Giant Coronary Artery Aneurysm Causing Acute Anterior Myocardial Infarction.

A 70-year-old man with hypertension was admitted to our coronary ICU with acute anterior MI. Emergent primary PCI was planned and coronary angiography was performed. LAD artery was totally occluded in the proximal segment just after a huge 32 × 26 mm sized aneurysm. Emergent CABG operation was performed in 75 minutes because of multivessel disease including the RCA and left circumflex artery. Aneurysm was ligated and coronary bypass was performed using LIMA and saphenous grafts. The postoperative course of the patient was uneventful. He was discharged with medical therapy including ASA, clopidogrel, and atorvastatin. He was asymptomatic at his polyclinic visit in the first month.

Statin pre-treatment protects brain against focal cerebral ischemia in diabetic mice.

BACKGROUND: Cerebrovascular diseases and other vascular complications are common and cause considerable mortality and morbidity in diabetes mellitus. Recent studies suggest that statins reduce the incidence of stroke in diabetic as well as non-diabetic patients. The outcome of stroke is shown to be worse in diabetics. However, the effect of statins on the outcome of stroke occurring in diabetics is not clear. The purpose of this study was to investigate the effect of pre-treatment with statins on focal cerebral ischemia in diabetic mice. MATERIALS AND METHODS: Swiss albino mice were randomized into two groups. Diabetes was induced in the first group by intravenous streptozotosin injection. The second group served as non-diabetic. After 4 weeks, half of the mice in diabetic and non-diabetic groups were randomized to receive intraperitoneal simvastatin 1 mg/kg/day or saline treatment for 14 days. Subsequently, mice were subjected to 90 min of proximal middle cerebral artery occlusion and 24 h of reperfusion. Sham-operation was also performed for each group. After 24 h of reperfusion, neurological deficits were scored and the infarct volume was measured on Nissl stained brain sections. RESULTS: Infarct volume (median, interquartile range) was significantly increased in the diabetic group (60.7 mm(3)) compared to non-diabetic group (53.4 mm(3)). Statin pre-treatment significantly reduced the infarct volume (to 40.4; 33.5 mm(3), respectively) and neurological disability scores both in diabetic and non-diabetic groups. CONCLUSIONS: These data suggest that diabetes aggravates the ischemic damage after focal cerebral ischemia and statin pre-treatment protects the brain in diabetic as well as healthy animals. Statin treatment may favorably affect stroke outcome in diabetic patients in addition to decreasing stroke incidence.

Simvastatin pretreatment reduces the severity of limb ischemia in an experimental diabetes model.

OBJECTIVE: The purpose of this study was to examine the effects of simvastatin pretreatment in the setting of acute limb ischemia-reperfusion injury in an experimental diabetes model that is associated with a high risk for limb loss. METHODS: Adult male Sprague-Dawley rats were randomized into two groups. Diabetes was induced in the first group by intravenous streptozotocin injection. The second group served as the nondiabetic group. Eight weeks after the streptozotocin injection, half of the rats in the diabetic and the nondiabetic groups were further randomized to receive either intraperitoneal simvastatin (1 mg/kg per day) or saline treatment for 6 weeks. Bilateral hind-limb ischemia was induced for 4 hours by the tourniquet method. After 24 hours of reperfusion, tissue samples were collected from the gastrocnemius and anterior tibial muscles bilaterally for measurement of muscle edema, percentage of necrosis, and malondialdehyde (MDA), glutathione, and myeloperoxidase (MPO) levels. RESULTS: Ischemic injury was more prominent in diabetic animals. The diabetic animals with limb ischemia exhibited a 7% increase in tissue edema, a 47% increase in muscle necrosis and MPO level, and a 15% reduction in glutathione levels compared with the nondiabetic animals (P < .05). Simvastatin treatment with 1 mg/kg for 6 weeks reduced the ischemic injury. Simvastatin pretreatment led to a 71% reduction in muscle necrosis in diabetic animals (P < .001). The protective effects of simvastatin pretreatment also correlated with a 23% improvement in tissue edema, a 75% reduction in tissue myeloperoxidase content, and a 71% increase in glutathione levels in diabetic animals (P < .01). Furthermore, skeletal muscle injury, characterized by tissue edema and leucosequestration, was significantly less severe with simvastatin pretreatment compared with the nondiabetic animals (P < .01). CONCLUSION: Simvastatin pretreatment reduced limb ischemia-reperfusion injury in diabetic and nondiabetic animals. We conclude that simvastatin pretreatment may be a potential therapeutic intervention for skeletal muscle ischemia-reperfusion injury in the clinical setting.