Loading Dose Of Atorvastatin Research Articles

GW25-e4571 The effects of a loading-dose of atorvastatin before primary percutaneous coronary intervention on coronary flow and serum sCD40L in patients with ST-segment elevation myocardial infarction

GW25-e4571 The effects of a loading-dose of atorvastatin before primary percutaneous coronary intervention on coronary flow and serum sCD40L in patients with ST-segment elevation myocardial infarction

Impact of a High Loading Dose of Atorvastatin on Contrast-Induced Acute Kidney Injury

A single high loading dose of atorvastatin administered ≤24 hours before contrast media (CM) exposure reduces the rate of contrast-induced acute kidney injury (CIAKI). The benefit is only seen in patients at low to medium risk.

Administration of a Loading Dose of Atorvastatin Before Percutaneous Coronary Intervention Prevents Inflammation and Reduces Myocardial Injury in STEMI Patients: A Randomized Clinical Study

BackgroundAdministration of a loading dose of atorvastatin 80 mg/d has been shown to be beneficial in patients with stable coronary artery disease and acute coronary syndromes. However, little is known about the impact and mechanism behind the beneficial effects of loading-dose atorvastatin treatment before percutaneous coronary intervention (PCI), especially for those patients experiencing cardiovascular inflammation in ST-segment elevation myocardial infarction (STEMI). ObjectiveThe goal of this randomized clinical study was to investigate whether, before emergency PCI, administration of loading-dose atorvastatin therapy in STEMI patients inhibits inflammation and improves cardiac function during 24 weeks of follow-up. MethodsA total of 102 STEMI patients were enrolled into 3 groups: group A (n = 32) received 80 mg of atorvastatin before emergency PCI, post-PCI follow-up atorvastatin 40 mg for 4 weeks, and atorvastatin 20 mg for 20 weeks; group B (n = 32) received no pre-PCI loading dose of atorvastatin but did receive atorvastatin 40 mg for 4 weeks and then atorvastatin 20 mg for 20 weeks; and group C (n = 38) received only post-PCI atorvastatin 20 mg for 24 weeks. ResultsNo differences were found in baseline demographic and angiographic characteristics among the 3 groups. Patients in group A had the lowest plasma levels of high-sensitivity C-reactive protein (hs-CRP), B-type natriuretic peptide (BNP), and matrix metalloproteinase type 9 (MMP-9) (P < 0.05). Patients in group A also showed improvement in heart performance, with significant increases in their left ventricular ejection fraction. To a lesser extent, group B displayed reductions in the plasma levels of hs-CRP, BNP, and MMP-9 at later time points (P < 0.05). Compared with those in group C, patients in group B also exhibited significant improvement in left ventricular ejection fraction (P < 0.05). ConclusionsLoading-dose atorvastatin therapy before emergency PCI reduced the inflammatory response and myocardial dysfunction in these STEMI patients by lowering hs-CRP, BNP, and MMP-9. Pre-PCI loading-dose atorvastatin treatment may help prevent inflammatory response and improve cardiac function in patients with acute coronary syndromes undergoing emergency PCI. ClinicalTrials.gov identifier: NCT01334671.

Effect of a Single High Loading Dose of Rosuvastatin on Percutaneous Coronary Intervention for Acute Coronary Syndromes

A high loading dose of atorvastatin has been confirmed to reduce postprocedural events in patients undergoing percutaneous coronary intervention (PCI). In this study, we sought to investigate the protective effects of rosuvastatin in patients with acute coronary syndromes (ACS) undergoing PCI and to determine the effect of rosuvastatin pretreatment on the postprocedural levels of high-sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), and monocyte chemotactic protein 1 (MCP-1). A total of 125 patients with non-ST-segment elevation ACS were randomized to pretreatment with rosuvastatin (20 mg 2-4 hours before PCI [n = 62]) or placebo (n = 63). All the patients received subsequent long-term rosuvastatin treatment (10 mg/d). The main end point of the trial was the 30-day incidence of major adverse cardiac events (death, myocardial infarction, or unplanned revascularization). Plasma levels of hs-CRP, IL-6, and MCP-1 were detected before PCI and 6 hours, 24 hours, and 3 days after PCI. The primary end point occurred in 8.1% of the patients in the rosuvastatin arm and 22.2% in the placebo arm (P < .01); this difference was entirely attributed to a reduced incidence of myocardial infarction (8.1% vs 22.2%; P < .01). The postprocedural elevation in creatine kinase-MB and troponin I was also significantly lower in the rosuvastatin group at 6 hours, 24 hours, and 3 days. Plasma levels of hs-CRP, IL-6, and MCP-1 increased significantly after PCI in both the rosuvastatin and control groups; however, the postprocedural elevations in hs-CRP and IL-6 levels were significantly lower in the rosuvastatin group than the control group. A single, high dose (20 mg) of rosuvastatin prior to PCI reduces postprocedural myocardial injury in patients with ACS, with a concomitant attenuation of the postprocedural increase in hs-CRP and IL-6 levels.

Circulation: Clinical Summaries

<i>Circulation:</i> Clinical Summaries

Impact of a High Loading Dose of Atorvastatin on Contrast-Induced Acute Kidney Injury

The role of statins in the prevention of contrast-induced acute kidney injury (CIAKI) is controversial. First, we investigated the in vivo effects of atorvastatin on CIAKI. Patients with chronic kidney disease enrolled in the Novel Approaches for Preventing or Limiting Events (NAPLES) II trial were randomly assigned to (1) the atorvastatin group (80 mg within 24 hours before contrast media [CM] exposure; n=202) or (2) the control group (n=208). All patients received a high dose of N-acetylcysteine and sodium bicarbonate solution. Second, we investigated the in vitro effects of atorvastatin pretreatment on CM-mediated modifications of intracellular pathways leading to apoptosis or survival in renal tubular cells. CIAKI (ie, an increase >10% of serum cystatin C concentration within 24 hours after CM exposure) occurred in 9 of 202 patients in the atorvastatin group (4.5%) and in 37 of 208 patients in the control group (17.8%) (P=0.005; odds ratio=0.22; 95% confidence interval, 0.07-0.69). CIAKI rate was lower in the atorvastatin group in both diabetics and nondiabetics and in patients with moderate chronic kidney disease (estimated glomerular filtration rate, 31-60 mL/min per 1.73 m(2)). In the in vitro model, pretreatment with atorvastatin (1) prevented CM-induced renal cell apoptosis by reducing stress kinases activation and (2) restored the survival signals (mediated by Akt and ERK pathways). A single high loading dose of atorvastatin administered within 24 hours before CM exposure is effective in reducing the rate of CIAKI. This beneficial effect is observed only in patients at low to medium risk.

The effects of high loading and high maintenance doses of atorvastatin on platelet activity and vascular endothelium function as well as prognosis in patients with acute coronary syndrome undergoing percutaneous coronary intervention

ObjectiveTo observe the effects of high loading doses and high maintenance dose of atorvastatin on platelet activity, function of vascular endothelium and inflammation as well as prognosis in patients with...

Effects of loading dose of atorvastatin before percutaneous coronary intervention on periprocedural myocardial injury

To investigate the effects of loading dose of atorvastatin on periprocedural myocardial injury and inflammatory reaction in patients with non-ST segment elevation (NSTE) acute coronary syndromes (unstable angina or NSTE acute myocardial infarction). A total of 81 patients with NSTE-acute coronary syndromes were randomly divided into the pretreatment with atorvastatin group [80 mg 12 h before percutaneous coronary intervention (PCI), with a further 40 mg preprocedure dose] (n=41) or the placebo group (n=40). The main end point was a 30-day incidence of major adverse cardiac events (cardiac death, nonfatal acute myocardial infarction, or revascularization with either PCI or coronary artery bypass grafting). Creatine kinase-MB, cardiac troponin I, and high-sensitivity C-reactive protein levels were measured at the baseline and at 8 and 24 h after the procedure. Major adverse cardiac events occurred in 2.4% of patients in the atorvastatin group and 22.5% of those in the placebo group (P=0.0161). This difference was mostly because of reduction in the incidence of myocardial infarction (2.4 vs. 20.0%; P=0.0307). Markers of the two groups were elevated after PCI; however, the higher values of creatine kinase-MB, cardiac troponin I, and high-sensitivity C-reactive protein in the atorvastatin treatment group were significantly lower than those in the placebo group (P<0.01). Short-term pretreatment with a high dose of atorvastatin significantly reduces procedural myocardial injury in early PCI.

Effect of different loading doses of atorvastatin on percutaneous coronary intervention for acute coronary syndromes

Percutaneous coronary intervention (PCI)-induced myocardial damage is associated with late cardiovascular events. Treatment with atorvastatin before PCI can reduce myocardial damage during the peri-PCI period. To compare the safety and myocardial effects of different atorvastatin loading doses and dosing frequency before PCI in non-ST segment elevation acute coronary syndrome (NSTE-ACS) patients. Eighty NSTE-ACS patients were randomly divided into four groups (20 patients per group). The control group was given 40 mg atorvastatin each night. The three loading dose groups were treated the same as in the control group, but were given 80 mg atorvastatin 12 h before PCI (lowload group) in combination with 40 mg atorvastatin 2 h to 4 h before PCI (mid-load group) or 60 mg atorvastatin 2 h to 4 h before PCI (high-load group). All patients underwent PCI within 48 h to 72 h of admission, and received 40 mg atorvastatin for at least one month after PCI. Changes in myocardial markers and highly sensitive C-reactive protein were analyzed. Patients were followed up for 30 days to monitor the incidence of major adverse cardiac events (MACE). No deaths or revascularizations were recorded. The incidences of MACE differed significantly between the four groups (40%, 25%, 10% and 0% for the control, low-load, mid-load and high-load groups, respectively; P<0.05). The incidence of MACE and cardiac troponin I level above the normal range, and post-PCI increases in creatine kinase-MB and highly sensitive C-reactive protein were significantly higher in the control group than in the high-load group (all P<0.007). The post-PCI alanine aminotransferase levels in all four groups were significantly higher than the pre-PCI levels, but were within normal ranges. No myalgia or myasthenia was observed. The results of the present study show that short-term atorvastatin loading before PCI was well tolerated and had beneficial myocardial effects in patients with NSTE-ACS.

E0468 Effect of different loading doses of atorvastatin on percutaneous coronary intervention for acute coronary syndromes

BackgroundPercutaneous coronary intervention (PCI)-induced myocardial damage is a major cause of late cardiovascular events. Treatment with atorvastatin before PCI can reduce myocardial damage during the peri-PCI period. Objectives: To compare...

Novel Approaches for Preventing or Limiting Events (Naples) II Trial: Impact of a Single High Loading Dose of Atorvastatin on Periprocedural Myocardial Infarction

Atorvastatin administered at least 7 days before the percutaneous coronary intervention (PCI) reduces the rate of periprocedural myocardial infarction (MI). It is unknown whether a single, high (80 mg) loading dose of atorvastatin may reduce the rate of periprocedural MI. Periprocedural MI is a prognostically important complication of PCI. The day before the elective PCI, 668 statin-naive patients were randomly assigned to atorvastatin 80 mg (atorvastatin group; n = 338) or no statin treatment (control group; n = 330). Creatine kinase-myocardial isoenzyme (CK-MB) (upper limit of normal [ULN] 3.5 ng/ml) and cardiac troponin I (ULN 0.10 ng/ml) were assessed before and 6 and 12 h after the intervention. Periprocedural MI was defined as a CK-MB elevation >3x ULN alone or associated with chest pain or ST-segment or T-wave abnormalities. The incidence of a periprocedural MI was 9.5% in the atorvastatin group and 15.8% in the control group (odds ratio: 0.56; 95% confidence interval: 0.35 to 0.89; p = 0.014). Median CK-MB peak after PCI was 2.10 ng/ml (interquartile range 1.00 to 12.50 ng/ml) in the atorvastatin group and 3.20 ng/ml (interquartile range 1.37 to 16.07 ng/ml) in the control group (p = 0.014). The incidence of cardiac troponin I elevation >3x ULN was 26.6% in the atorvastatin group and 39.1% in the control group (odds ratio: 0.56; 95% confidence interval: 0.40 to 0.78; p < 0.001). A single, high (80 mg) loading (within 24 h) dose of atorvastatin reduces the incidence of periprocedural MI in elective PCI.