Postoperative levels of cardiac troponin versus CK-MB and high-sensitivity C-reactive protein for the prediction of 1-year cardiovascular outcome in patients undergoing vascular surgery.

OBJECTIVE: This study evaluated comparatively the predictive value of postoperative cardiac troponin I (cTnI), creatinine kinase (CK)-MB, and high-sensitivity C-reactive protein (hs-CRP) in 1-year cardiovascular mortality and morbidity in patients undergoing elective vascular surgery. METHODS: A total of 295 consecutive patients undergoing elective noncardiac vascular surgery were prospectively followed-up over a period of 12 months. The levels of cTnI, CK-MB, and hs-CRP were measured preoperatively and 24 h after operation. The primary endpoint was the composite of cardiovascular death, nonfatal acute myocardial infarction, ischemic stroke, and unstable angina. RESULTS: The primary endpoints occurred in 11 patients (3.8%). Receiver operating characteristic curve analysis showed that postoperative cTnI was a strong predictor of a cardiovascular event during 1-year follow-up (area under the curve, 0.852; P<0.001). Areas under the curve for hs-CRP and for CK-MB were 0.734 (P=0.008) and 0.494 (P=0.947). A threshold cTnI value of 0.4 ng/ml was highly associated with the occurrence of a cardiovascular event, with a sensitivity of 80% and specificity of 81%. Furthermore, cTnI levels provided a significantly better prediction than CK-MB levels (P=0.009) and tended to be superior to hs-CRP (P=0.2). CONCLUSION: Postoperative cTnI levels seem to be superior to CK-MB and hs-CRP levels for the prediction of 1-year cardiovascular mortality and morbidity in patients undergoing elective vascular surgery.

Starting with rosuvastatin in primary hyperlipidemia--Is there more than lipid lowering?

The authors investigated the effects of rosuvastatin, beyond its lipid-lowering activity, on several nonlipid metabolic variables, along with its safety and tolerability, in patients treated for primary hyperlipidemia. Patients (n = 55) with primary hyperlipidemia were open-label assigned to the recommended starting dose of rosuvastatin 10 mg/day, and serum metabolic variables were measured at baseline and after 8 and 20 weeks. Treatment with rosuvastatin produced significant reductions in total cholesterol, low-density lipoprotein cholesterol (LDL-C), apolipoprotein B, nonhigh-density lipoprotein cholesterol (non HDL-C), and triglyceride concentrations, whereas HDL-C, apolipoprotein A-I, and lipoprotein(a) levels did not change significantly from baseline. The LDL-C treatment target was achieved in 71% of patients. No significant variations in renal function parameters (serum creatinine and creatinine clearance), insulin resistance estimates, and serum concentrations of uric acid, total homocysteine, vitamin B12, and folic acid were observed during the period of treatment. High-sensitivity C-reactive protein levels were significantly lowered by rosuvastatin therapy (median values, 3.1 vs 2.0 vs 1.9 mg/L, at 0, 8, and 20 weeks, respectively; p < 0.0001). In conclusion, rosuvastatin at 10 mg/day is a highly effective, safe, and well-tolerated monotherapy option for patients with primary hyperlipidemia, with a favorable antiinflammatory potential and nondeteriorating effects on renal function.

Comparative effects of atorvastatin, simvastatin, and fenofibrate on serum homocysteine levels in patients with primary hyperlipidemia.

Hyperhomocysteinemia is regarded as an independent risk factor for cardiovascular disease. Lipid-lowering agents, such as fibrates, can modify homocysteine levels. However, less is known about the effect of statin therapy on homocysteine. The authors compared the effects of atorvastatin (40 mg/day), simvastatin (40 mg/day), and micronized fenofibrate (200 mg/day) on the serum concentrations of total homocysteine, vitamin B12, and folic acid in patients with primary hyperlipidemia. A total of 128 patients with primary hyperlipidemia (total cholesterol > 240 mg/dL and triglycerides < 350 mg/dL) were assigned to atorvastatin, simvastatin, or fenofibrate. Serum lipid and metabolic parameters were measured at baseline and at 6 and 12 weeks of treatment. Homocysteine correlated positively with serum creatinine and uric acid levels and inversely with serum folic acid levels. All treatment modalities reduced total, low-density lipoprotein (LDL) cholesterol, and triglyceride concentrations. High-density lipoprotein (HDL) cholesterol levels significantly increased only in the fenofibrate-treated patients (47.9 +/- 12.5 vs. 50.7 +/- 12.6 vs. 51.2 +/- 12.8 mg/dL, p < 0.01). Atorvastatin and fenofibrate treatment resulted in a significant reduction of serum uric acid levels (5.3 +/- 1.6 vs. 4.9 +/- 1.4 vs. 4.8 +/- 1.4 mg/dL, p < 0.0001 for atorvastatin; 5.6 +/- 1.6 vs. 4.3 +/- 1.4 vs. 4.4 +/- 1.4 mg/dL, p < 0.0001 for fenofibrate). Homocysteine levels were significantly increased only by fenofibrate (10.3 +/- 3.3 vs. 14.1 +/- 3.8 vs. 14.2 +/- 3.6 microU/L, p < 0.001) but did not change from baseline following statin treatment. Neither statins nor fenofibrate had any effect on serum vitamin B12 and folic acid levels. In contrast to fenofibrate, therapeutic dosages of atorvastatin and simvastatin have a neutral effect on serum homocysteine levels, which is in favor of their "cardioprotective" properties.