atorvastatin improves reflow after percutaneous coronary intervention in patients with acute st segment elevation myocardial infarction by decreasing serum uric acid level
Male
Percutaneous Coronary Intervention
Heptanoic Acids
Risk Factors
Acute Disease
Atorvastatin
Humans
ST Elevation Myocardial Infarction
Female
Myocardial Reperfusion
Pyrroles
Hyperuricemia
Uric Acid
DOI:
10.3785/j.issn.1008-9292.2016.09.12
Publication Date:
2016-05-25
AUTHORS (5)
ABSTRACT
Objective: To investigate the effect of atorvastatin on reflow in patients with acute ST-segment elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI) and its relation to serum uric acid levels. Methods: One hundred and fourteen STEMI patients undergoing primary PCI were enrolled and randomly divided into two groups:55 cases received oral atorvastatin 20 mg before PCI (routine dose group) and 59 cases received oral atorvastatin 80 mg before PCI (high dose group). According to the initial serum uric acid level, patients in two groups were further divided into normal uric acid subgroup and hyperuricemia subgroup. The changes of uric acid level and coronary artery blood flow after PCI were observed. Correlations between the decrease of uric acid, the dose of atorvastatin and the blood flow of coronary artery after PCI were analyzed. Results: Serum uric acid levels were decreased after treatment in both groups (all P<0.05), and patients with hyperuricemia showed more significant decrease in serum uric acid level (P<0.05). Compared with the routine dose group, serum uric acid level in patients with hyperuricemia decreased more significantly in the high dose group (P<0.05), but no significant difference was observed between patients with normal serum uric acid levels in two groups (P>0.05). Among 114 patients, there were 19 cases without reflow after PCI (16.7%). In the routine dose group, there were 12 patients without reflow, in which 3 had normal uric acid and 9 had high uric acid levels (P<0.01). In the high dose group, there were 7 patients without reflow, in which 2 had normal uric acid and 5 had high uric acid (P<0.05). Logistic regression analysis showed that hyperuricemia was one of independent risk factors for no-reflow after PCI (OR=1.01, 95% CI:1.01-1.11, P<0.01). The incidence of no-flow after PCI in the routine dose group was 21.8% (12/55), and that in the high dose group was 11.9% (7/59) (P<0.01). Conclusion: High dose atorvastatin can decrease serum uric acid levels and improve reflow after PCI in patients with STEMI.
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