Abstract
Background: Coronary slow flow (CSF) is characterized by reduced coronary circulation and delayed contrast media opacity during angiography. Inflammatory responses have been observed in CSF. The correlation between lipoprotein-associated phospholipase A2 (LpPLA2) as a vascular inflammatory factor and the prognosis of CSF patients remains unclear. This study aims to investigate the potential correlation between plasma LpPLA2 levels and the occurrence of major adverse cardiovascular events (MACE) in CSF patients.
Methods: A retrospective study was conducted on 285 patients with CSF who were admitted to Anqing Municipal Hospital from January 2019 to March 2023. LpPLA2 plasma levels and baseline data were collected from hospital records, mean thrombolysis in myocardial infarction frame count (mTFC) was calculated for each patient. Follow-up was conducted by telephone call or cardiology clinic data, and the occurrence and timing of MACE were recorded.
Results: The median follow-up duration was 25 (95%CI: 23-27) months. During follow-up, MACE occurred in 54 patients (18.9%), including 4 individuals had non-fatal myocardial infarction, 6 had arrhythmias (4 of atrial fibrillation, 2 of frequent ventricular premature beats), and 44 had rehospitalizations due to unstable angina pectoris. No cardiac death or cerebrovascular events occurred during follow-up. We categorized LpPLA2 into quartiles, and multivariable adjusted Cox models showed an association between LpPLA2 levels and MACE incidence among CSF patients. Compared to the lowest quartiles, the hazard ratios (HR) for the highest quartiles of LpPLA2 levels was 3.34(95%CI: 1.09-10.22) (p-trend < 0.01). Though the restricted cubic spline (RCS) curve indicates a linear relationship between LpPLA2 and MACE incidence in patients with CSF (p for non-linearity = 0.212), the risk of MACE was relatively flat until 247.7 ng/ml of predicted LpPLA2 levels and increased afterwards, with a HR of 1.78 (95%CI: 1.17 to 2.71) per standard deviation. Kaplan-Meier survival assessments revealed that patients in the highest LpPLA2 quartile exhibited a worse prognosis for MACE compared to those in the lower quartiles of LpPLA2 levels (log-rank p = 0.002). Additionally, multivariable Cox regression analyses identified mTFC, LDL-C, and diabetes as other factors associated with occurrence of MACE in patients with CSF.
Conclusion: Elevated plasma LpPLA2 levels may serve as an independent predictor of MACE in patients with CSF. In addition to LpPLA2, dyslipidemia, diabetes, and mTFC may also be correlated with the prognosis of CSF.