Intensive Atorvastatin Therapy Decreases No Reflow In Patients Undergoing Elective PCI Which Is Associated With Decreased CRP And Increased Adiponectin

Background:Outline of the Report on Cardiovascular Disease in China,2010, shows that the risk factors of cardiovascular disease (CVD) are increasing persistently in China. The morbidity and mortality of CVD are still at a high level. The burden of CVD is aggravated, and CVD has become an important issue of public health. So the prevention and treatment of CVD should be reinforced immediately. Coronary heart disease (CHD) is one of the main causes of death in CVD. The prevention and treatment of CHD is very important. Adiponectin and C reactive protein (CRP) are prognostic and predictive factors in CHD. APN and CRP displays various actions on the development of CHD. Statins have the effects of lipid-lowering, anti-inflammatory and plaque stabilization, which can decrease the risk of CHD.Objectives:Percutaneous coronary intervention (PCI) is a more important method of treatment of CHD, which can improve the symptoms of myocardial ischemia. slow flow/No reflow, which partly attributes to inflammatory injury, is a common complication in the patients undergoing PCI. When the blood flow of infarcted arterial reaches TIMI3, reperfusion is regarded as Success. Corrected TIMI Frame Count (CTFC) is an index introduced to quantitatively assess coronary blood flow in recent years. It is shown that intensive atorvastatin therapy could reduce inflammatory factors and improve the prognosis in patients undergoing PCI. Adiponectin (APN) is an adipose tissue-derived hormone, which displays protective actions on the development of CHD. APN attenuates inflammatory responses to multiple stimuli by modulating signaling pathways in variety of cell types. The anti-inflammatory properties of APN may be a major component of its beneficial effects on atherosclerosis. High sensitivity C-reactive protein (hs-CRP) is associated with atherosclerosis and lipoprotein altering therapy can decrease inflammatory markers. These findings are important which support the inflammatory disease hypothesis of atherosclerosis. Hs-CRP has been used to assess risk of CHD for clinical purposes. However, though statin therapy has an effect on CHD, many patients with CHD have a high CRP level. Intensive statin therapy would be an independent predictor of a lower hs-CRP irrespective of risk factor burden. However, the role of intensive atorvastatin therapy in patients undergoing elective PCI is still unclear. This study is to investigate whether intensive atorvastatin therapy could decrease the rate of slow flow/no reflow phenomenon and investigate the effect of intensive atorvastatin therapy on APN and hsCRP.Methods:78patients with stable angina, significant coronary artery disease, and the indication for elective coronary angioplasty were enrolled. All patients were randomly divided into intensive atorvastatin therapy group (39patients) and moderate atorvastatin therapy group (39patients). The patients in intensive atorvastatin therapy group were given atorvastatin80mg/d for2days before PCI, followed by40mg/d for30days after PCI. The patients in moderate atorvastatin therapy group were given atorvastatin40mg/d for2days before PCI, followed by20mg/d for30days after PCI. All the patients were followed up for6months. The30-day incidence of main end point events (death, myocardial infarction, unplanned revascularization, heart failure, stroke or acute coronary syndrome) and the incidence of slow flow/no reflow was recorded. Plasma levels of hs-CRP, adiponectin and myocardial injury markers (CK-MB and cTnI) were tested in the two groups.Results:The main end point events did not happened in the two groups after one month. No severe adverse effects were found in two groups. Both group increased the CK-MB and cTnI level after PCI. Moderate atorvastatin therapy increased the CK-MB and cTnI level (P<0.05, vs Intensive group). Both group were increased the plasma APN and HDL-C and decreased the hsCRP and LDL-C after3months therapy.3months hsCRP and LDL-C levels were significant lower in moderate group before versus after therapy(5.0±0.6vs3.5±0.5mg/L,P<0.05;3.9±0.6vs2.8±0.6mmol/L,P<0.05).3months hsCRP and LDL-C levels were significant lower in intensive group before versus after therapy (4.9±0.6vs1.7±0.4mg/L,P<0.05;4.0±0.6vs1.7±0.6,P<0.05).3months hsCRP and LDL-C levels were significant lower in Intensive group versus moderate group (1.7±0.4vs3.4±0.5,P<0.05;2.8±0.6vs1.7±0.5, P<0.05).3months APN and HDL-C levels were significant higher in moderate group before versus after therapy (3.7±0.9vs5.7±0.9,P<0.05;0.8±0.3vs1.2±0.4,P<0.05).3months APN and HDL-C levels were significant higher in Intensive group before versus after therapy (3.7±0.8vs9.8±1.1,P<0.05;0.8±0.3vs1.7±0.3,P<0.05).3months APN and HDL-C levels were significant higher in Intensive group versus moderate group (9.8±1.1vs5.7±0.9,P<0.05; 1.7±0.3vs1.2±0.4,P<0.05). Intensive atorvastatin therapy decreased the incidence of slow flow/no reflow compared with moderate atorvastatin therapy (2/39in intensive atorvastatin therapy group,5/39in moderate atorvastatin therapy group,P<0.05).Conclusions:Intensive statin therapy is effective and safe in CHD patients. Intensive statin therapy can significantly increase plasma APN and decrease hsCRP. The incidence of slow flow/no reflow were negatively correlated with APN level and positively correlated with CRP level. Intensive statin therapy significantly decreases the incidence of slow flow/no reflow in patients undergoing elective PCI, which is possibly associated with decreased CRP and increased plasma adiponectin.