Impact of Chronic Pre-Treatment of Statins on the Level of Systemic Inflammation and Myocardial Perfusion in Patients Undergoing Primary Angioplasty (original) (raw)

Timing and Dose of Statin Therapy Define Its Impact on Inflammatory and Endothelial Responses During Myocardial Infarction

… and Vascular Biology, 2011

Objective-Clinical trials of statins during myocardial infarction (MI) have differed in their therapeutic regimes and generated conflicting results. This study evaluated the role of the timing and potency of statin therapy on its potential mechanisms of benefit during MI. Methods and Results-ST-elevation MI patients (nϭ125) were allocated into 5 groups: no statin; 20, 40, or 80 mg/day simvastatin starting at admission; or 80 mg/day simvastatin 48 hours after admission. After 7 days, all patients switched their treatment to 20 mg/day simvastatin for an additional 3 weeks and then underwent flow-mediated dilation in the brachial artery. As of the second day, C-reactive protein (CRP) differed between non-statin users (12.0Ϯ4.1 mg/L) and patients treated with 20 (8.5Ϯ4.0 mg/L), 40 (3.8Ϯ2.5 mg/L), and 80 mg/day (1.4Ϯ1.5 mg/L), and the daily differences remained significant until the seventh day (PϽ0.0001). The higher the statin dose, the lower the elevation of interleukin-2 and tumor necrosis factor-␣, the greater the reduction of 8-isoprostane and low-density lipoprotein(Ϫ), and the greater the increase in nitrate/nitrite levels during the first 5 days (PϽ0.001). Later initiation of statin was less effective than its early introduction in relation to attenuation of CRP, interleukin-2, tumor necrosis factor-␣, 8-isoprostane, and low-density lipoprotein(Ϫ), as well as in increase in nitrate/nitrite levels (PϽ0.0001). At the 30th day, there was no longer a difference in lipid profile or CRP between groups; the flow-mediated dilation, however, was proportional to the initial statin dose and was higher for those who started the treatment early (Pϭ0.001). Conclusion-This study demonstrates that the timing and potency of statin treatment during MI are key elements for their main mechanisms of benefit. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT00906451.

Effect of statin pretreatment on the outcome of ST-segment elevation myocardial infarction in patients without prior history of coronary artery disease

Hellenic journal of cardiology : HJC = Hellēnikē kardiologikē epitheōrēsē

Early statin treatment has beneficial effects on the prognosis after acute coronary syndromes. We investigated the impact of prior statin treatment on the outcome of patients without a prior history of coronary artery disease (CAD) who presented with ST-elevation myocardial infarction (STEMI) and were treated with thrombolysis. The study enrolled 1032 consecutive patients who satisfied the above criteria. They were categorized into two groups, based on their prior statin treatment for at least 3 months before admission: the statin pretreatment group (n=124) and the statin-naïve group (n=908). All patients received high-dose statins during hospitalization and were prescribed statins after discharge. The primary outcome was the incidence of successful thrombolysis, as expressed by the percentage of patients with 50% ST-segment resolution and complete retrosternal pain resolution at 90 minutes. Secondary outcomes included reduction in high-sensitivity C-reactive protein (hs-CRP) and CK...

452 Timing and Dose of Statin Therapy Define Its Impact on Inflammatory and Endothelial Responses During Myocardial Infarction

Atherosclerosis Supplements, 2011

Objective-Clinical trials of statins during myocardial infarction (MI) have differed in their therapeutic regimes and generated conflicting results. This study evaluated the role of the timing and potency of statin therapy on its potential mechanisms of benefit during MI. Methods and Results-ST-elevation MI patients (nϭ125) were allocated into 5 groups: no statin; 20, 40, or 80 mg/day simvastatin starting at admission; or 80 mg/day simvastatin 48 hours after admission. After 7 days, all patients switched their treatment to 20 mg/day simvastatin for an additional 3 weeks and then underwent flow-mediated dilation in the brachial artery. As of the second day, C-reactive protein (CRP) differed between non-statin users (1.2Ϯ4.

Effect of Previous Treatment With Statins on Outcome of Patients With ST-Segment Elevation Myocardial Infarction Treated With Primary Percutaneous Coronary Intervention

The American Journal of Cardiology, 2009

Beyond lipid-lowering effects, statins have favorable effects on platelets, endothelial function, plaque stability, and inflammation. These "pleiotropic" effects could contribute to microvascular function preservation during ischemia. Data are limited about the impact of previous treatment with statins on outcomes of patients with ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI). Accordingly, the aim was to evaluate the effect of previous statin treatment on clinical outcomes of such patients. A total of 950 consecutive patients with STEMI treated with primary PCI who were included in our primary PCI registry from January 2001 to July 2007 were studied. Excluded were patients with cardiogenic shock. Patients were allocated into 2 groups: those who received previous statin treatment (n ‫؍‬ 327) and those who did not (n ‫؍‬ 623). Patients who received previous statin treatment were older and more likely to be women; have diabetes, hypertension, hyperlipidemia, renal insufficiency, and anemia; or have had a previous myocardial infarction. Procedural characteristics were similar between the 2 groups. Despite the higher risk profile, patients who received previous statin treatment had a lower 30-day mortality rate (1.5% vs 3.8%; p ‫؍‬ 0.05). However, at 6 months, mortality differences were no longer evident and patients who received previous statin therapy had a higher rate of target-vessel revascularization (12.4% vs 7.6%; p ‫؍‬ 0.02). Multivariate analysis showed that previous statin treatment was associated with an odds ratio of 0.4 (95% confidence interval 0.13 to 0.96, p ‫؍‬ 0.045) for 30-day mortality. In conclusion, the present study suggested that previous therapy with statins in patients with STEMI treated using primary PCI may be associated with reduced short-term mortality. © 2009 Elsevier Inc. (Am J Cardiol 2009;103:165-169)

Clinical Benefit of Statin Pretreatment in Patients Undergoing Percutaneous Coronary Intervention

Circulation, 2011

Background— Previous studies suggested that statin pretreatment reduces cardiac events in patients undergoing percutaneous coronary intervention. However, most data were observational, and single randomized trials included limited numbers of patients. Methods and Results— We performed a collaborative meta-analysis using individual patient data from 13 randomized studies in which 3341 patients received either high-dose statin (n=1692) or no statin/low-dose statin (n=1649) before percutaneous coronary intervention, with all patients receiving statin therapy after intervention. Occurrence of periprocedural myocardial infarction, defined as postintervention creatine kinase–MB increase ≥3 times the upper limit of normal, and 30-day major adverse cardiac events (death, myocardial infarction, target-vessel revascularization) was evaluated. Incidence of periprocedural myocardial infarction was 7.0% in the high-dose statin versus 11.9% in the control group, which corresponds to a 44% risk re...

Statins and Their Role in Pre-Percutaneous Coronary Intervention

Current Cardiology Reports, 2010

Lipid-lowering therapy with statins reduces the risk of cardiovascular events in patients with coronary artery disease. Recent in vitro and in vivo studies demonstrated a low-density lipoprotein-independent action of this class of drugs, which appears to modulate endothelial function, inflammation, and thrombosis. Randomized studies showed a beneficial effect of short-term statin pretreatment in reducing periprocedural cardiac marker release in patients undergoing percutaneous coronary intervention (PCI). In particular, the ARMYDA (Atorvastatin for Reduction of Myocardial Damage During Angioplasty) investigatorsinitially in stable angina patients, then in patients with acute coronary syndrome, and then in patients already on chronic statin therapy-demonstrated an improvement in 30-day major adverse cardiac event rates, which were driven by a reduced rate of periprocedural myocardial infarction. Moreover, statin therapy at the time of PCI significantly decreased the incidence of contrast-induced nephropathy. These observations support high-dose statin pretreatment in all patients who are candidates for PCI.

Statin administration before percutaneous coronary intervention: impact on periprocedural myocardial infarction

European Heart Journal, 2004

Aims Peri-procedural non-Q-wave myocardial infarction is a frequent and prognostically important complication of percutaneous coronary intervention (PCI). It has been postulated that statins may reduce the rate of myocardial injury after PCI. Methods and Results Four hundred and fifty-one patients scheduled for elective PCI and not on statins were randomly assigned to either no treatment or to statin treatment. Statin administration was started at least 3 days before the procedure.Incidence of periprocedural myocardial injury was assessed by analysis of creatinine kinase myocardial isoenzyme (CK-MB: upper limit of normal [ULN] 3.5 ng/ml) and cardiac troponin I (cTn I, ULN 0.10 ng/ml) before, 6 and 12 h after the intervention. A large non-Q-wave myocardial infarction was defined as a CK-MB elevation >5 times ULN alone or associated with chest pain or ST segment or T wave abnormalities. Median CK-MB peak after PCI was 1.70 (interquartile ranges 1.10-3.70) ng/ml in the Statin group and 2.20 (1.30-5.60) ng/ml in the Control group (p = 0.015). Median peak of cTnI after PCI was 0.13 (0.05-0.45) ng/ml in the Statin group and 0.21 (0.06-0.85) ng/ml in the Control group (p = 0.033). The incidence of a large non-Q-wave myocardial infarction was 8.0% in the Statin group and 15.6% in the Control group (p = 0.012: OR = 0.47; 95% CI = 0.26-0.86). The incidence of cTnI elevation >5 times ULN was 23.5% in the Statin group and 32% in the Control group (p = 0.043: OR = 0.65; 95% CI = 0.42-0.98). By logistic regression analysis, the independent predictors of CK-MB