Walter J. McCarthy

Collagen types and matrix protein content in human abdominal aortic aneurysms

Deficiencies of total collagen, type III collagen, and elastin have been proposed to explain aneurysm formation. Infrarenal aortas were collected from 19 patients (age 70 +/- 7 years) undergoing operative repair of abdominal aortic aneurysms (diameter 7 +/- 2 cm) and from 13 autopsies (age 63 +/- 17 years) of patients without aneurysm disease (controls). Wall thickness and collagen and elastin concentration were determined in full-thickness aorta. Collagen types I and III were measured after digestion with cyanogen bromide, which solubilized nearly 90% of total collagen for typing. Cyanogen bromide peptides were separated by sequential carboxymethylcellulose and agarose chromatography and quantified by peak area measurement with computerized image analysis. Histologic examination revealed prominent inflammatory cell infiltration and deficient, fragmented elastin in the aneurysms. Aortic wall thickness was similar in aneurysms and in control specimens. In the aneurysms, collagen was increased (37% +/- 16% vs 24% +/- 5%; p less than 0.05) and elastin was decreased (1% +/- 1% vs 12% +/- 7%; p less than 0.001), expressed as a percentage of delipidized, decalcified dry weight. Collagen type I accounted for 74% +/- 4% of aneurysm and 73% +/- 4% of control collagen solubilized for typing, and collagen type III accounted for 26% +/- 4% of aneurysm and 27% +/- 4% of control collagen solubilized for typing. Neither patients with a family history of aneurysms nor those without a history of aneurysms had collagen type III deficiency. Atherosclerotic abdominal aortic aneurysms are associated with an inflammatory process and may result from elastin degradation and not a deficiency of type III collagen.

Effect of Cilostazol on treadmill walking, community-based walking ability, and health-related quality of life in patients with intermittent claudication due to peripheral arterial disease: Meta-analysis of six randomized controlled trials

OBJECTIVES: To assess whether cilostazol, a phosphodiesterase III inhibitor, improves treadmill and community‐based walking ability and health‐related quality of life (HQL) in patients with intermittent claudication resulting from peripheral arterial disease (PAD).

Reduction in aortic aneurysm size: Early results after endovascular graft placement

PURPOSE Previous reports demonstrate initial technical success with transluminally placed endovascular grafts (TPEG) for the treatment of abdominal aortic aneurysms. However, long-term changes in the size of the aorta and aneurysmal segments are unknown. The purpose of this study was to determine aortic dimensions at several levels by computed tomographic (CT) scans 1 year after TPEG. METHODS Thirty-four patients underwent TPEG with 1-year CT scans. Patients were divided into three groups: group I, no perigraft leak; group II, early perigraft leak that sealed during the first year; and group III, persistent perigraft leak. Aortic minor and major diameters, perimeter, and area were measured at four locations: the celiac aorta, proximal neck, maximal aneurysm size, and distal neck. RESULTS There were 32 men and two women, with a mean age of 73 +/- 8 years. In group I there were 20 patients (58%), and groups II and III had seven patients (21%) each. The overall mean aneurysm minor diameter decreased from 4.79 +/- 0.68 cm at implantation to 4.39 +/- 0.86 cm at 1 year (p < 0.0001). The aneurysm sac decreased by 0.63 +/- 0.58 cm in group I, and by 0.34 +/- 0.24 cm in group II. In group III, however, the aneurysm sac increased by 0.19 +/- 0.21 cm. Aneurysm size change did not correlate with inferior mesenteric or lumbar artery patency. The dimensions of the celiac aorta and proximal neck did not change significantly. However, diameter of the distal neck enlarged by 0.12 +/- 0.27 cm (p < 0.01). CONCLUSIONS TPEG exclusion is associated with reduction of aneurysm size 1 year after implantation. Expansion of the aneurysms occurred with persistent perigraft leak. The aortic size at the celiac artery and proximal neck did not change. Dilation of the distal neck was minor but requires further long-term follow-up to determine clinical significance.

Arterial injuries in the thoracic outlet syndrome

PURPOSE This article reviews experience with arterial injury caused by thoracic outlet syndrome. Special emphasis is placed on the influence of athletic or work activities on the axillary-subclavian artery system and the mechanism by which the humeral head compresses the axillary artery and the circumflex humeral arterial branches. METHODS Retrospective review identified 34 patients (age range 13 to 67 years) treated for upper extremity symptoms or ischemic complications of thoracic outlet syndrome from 1983 to 1993. Evaluation included assessment of occupational and recreational activities plus duplex ultrasonography and contrast arteriography with positional maneuvers. RESULTS Twenty-two patients (27 arms) had subclavian artery injury, which was most commonly caused by compression by a bony abnormality (cervical rib, 16; anomalous first rib, two; cervical rib and anomalous first rib, two). Fourteen of the 27 arms had distal embolization. All 27 had surgical decompression of the subclavian artery; 15 required concomitant arterial reconstruction. Twelve additional patients (nine athletes) had axillary artery involvement, all from arterial compression by the head of the humerus during abduction maneuvers; all had concomitant compression of the posterior circumflex humeral artery. Axillary arterial injury included thrombosis (one), aneurysm (two), and symptomatic extrinsic compression only (nine). Five patients with axillary artery involvement were treated without a surgical procedure; of the remainder, three underwent decompression procedures only, and four had direct arterial repair. In both groups all subclavian and axillary artery reconstructions were patent at last follow-up examination (mean 31 months). CONCLUSION Most patients with thoracic outlet syndrome who have arterial involvement have a bony anomaly causing subclavian artery compression. This study demonstrates that humeral head compression of the axillary artery and its circumflex branches is a surprisingly common pathologic mechanism. Awareness of this condition affords a better therapeutic approach to arterial injuries caused by thoracic outlet syndrome.

Carotid plaque morphology correlates with presenting symptomatology

PURPOSE In carotid artery disease, correlation of carotid plaque morphology with the patients presenting symptoms has drawn conflicting conclusions. The purpose of this series was to correlate carotid plaque characteristics with the presenting symptoms from a large cohort of patients who underwent operation for carotid artery disease. METHODS From a series of 1252 consecutive patients who underwent carotid endarterectomy, presenting symptoms were divided into three groups: transiently symptomatic (transient ischemic attack [TIA] or amaurosis fugax), prior stroke, and asymptomatic. Plaque characteristics, including ulceration, intraplaque hemorrhage, and degree of stenosis, were recorded prospectively for 1008 procedures. All endarterectomy specimens were inspected during the procedure, and plaque characteristics were recorded immediately after operation. RESULTS There was a higher incidence of plaque ulceration in the transiently symptomatic and prior stroke groups (391 of 508 [77%] and 91 of 115 [79%]) than in the asymptomatic cohort (231 of 385 [60%]; p < 0.0001, chi2 test). There was no significant difference in the incidence of plaque hemorrhage between the transiently symptomatic and prior stroke patients compared with the asymptomatic patients. There was no statistical difference for ulcerated plaque or plaque hemorrhage between the transiently symptomatic and prior stroke group. Intraplaque hemorrhage occurred more frequently in patients with high-grade stenosis (90% to 99%) than in those with less than 90% stenosis (202 of 299 [68%] versus 97 of 299 [32%]; p = 0.01, chi2 test). CONCLUSIONS On gross examination of the carotid specimen in the operating room, plaque ulceration correlates with an initial presentation of amaurosis fugax, TIA, or prior stroke compared with patients operated on for asymptomatic disease. The presence of intraplaque hemorrhage is associated with more advanced stenosis of the internal carotid artery. These findings suggest that plaque morphology does play an important role in the presentation of carotid artery disease.

Surgical management of atheroembolization

PURPOSE Atheroembolization may cause limb loss or organ failure. Surgical outcome data are limited. We report the largest series of atheroembolization focusing on patterns of disease, surgical treatment and outcome. METHODS One hundred patients (70 men), mean age 62 +/- 11 years, operated on for lower extremity, visceral, or nonthoracic outlet upper extremity atheroemboli were identified prospectively and monitored over a 12-year period. The atheroembolic source was localized by use of a combination of computed tomography scanning (n = 55), arteriography (n = 93), duplex scanning (n = 25), transesophageal echocardiography (n = 6), and magnetic resonance imaging (n = 4). Occlusive aortoiliac disease (47 patients) and small aortic aneurysms (20 patients; mean aneurysm size 3.5 +/- 0.8 cm) were the most common source of atheroemboli. Imaging studies revealed 12 patients with extensive suprarenal aortic thrombus. Correction of the embolic source was achieved with aortic bypass (n = 52), aortoiliac endarterectomy and patch (n = 11), femoral or popliteal endarterectomy and patch (n = 11), infrainguinal bypass (n = 3), extraanatomic reconstruction (n = 6), graft revision (n = 3), upper extremity bypass (n = 11), or upper extremity endarterectomy and patch (n = 3). RESULTS All four deaths within 30 days and all seven deaths within the first 6 months after operation were among the 12 patients with suprarenal aortic thrombus. The cumulative survival probabilities for all patients at 1, 3, and 5 years were 89%, 83%, and 73%, respectively. After operation, nine patients required major leg amputations and 10 required toe amputations. Renal atheroemboli led to hemodialysis in 10 patients. Recurrent embolic events occurred in five of 97 patients monitored for a mean of 32 months. All five recurrences occurred in the first 8 months after operation. Three patients with recurrent emboli had suprarenal aortic disease, one of whom had undergone axillofemorofemoral bypass. Four of 15 patients receiving postoperative warfarin anticoagulation had development of recurrent embolism. Only one patient not receiving postoperative warfarin had a recurrent event (p < 0.05 by Fisher exact test). CONCLUSION The atheroembolic source is the aorta or iliac arteries in two thirds of patients who underwent operation. Computed tomography scanning of the aorta is a useful diagnostic technique. The source of the emboli can be eliminated surgically with low mortality or limb loss rates except when the suprarenal aorta is involved.

Carotid endarterectomy with an occluded contralateral carotid artery

Five hundred twenty-six patients who underwent carotid endarterectomy were separated by reviewing those 81 (15%) patients with an occluded contralateral carotid artery and those 445 (85%) with nonocclusion. The population characteristics and surgical indications were similar between the occluded and nonoccluded groups. Ipsilateral plus contralateral perioperative stroke occurred during 11 of 445 operations (2.5%) in which the contralateral carotid was patent, and during which no patient was hemorrhagic. Those patients with contralateral artery occlusion had ipsilateral plus contralateral stroke in 4 of 81 cases of (4.9%) (NS). Intracerebral hemorrhage was responsible for two of four strokes after carotid endarterectomy with contralateral occlusion (p = 0.001). Restenosis to greater than 50% by duplex scanning was more rapid in the occluded group with primary closure (no patch) (p = 0.025) and for men (p = 0.025). Although perioperative safety is comparable, patients with contralateral carotid occlusion may have a greater risk of intracranial hemorrhage and a more rapid rate of restenosis in some subgroups.

Combined arterial reconstruction and free tissue transfer for limb salvage.

PURPOSE Lower-extremity arterial anatomy that is insufficient for successful vein bypass grafting and major proximal foot wounds often lead to leg amputation in patients with severe ischemia. Free tissue transfer, which can provide limb salvage in these patients after arterial reconstruction, was studied. METHODS During a 45-month period, 21 patients who otherwise would have undergone leg amputation were treated with arterial bypass by means of vein grafting and free tissue transfer. Ages of the patients ranged from 40 to 73 years (average, 59 years); 18 of the 21 patients had diabetes mellitus; and all patients except one were men. Arterial reconstruction was performed from the femoral (nine of 21 patients) or popliteal artery (12 of 21 patients) to the posterior tibial (eight patients), dorsalis pedis (five patients), peroneal (three patients), popliteal (one patient), or anterior tibial artery (one patient), or directly to the free flap (three patients). The tissue transferred included latissimus dorsi (five patients), rectus abdominus (five patients), omentum (five patients), gracilis (two patients), radial forearm flaps (three patients), and a scapular flap (one patient). Foot defects were debrided, including the appropriate toe or transmetatarsal amputation, covered with the transferred flap, and then split-thickness skin grafted. Arterial flow for all flaps was through the vein grafts, with direct arterial anastomosis and with venous outflow through adjacent tibial veins. RESULTS All 21 procedures were successful initially, without operative mortality, but three failed within 4 weeks because of uncontrolled infection (two) or embolization from a remote site (one) and required below-knee amputation. Grafts remained patent in 18 procedures, and follow-up of this cohort ranged from 1 to 45 months (mean, 13.3 months). Two patients died, one after 4 months and one after 6 months, of unrelated illness; at the time of death, they had functioning grafts. The remaining 19 patients are alive. Of these, 15 have patent arterial grafts, all viable free flaps. Thus, limb salvage was accomplished in 18 of 21 (86%) patients who otherwise would have required below-knee amputation. CONCLUSION Patients destined for leg amputation despite aggressive traditional arterial bypass grafting methods can achieve limb salvage with the additional technique of free tissue transfer.

Arterial abnormalities of the shoulder in athletes

Vascular lesions of the shoulder may be misinterpreted as one of the more familiar shoulder abnormalities by a treating physician. We are reporting on 13 athletes who were found to have symptoms related to compression of the subclavian or axillary artery or their tributaries. Nine were amateur or professional baseball pitchers. Severe arm fatigue or finger ischemia, secondary to embolization, were presenting symptoms. Arm fatigue was noted in all pitchers. After complete history and physical examination, including auscultation for bruits in functional positions, all athletes were evaluated by noninvasive tests (Doppler and Duplex scanning). Ar teriography was performed with positional testing, re creating overhead activity, and complete radiographic visualization of the dye to the digital arteries. Two patients were found to have subclavian artery aneu rysm. The remaining athletes were found to have compression of the subclavian artery beneath the an terior scalene muscle (five patients), the axillary artery beneath the pectoralis minor (two patients), both arterial segments (two patients), and one was found to have arterial compromise at the level of the humeral head. Branch artery compression was also noted. One pitcher occluded the posterior circumflex humeral artery with embolization to the digit. The two patients with subclavian aneurysms under went saphenous vein bypass with cervical rib resection. All of the other athletes except one underwent resection of a 2 to 3 cm segment of the anterior scalene muscle or pectoralis minor muscles. All returned to their pre vious level of activity except one patient who developed impingement type symptoms and required acromio plasty. He is currently undergoing rehabilitation. Proper recognition of vascular compromise in the upper extremity of athletes is essential to avoid the catastropic complications of arterial thrombosis.

Physical activity during daily life and brachial artery flow-mediated dilation in peripheral arterial disease

Abstract We determined whether higher levels of physical activity in daily life are associated with better brachial artery flow-mediated dilation (FMD) among individuals with lower extremity peripheral arterial disease (PAD). Participants were 111 men and women with PAD (ankle–brachial index (ABI) ≤ 0.95) who completed baseline testing in the Study to Improve Leg Circulation (SILC). We evaluated FMD of the brachial artery at baseline and at 60 seconds following 4 minutes of suprasystolic blood pressure cuff inflation. Physical activity was measured continuously over 7 days using a vertical accelerometer (Caltrac) and a pedometer (Digiwalker). Adjusting for age, sex, race, ABI, cardiovascular risk factors and other potential confounders, higher levels of physical activity were associated with a greater percent change in brachial artery FMD at 60 seconds post cuff deflation for both Caltrac (1st tertile of activity +4.81% change; 2nd tertile +4.60% change; 3rd tertile +7.23% change; p-trend = 0.018) and the Digiwalker (1st tertile of activity +3.76% change; 2nd tertile +6.25% change; 3rd tertile +7.25% change; p-trend = 0.001). Similar findings were observed for absolute change in brachial artery FMD 60 seconds after cuff deflation. In conclusion, higher levels of physical activity during daily life are associated significantly and independently with better brachial artery FMD among individuals with PAD, even after adjusting for confounders. ClinicalTrials.gov Identifier: NCT00106327.