the lupus anticoagulant should be sought, particularly in those less than 40 years of age.

Chronic intravascular coagulation was produced in eight dogs by continuous intravenous infusion of dog brain thromboplastin for 3 days to 18 days. About the third day of infusion there was a decrease in platelet count to 32% of the original value and an increase in plasma platelet factor 4-like (PF4-like) activity to 65% of the entire releasable PF4 of circulating platelets. These platelets released about twice the normal amount of PF4-like activity when aggregated in vitro with ADP. Turnover ( 51 Cr-labeled) was 2 times faster than normal. The level of plasma PF4-like activity seems to reflect the rate of platelet consumption in intravascular coagulation and provides information about platelet kinetics.

We studied the reproducibility of four tests of peripheral occlusive arterial disease in 54 subjects, 32 of whom had this disease. We found that the reproducibility of systolic blood pressures obtained at rest from the thighs, calves, and ankles approximated that of arm systolic and diastolic blood pressures, as did the ankle-to-arm systolic blood pressure ratios. The average of the tenth and ninetieth percentile ranges of the resting systolic blood pressure ankle-to-arm rations was ± 0.10. Systolic blood pressures from the fingers were somewhat less reproducible, and those from the toes were even more variable. Systolic blood pressure ankle-to-arm ratios measured after the patient had exercised were less reproducible than resting ratios. The average of the tenth and ninetieth percentile ranges of the 1-, 3-, 5-, and 10-minute ratios after exercise was −0.13 to +0.16. Skin temperatures from the fingers and toes were approximately as reproducible as systolic blood pressures from the arms and legs and as the resting ankle-to-arm blood pressure ratios. Pulse-volume recordings from the thighs, calves, ankles, feet, toes, and fingers were very poorly reproducible. We conclude that information on the reproducibility of these measurements is essential in the evaluation of noninvasive arterial tests that are used to determine the course of peripheral occlusive arterial disease. (J VASC SURG 1985;2:678-83.)

Two patients with giant cell arteritis and visual deficits were found to have pituitary tumors, which accounted for the optic findings. The various ophthalmologic abnormalities in these two conditions, which were apparently coincidentally associated in these two patients, are compared. These cases illustrate the importance of careful neuro-ophthalmologic examination and roentgenograms of the head in patients with giant cell arteritis who have visual field loss.

Twelve affected persons in the third decade of life or later, and the 14 nearest age- and sex-matched unaffected relatives, of a large kindred with autosomal dominant hereditary motor and sensory neuropathy not linked to the Duffy blood group (HMSN type IA) were assessed for arrhythmia and cardiomyopathy. Cardiac abnormalities were no more frequent in the affected persons than in the unaffected relatives. The heart of a patient with HMSN type II who had died of complications of cardiomyopathy was found to have rheumatic disease-type myocarditis with Aschoff bodies. The results of this study provide further evidence against an association of cardiomyopathy and HMSN.

Thirty-two patients (26 female, 6 male) with angiographically diagnosed Takayasu arteritis were seen at the Mayo Clinic between 1971 and 1982. Racial composition of this group was 23 North American Caucasians, 4 Mexicans, 3 Orientals, 1 Native American, and 1 patient of Middle Eastern origin. Incidence of the disease in Olmsted County, Minnesota, was 2.6/million/year. Diagnosis was often delayed for long periods of time, with a median delay of 18 months. Patients had both non-vascular symptoms (arthralgias in 56%, fever in 44%, weight loss in 38%) and symptoms of vascular stenosis such as arm claudication (47%) and hypertension due to renal artery stenosis (41%). All patients had either multiple vascular bruits (94%) or absent pulses (50%). Laboratory findings included anemia (44%) and elevations of erythrocyte sedimentation rate (78%). Almost all patients had multiple sites of arterial involvement documented by angiogram with various combinations of stenosis, luminal irregularity and aneurysm formation. Response to corticosteroid treatment was usually very good, with dramatic improvement in non-vascular symptoms and return of pulses in 8 of the 16 patients with absent pulses prior to treatment. Five-year survival rate from time of diagnosis was 94%. Twelve patients underwent surgical procedures involving the carotid arteries (5 cases), subclavian artery (4 cases) and renal arteries (3 cases). Three aneurysms were resected, one had aortic valve replacement for severe aortic regurgitation, and two patients underwent transluminal angioplasty. Pathologic changes were restricted to the media and adventitial layers of the vessel wall and were indistinguishable from those of giant-cell or temporal arteritis. Takayasu arteritis is more common than previously suspected in North America, is not restricted to any one racial group, and is readily treatable with corticosteroids and surgical vascular reconstruction.

Two patients with hypertensive crises due to pheochromocytoma presented with unusual features suggestive of cardiovascular disorders other than pheochromocytoma. These features included transient cortical blindness and other neurologic deficits, electrocardiographic changes indicative of transmural infarction and peripheral arterial spasm. In both patients the diagnosis of pheochromocytoma was made later; removal of the tumor was followed by ready reversal of the clinical and biochemical abnormalities. Management of such cases includes suspicion of the diagnosis in the presence of atypical features, early initiation of therapy with alpha and beta adrenergic blocking agents and a definitive surgical procedure before peripheral vascular changes become irreversible. When an apparent myocardial infarction occurs, the diagnosis of coronary artery disease cannot always be excluded, but rapid stabilization of the clinical and electrocardiographic changes after adrenergic blockade would favor the diagnosis of a catecholamine-induced myocarditis. The coexistence of coronary artery disease and uncontrollable arrhythmias presents an increased risk but, if pheochromocytoma is suspected, surgery may be necessary despite the increased risk.

The effect of oral aspirin in doses known to influence in vitro platelet aggregation was evaluated in patients undergoing brachial artery catheterization. Neither arterial thrombus formation nor pulse reduction was affected in patients given aspirin when compared to controls. Aspirin in small doses does not decrease the incidence of vascular occlusion after brachial artery catheterization.

SummaryThe role of platelets in the initation of arterial thrombosis is clear. In venous thrombosis as well, platelets may in some circumstances play a significant role.For these reasons, and because of the complications and limitations of anticoagulant therapy, antithrombotic trials have been launched with several agents which inhibit platelet function.Regarding postoperative deep vein thrombosis, neither aspirin nor dipyridamole alone appears effective, although the combination offers promise. Results with the dextrans are conflicting. In recurrent idiopathic deep vein thrombosis, sulfinpyrazone may be beneficial.On the arterial side, transient cerebral ischemic attacks may be favorably affected by either aspirin or sulfinpyrazone. Prevention of thromboembolism associated with prosthetic heart valves appears possible with combination warfarin-dipyridamole therapy, and the beneficial effect of sulfinpyrazone on shortened platelet survival in this group suggests that this agent may also be effective. Sulfinpyrazone may also be beneficial in preventing thrombosis in arteriovenous canulas.The issue which has attracted the greatest attention and about which no clear answer exists at present is whether antiplatelet agents can modify the course of acute myocardial infarction. Several trials with aspirin are currently underway, and it would be premature to recommend its use in this condition until the results of these trials are available, probably in 1975.

Vaginal insufflation in pregnant women leading to acute venous air embolism has been appreciated by obstetricians and pathologists for several decades. Initially described as a complication of powder insufflation for treatment of trichomonal vaginitis, insufflation-induced air embolism has been more recently associated with orogenital sex. The case herein illustrates a typical history that is almost pathognomonic. Clinical and laboratory abnormalities as well as treatment measures are briefly described. Familiarity with this syndrome is essential if prompt and appropriate therapy is to be rendered.

BG 0 patients (pts) have lower risk for cardiovascular-thromboembolic disease than A-AB-B pts, particularly males. This might be related to blood hypocoagulability (lower Factor VIII). We report BG frequencies in our Caucasian renal transplant population divided in two groups, ES reflux nephropathy (RN) and ESRD of other etiologies excluding diabetes mellitus.BG 0 male pts are protected, especially for ESRN. To determine whether this sex dependency could be related to different VIII: RWF levels or PS, VIII:RWF levels (n=82) and 51Cr-labelled PS (n=74) were analyzed in controls according to sex and BG.VIII: RWF is sex independent and lower in BG 0. PS is BG independent and shortened in males. A hypercoagulable State reflected by high VIII: RWF and short PS might explain the increased risk of non-BG 0 males to develop ESRD. Non-BG 0 male pts with RN may be more susceptible to develop progressive RD.

Mayo Clinic, Mayo Foundation, Rochester, MinnesotaPlatelets are believed to play an important role in the pathogenesis of atherosclerosis and thrombotic occlusive arterial disease. As part of a prospective study of peripheral occlusive arterial disease in diabetes mellitus, platelet survival half-life (PS) was determined in years 1 and 2 from the disappearance pattern of 51cr-labeled platelets obtained by measuring radioactivity in serial samples over 8 days in four groups of patients age 50-70. Using computer assisted least-square analysis, a single exponent is fitted to the data and half-life determined.Groups included (1) normal subjects (NC); (2) subjects with clinical and objective evidence (transcutaneous doppler ultrasound and treadmill exercise) of peripheral arterial occlusive disease (AS0); (3) subjects with diabetes mellitus without AS0 (DM); (A) subjects with both diabetes mellitus and AS0 (DM+AS0). 112 subjects were tested in year 1 and 75 of these were available for retesting in year 2.In year 1, there is a difference in the distribution of platelet survival (PS) for the four groups (p=.002). PS is significantly short in groups AS0 and DM+AS0 compared with controls (NC), Year 2 values for PS (75 subjects) were compared to year 1. Using the t test on mean differences PS for each group was not significantly different year 2 vs year 1; mean percent differences year 2 vs year 1 were 1.2% (NC), 0.2% (ASO), 3.2% (DM), and -9.3% (9-3% lower than year 1 for DM+ ASO).Platelet survival half-life (PS) does distinguish popula tion groups and is reproducible when repeated.

To evaluate results of medical and surgical treatment of axillary-subclavian venous occlusion, the clinical courses of 95 patients were reviewed. Twenty-three patients had acute axillary-subclavian venous thrombosis, and 72 patients had chronic occlusion. Thirty-four patients with thoracic outlet syndrome and axillary-subclavian occlusion represented 3.5% of the 969 patients treated for thoracic outlet syndrome during the same period. Nonlethal pulmonary embolization from the axillary-subclavian vein occurred in four patients. Sixty percent of patients were asymptomatic or had mild symptoms during strenuous exercise at last follow-up (mean, 5.4 years). Forty-eight of these 56 patients had received anticoagulation during the acute phase of the disease. Twenty-seven percent of patients had symptoms with moderate exercise and 12.6% had symptoms at rest. Thirteen patients had operations, with improvement demonstrable in 10 patients. All five patients who underwent first rib resection for intermittent venous occlusion or for thoracic outlet syndrome after thrombosis occurred on the contralateral side did well. Axillary-subclavian venous occlusion is a nonlethal disease but late sequelae occur in one third of patients. Early anticoagulation appears to be beneficial and, in some patients with concominant thoracic outlet syndrome, first rib resection also appears to be helpful. Further data are needed to evaluate results of fibrinolytic treatment, thrombectomy, and venous reconstruction. (J VASC SURG 1986;4:333-7.)

We reviewed the records of all patients who underwent carotid endarterectomy at our institution during the period from January 1970 through December 1986 to determine the frequency of postoperative occlusions and the role of heparin-induced thrombosis in patients with such occlusions. After 2,527 carotid endarterectomies, a total of 19 occlusions occurred in 18 patients. Of these 18 patients, 6 had an associated heparin-induced coagulation disorder, 3 of whom are described in detail. Although heparin is a useful anticoagulant, it may precipitate occlusion of vessels after an endarterectomy procedure, either at the endarterectomy site or elsewhere. Physicians should be aware of the potentially increased risk for embolic or thrombotic cerebrovascular events in patients who receive heparin therapy.

• Between 1970 and 1976,1,112 patients underwent abdominal aortic aneurysm repair. Follow-up, ranging from six to 12 years, was complete in 1,087 patients (97.7%). The most frequent cause of late deaths was coronary artery disease (45.6%), but significant morbidity related to the peripheral vascular system had developed in 94 patients, and led to 8.4% (48 patients) of all late deaths. Forty-nine true, 14 anastomotic, and five dissecting aneurysms were detected in 59 patients (5.4%) a mean ( ± SD) of 5.2 ± 3.1 years after the initial aneurysm repair. These aneurysms were located in the thoracic (24), thoracoabdominal (five), or abdominal aorta (11), and in the iliac (six), femoral (17), popliteal (four), and renal arteries (one). Only one of 26 patients presenting with a rupture of one of these secondary aneurysms survived. There was a significant association between preoperative hypertension and recurrent aneurysm. These findings suggest that subsequent vascular disease, including recurrent aneurysms and graft complications, cause significant late morbidity and mortality after repair of abdominal aortic aneurysm. Careful follow-up and adequate control of hypertension may allow reduction in morbidity and an improvement in late survival. ( Arch Surg 1985;120:590-594)

Levels of three factor VIII-von Willebrand factor components (von Willebrand antigen, ristocetin cofactor, and factor VIII coagulant) were higher in specimens of plasma from 27 patients with giant cell arteritis and 18 patients with polymyalgia rheumatica than in specimens from 21 normal control subjects. Values in patients with active giant cell arteritis were higher than those in patients with either inactive giant cell arteritis or active polymyalgia rheumatica. Levels of factor VIII-von Willebrand factor components tended to decline gradually after disease activity had been suppressed by corticosteroid therapy and therefore may be indicators of vascular damage. These levels, however, did not revert to normal rapidly in response to corticosteroid therapy as did the patients' symptoms and the usual laboratory measurements indicative of inflammation; thus, measurements of these components are unlikely to be useful in day-to-day management of these diseases. Electrophoretic analysis suggested that the elevated values are due to increased amounts of normal factor VIII-von Willebrand factor rather than to the presence of an abnormal molecule.

Distinguishing between in vitro and in vivo release of platelet specific proteins has led to problems in interpretation of clinical studies with PF4, and with BTG.As part of a prospective study of peripheral occlusive arterial disease in diabetes mellitus PF4 and BTG were measured together by specific radioimmunoassay in four groups of subjects age 50-70 years. Groups included (1) 106 normal subjects (NC); (2) 126 with clinical and objective evidence (transcutaneous doppler ultrasound and treadmill exercise) of peripheral arterial occlusive disease (ASO); (3) 244 with diabetes mellitus without ASO and (4) 101 with both diabetes mellitus and ASO.PF4 did not distinguish among the four groups: NC vs ASO p=. 18, NC vs DM p=.52, NC vs DM+ASO p=.73, NC vs all diabetics p=.61, and NC vs all ASO p=.46. However, BTG did distinguish the groups with vascular disease from NC: NC vs ASO p=.02, NC vs DM+ASO pNormal range for PF4 is 0-13 ng/ml with a median of 3.0 ng/ml, a mean of 3.0 ng/ml, and SD 1.97. Normal range for BTG is 14-46 ng/ml with a median of 26 ng/ml, a mean of 27.2 ng/ml, and SD 10.3. When PF4 and BTG are correlated (all groups included) r=.41 pPF4 and BTG levels should be performed together. When done together low PF4 levels support the absence of in vitro platelet release due to sample collection and handling. BTG levels are significantly increased in subjects with peripheral arterial disease, supporting the active role of platelets in thrombotic occlusive arterial disease.

Clinically, penetrating atheromatous ulceration of the aortic wall may be confused with either symptomatic thoracic aneurysm or classic spontaneous aortic dissection. Aortography and computed tomographic (CT) scanning of the thoracic aorta provide specific diagnostic information which permits one to distinguish this lesion from atherosclerotic aneurysm and classic dissection. Hallmarks of findings on aortography and CT scan include the presence of the ulcer and an intramural hematoma. Since the findings may be disarmingly subtle, the potentially progressive and serious nature of this condition may remain unappreciated. Recognition of the penetrating atheromatous ulcer and distinguishing it from aortic dissection arising just distal to the origin of the left subclavian artery is mandatory. Resection of only a conservative segment of the proximal descending aorta suffices for classic dissection in the upper descending thoracic aorta, but the penetrating aortic ulcer requires graft replacement in the area of the ulcer and intramural hematoma.

Collective experience at the Mayo Clinic with nine cases of acquired aortocaval fistula revealed a difference between the presenting features of patients with traumatic fistula and those of patients with spontaneous fistula. In addition, patients with spontaneous aortocaval fistula, rather than presenting with a single distinct clinical syndrome, present with at least three different clinical pictures: (1) the classic syndrome of high-output heart failure of recent onset with palpable aneurysm and continuous bruit, (2) hypotension and oliguria or anuria in the presence of an abdominal aortic aneurysm, which may not be tender and in which a characteristic bruit may be absent and (3) back pain or abdominal pain associated with a tender pulsatile mass, shock and retroperitoneal hemorrhage. (The fistula may not be suspected prior to surgery.)

In THE MORE than two decades since Campbell and Link1isolated bishydroxycoumarin as the hemorrhagic agent in spoiled sweet clover, numerous other coumarins and the related indandione derivatives have been developed and widely used as anticoagulants.2Studies of the effect of these oral anticoagulants on blood coagulation have indicated that most of these drugs depress not only prothrombin,3but three other clotting activities as well—factors VII,4IX,5and X6—although evidence has been presented7,8that certain anticoagulant drugs differ qualitatively in their effect on the clotting mechanism. Furthermore, despite numerous isolated studies on individual drugs, the exact sequence in which the levels of various affected clotting factors decrease with coumarin or indandione therapy is not a matter of general agreement.9A systematic study of the effect of commonly used coumarin and indandione drugs using specific assays for each of the four coagulation factors were the same as those usually observed during

Chronic constrictive pericarditis impairs normal diastolic filling of the heart and usually results in the classic clinical triad of increased venous pressure, ascites and a small quiet heart.1 Occasionally, however, this process may simulate other cardiac abnormalities, as illustrated by the following case.

• We conducted a noncurrent prospective study of all Olmsted County, Minnesota, residents who had had a lowerextremity venogram, pulmonary angiogram, or lung scan performed because of suspicion of deep venous thrombosis or pulmonary emboli. One hundred thirteen cancer-free patients were followed for 386 person-years from the date of procedure. Nine subsequent cancers were observed compared with 4.5 expected (relative risk, 2.0; 95% confidence interval, 0.9 to 3.8), using total cancer incidence rates for the Rochester, Minn, population. Five hundred seventeen cancer-free controls were followed for 2072 person-years. Twenty subsequent cancers were observed compared with 11.6 expected, yielding a relative risk of 1.7 (95% confidence interval, 1.1 to 2.7). When cases and controls were compared directly, no statistically significant difference in cancer-free survival was found. ( Arch Intern Med 1987;147:1907-1911)

A patient with Fabry's disease underwent cadaveric renal transplantation. Unusual features of this case were as follows: (1) partial correction of the enzyme deficiency typical of the disease by the renal allograft; (2) the development of rapidly progressive pulmonary vascular obstruction and eventual fatal pulmonary embolism from subclavian vein thrombosis; and (3) surgical clipping of the inferior vena cava. This was done because of failure of and complications from anticoagulant therapy and did not in any way alter allograft function.