Cholesterol embolization syndrome following thrombolysis during acute myocardial infarction.

BACKGROUND: Cholesterol embolization syndrome (CES) is the result of atherosclerotic plaque erosion and subsequent dislodgement of cholesterol crystals from the core of the plaque to the peripheral arteries. The source of emboli is usually located in the aorta, whereas the most commonly affected organs are the skin and the kidneys. CASE REPORT: The case of a 69-year-old male with cyanotic painful discoloration of his toes following thrombolysis for acute myocardial infarction 1 month previously is presented. Both transesophageal echocardiography and magnetic resonance aortography showed a diffuse ulcerated atherosclerotic plaque in the course of descending thoracic aorta, while a skin biopsy of the cyanotic toes revealed cholesterol crystals in the lumen of the small diameter arteries. CONCLUSION: Cholesterol embolizations from the aorta are difficult to treat and may end in renal failure. Since treatment options are limited without proven efficacy, increased awareness by the clinicians is needed.

Non-diabetic hyperglycaemia correlates with angiographic coronary artery disease prevalence and severity.

AIM: The role of glycaemia as a coronary artery disease (CAD) risk factor is controversial, and the optimal glucose level is still a matter of debate. For this reason, we assessed the prevalence and severity of angiographic CAD across hyperglycaemia categories and in relation to haemoglobin A(1c) (HbA(1c)) levels. METHODS: We studied 273 consecutive patients without prior revascularization undergoing coronary angiography for suspected ischaemic pain. CAD severity was assessed using three angiographic scores: the Gensini's score; extent score; and arbitrary index. Patients were grouped, according to 2003 American Diabetes Association criteria, into those with normal fasting glucose (NFG), impaired fasting glucose (IFG) and diabetes mellitus (DM). RESULTS: CAD prevalence was 2.5-fold higher in both the IFG and DM groups compared with the NFG group. Deterioration of glycaemic profile was a multivariate predictor of angiographic CAD severity (extent score: P=0.027; arbitrary index: P=0.007). HbA(1c) levels were significantly higher among CAD patients (P=0.016) and in those with two or more diseased vessels (P=0.023) compared with the non-CAD group. HbA(1c) levels remained predictive of CAD prevalence even after adjusting for conventional risk factors, including DM (adjusted OR: 1.853; 95% CI: 1.269-2.704). CONCLUSION: Non-diabetic hyperglycaemia, assessed either categorically by fasting glucose categories or continuously by HbA(1c) levels, correlates with the poorest angiographic outcomes.