Atorvastatin has an important acute anti-inflammatory effect in patients with acute coronary syndrome: results of a randomized, double-blind, placebo-controlled study.

BACKGROUND: C-reactive protein (CRP) levels are associated with cardiovascular risk. We assessed the hypothesis that atorvastatin might have anti-inflammatory effects in acute coronary syndromes (ACS) as shown by CRP reduction. METHODS: This study was a prospective, randomized, double-blind, placebo-controlled study of 90 consecutive patients admitted within 48 hours of onset of ACS with CRP levels > or =1.4 mg/dL. Patients were assigned to atorvastatin 40 mg daily or placebo over 30 days. C-reactive protein levels, lipid profiles, serum fibrinogen, white cell count, and erythrocyte sedimentation rate were measured at entry, hospital discharge, and 1 month later. RESULTS: Baseline clinical characteristics did not differ between atorvastatin and placebo groups (mean age 59.3 +/- 13.4 vs 61.1 +/- 11.5, P = ns); myocardial infarction 52.3% versus 67.4% ( P = ns). In both groups, median baseline CRP levels were comparable (5.97 +/- 6.2 vs 4.64 +/- 4.2 mg/dL, P = ns). C-reactive protein levels were lower in the atorvastatin group versus control group at discharge (1.68 +/- 1.65 vs 4.12 +/- 4.18 mg/dL) and at 30 days (0.50 +/- 0.71 vs 2.91 +/- 2.68 mg/dL, both P < .0001). C-reactive protein levels significantly decreased from baseline to discharge and 1 month later in placebo and atorvastatin groups (both P < .0001); however, the reduction was greater in the atorvastatin group (62% vs 11% at discharge [P < .0001]; 84% vs 30% at 1 month [P < .0001]). In addition, atorvastatin was associated with a reduction in total and low-density lipoprotein cholesterol and erythrocyte sedimentation rate at discharge and at 30 days (P < .0001 for all comparisons). No correlation was found between changes in CRP and cholesterol levels. CONCLUSIONS: C-reactive protein levels in ACS were rapidly reduced with atorvastatin. These data provide evidence that statins have fast and early anti-inflammatory effects in addition to lipid-lowering effects in ACS.

Ongoing myocardial injury in stable severe heart failure: value of cardiac troponin T monitoring for high-risk patient identification.

BACKGROUND: The progression of chronic heart failure (CHF) is related to ongoing myocyte loss, which can be detected by cardiac troponin T (cTnT). We examined the prevalence and prognostic value of increased cTnT concentrations in serial blood specimens from patients with severe CHF. METHODS AND RESULTS: Clinical, echocardiographic, and 6-minute walk test data were collected prospectively at baseline and at 1 year in 115 outpatients (mean age, 61+/-11 years; 75% men; 62% coronary heart disease) with CHF and a left ventricular ejection fraction <40%. Blood samples were collected at baseline and at 3, 6, and 12 months of follow-up. cTnT concentrations > or =0.02 ng/mL were considered abnormal, and a Tn index (highest cTnT measurement/0.02 ng/mL) was calculated. In 62 patients (54%), cTnT was consistently <0.02 ng/mL (group 1); 28 (24%) had a single abnormal cTnT result (group 2); and 25 (22%) had > or =2 abnormal cTnT results (group 3). At 18 months, CHF hospitalization-free survival was 63%, 46%, and 17%, respectively (P=0.0001). In a Cox proportional-hazards model, hospitalization for worsening CHF in the previous year (HR=2.1; 95% CI, 1.1 to 4.1), functional class III-IV (HR=2.3; 95% CI, 1.1 to 4.6), and number of abnormal cTnT samples (HR=1.6; 95% CI, 1.1 to 2.4) were independently associated with prognosis. A cTnT rise of 0.020 ng/mL in any sample was associated with an excess of 9% (95% CI, 1% to 18%) in the incidence of combined end point. CONCLUSIONS: Abnormal cTnT concentrations were detected in >50% of outpatients with advanced CHF. This ongoing myocardial necrosis was a strong predictor of worsening CHF, suggesting a role of cTnT-based monitoring to identify high-risk patients.