Atheroembolism in an endomyocardial biopsy from a cardiac transplant recipient after coronary angioplasty.
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A case of a coronary atheroembolism after coronary angioplasty was detected by routine myocardial biopsy six years after cardiac transplant. The patient had had three balloon angioplasties within a five week interval for symptomatic accelerated coronary artery disease. Histological examination clearly identified atheromatous debris in a small intramyocardial artery with a secondary inflammatory response. This complication of angioplasty has been identified at necropsy in association with new myocardial infarction. It is unusual to identify this complication in a survivor, and in a case in which there was no clinical evidence of myocardial infarction. Myocardial biopsy samples a relatively small amount of myocardium, and this case suggests that coronary atheroembolism may not be an uncommon complication of angioplasty. (+info)
Clinical and biochemical analysis in infection-associated stroke.
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BACKGROUND AND PURPOSE: Currently, recent infection (primarily bacterial infection) is discussed as a risk factor for cerebrovascular ischemia. The aim of this study was to investigate whether the association of ischemic stroke with recent infection is restricted to stroke subtypes and whether recent infection influences the severity of the postischemic deficit; we also aimed to define biochemical pathways linking infection and ischemic stroke. METHODS: Analyzing the data of a prospective case-control study, we classified the etiology of cerebrovascular ischemia on the basis of clinical, neuroradiological, sonographical, cardiological, and biochemical data in 159 patients without and in 38 patients with infection within 1 week before ischemia. We assessed the severity of neurological deficits using the Scandinavian Stroke Scale. RESULTS: In patients with recent infection compared with patients without infection, the neurological deficit on admission was more severe (median of scores, 41 versus 30.5; P < .005), cortical infarcts in the middle cerebral artery territory were more frequent (60% versus 26%; P < .001), the prevalence of extracranial artery stenoses was lower (9% versus 26%; P < .05), and definite or presumed cardioembolic stroke was more frequent (34% versus 19%; P < .05), as was stroke from cervical artery dissection (8% versus 1.3%; P = .05). Serum levels of C-reactive protein were higher in patients with (20.7 +/- 26.8 mg/L) than in those without infection (9.2 +/- 23.7 mg/L; P < .01). CONCLUSIONS: Recent infection may be associated with a more severe postischemic deficit and with an increased risk of stroke from cardioembolic origin and from cervical arterial dissection. (+info)
Cholesterol emboli following percutaneous transluminal coronary angioplasty as speculated by toe skin biopsy.
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A 55-year-old man required hemodialysis for acute renal failure 3 days after repeat percutaneous transluminal coronary angioplasty (PTCA). Bilateral acrocyanosis and necrotic lesions of the toes occurred 10 days after PTCA. Skin biopsy samples revealed needle-shaped cholesterol crystals of the intraluminal clefts in his small arteries. He was diagnosed with cholesterol emboli presenting as blue toe syndrome. The conditions improved with anticoagulation and vasodilation, but improvement in renal function was temporary. He later required maintenance hemodialysis. Cholesterol emboli following PTCA are life threatening because they are difficult to diagnose and can cause severe complications. (+info)
Surgical management of atheroembolization.
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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. (+info)
Foregut revascularization via retrograde splenic artery perfusion after resection of a juxtaceliac mycotic aneurysm: complicated by pancreatic infarction because of cholesterol emboli.
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A 66-year-old woman had development of a rapidly enlarging juxtaceliac mycotic aneurysm after therapy for lumbar osteomyelitis and a psoas abscess. The aneurysm was repaired through a thoracoabdominal approach with a Dacron aortic graft sewn end to end to the thoracic aorta and end to side to the infrarenal aorta. Perfusion was restored after oversewing the abdominal aorta above the superior mesenteric artery and oversewing the celiac trunk. After reperfusion the foregut remained critically ischemic despite a patent superior mesenteric artery. Foregut reperfusion was achieved by removing the spleen and anastomosing the distal splenic artery to the aortic graft. Recovery was complicated by infarction of the body of the pancreas because of cholesterol emboli, resulting in a large pleural effusion. After undergoing a subtotal pancreatectomy that preserved the splenic artery, the patient recovered without additional complications. During 8 years of follow-up, the patient has normoglycemia and has had no further infections complications. The distal splenic artery offers an excellent inflow for foregut revascularization; however, the pancreas is intolerant of atheromatous emboli. (+info)
Spontaneous cholesterol embolization. A rarely reported entity.
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Cholesterol embolization sometimes occurs after invasive procedures involving manipulation of the aorta or its major branches, and less commonly occurs after thrombolytic therapy for acute myocardial infarction. Rarer still is spontaneous cholesterol embolization, a case of which we now report. Our patient experienced peripheral embolization, the origin of which was traced to the infrarenal aortic segment and the common iliac vessels. Aortoiliac reconstruction was successful; we believe that surgical management of this condition should be performed in selected cases. (+info)
Myositis due to cholesterol emboli.
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Myositis due to spontaneous cholesterol embolization is uncommon and usually associated with cutaneous abnormalities at presentation. A case of myositis due to cholesterol emboli is reported. The patient presented with painful weak legs, and the diagnosis was confirmed by muscle biopsy. (+info)
Role of insulin resistance associated with compensatory hyperinsulinemia in ischemic stroke.
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BACKGROUND AND PURPOSE: Although insulin resistance and hyperinsulinemia play a crucial role in the pathogenesis of atherosclerosis, little is known about their roles in ischemic stroke. The purpose of this study was to clarify whether insulin resistance and hyperinsulinemia are causative factors in the pathogenesis of ischemic stroke. METHODS: Thirty-four consecutive patients with ischemic stroke, who were normotensive, nondiabetic, and not obese, were classified into three groups--atherothrombotic infarction (n = 16), lacunar infarction (n = 10), and cardioembolic infarction (n = 8)--based on clinical findings, brain imaging, and cerebral angiography. Both oral glucose tolerance tests and lipid analyses were performed. Insulin sensitivity was determined by the steady state plasma glucose method with the use of octreotide acetate. Data were compared with those of healthy control subjects (n = 15). RESULTS: Steady state plasma glucose levels were significantly higher in the atherothrombotic infarction group compared with control subjects and the other two stroke groups, indicating the presence of insulin resistance in patients with atherothrombotic infarction. In the atherothrombotic infarction group, the 2-hour insulin area (area under the plasma insulin concentration curve) during a 75-g oral glucose tolerance test was significantly increased and dyslipidemic changes (increased triglyceride and apolipoprotein B, decreased high-density lipoprotein) were observed, whereas these changes were not found in the lacunar infarction and cardioembolic stroke groups. CONCLUSIONS: Insulin resistance in association with compensatory hyperinsulinemia and dyslipidemia may be an important pathogenetic factor underlying the development of atherothrombotic infarction. (+info)