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Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
[Atorvastatin improves reflow after percutaneous coronary intervention in patients with acute ST-segment elevation
1Department of Cardiology, Tongling People's Hospital of Anhui Province, Tongling 244000, China.
Insights
High-dose atorvastatin significantly reduced serum uric acid levels and improved coronary artery reflow in ST-segment elevation myocardial infarction (STEMI) patients undergoing percutaneous coronary intervention (PCI). Hyperuricemia was identified as a risk factor for no-reflow post-PCI.
Area of Science:
- Cardiology
- Pharmacology
- Biochemistry
Background:
- Acute ST-segment elevation myocardial infarction (STEMI) is a critical condition requiring timely reperfusion.
- Percutaneous coronary intervention (PCI) is a primary treatment, but the no-reflow phenomenon can compromise outcomes.
- Serum uric acid levels have been implicated in cardiovascular disease, but their role in PCI outcomes requires further elucidation.
Purpose of the Study:
- To evaluate the impact of atorvastatin dosage on coronary artery reflow in STEMI patients post-PCI.
- To investigate the relationship between serum uric acid levels, atorvastatin treatment, and the incidence of no-reflow.
- To determine if hyperuricemia is an independent risk factor for no-reflow after PCI in STEMI patients.
Main Methods:
- A randomized controlled trial involving 114 STEMI patients undergoing primary PCI.
- Patients received either a routine dose (20 mg) or a high dose (80 mg) of atorvastatin before PCI.
- Subgroup analysis was performed based on initial serum uric acid levels (normal vs. hyperuricemia); changes in uric acid and reflow were assessed.
Main Results:
- Both atorvastatin doses reduced serum uric acid levels, with a more significant decrease observed in hyperuricemia patients treated with the high dose.
- The high-dose atorvastatin group showed a significantly lower incidence of no-reflow (11.9%) compared to the routine dose group (21.8%).
- Logistic regression identified hyperuricemia as an independent risk factor for no-reflow post-PCI (OR=1.01, 95% CI: 1.01-1.11).
Conclusions:
- High-dose atorvastatin effectively lowers serum uric acid levels in STEMI patients.
- High-dose atorvastatin improves coronary artery reflow following PCI in STEMI patients.
- Managing hyperuricemia may be crucial for improving PCI outcomes in STEMI patients.
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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