Effects of enalapril and folic acid tablets on hypertension patients with hyperhomocysteinemia and paroxysmal atrial fibrillation

Objective To observe the clinical effects of enalapril and folic acid tablets on hypertension patients with high homocysteine (Hcy) level and paroxysmal atrial fibrillation, so as to provide evidence for diagnosis and treatment. Methods A total of 108 hypertension patients with high Hcy level and paroxysmal atrial fibrillation were randomly divided into three groups (n=36), and treated with amlodipine, enalapril or enalapril folic acid tablets for 12 months. Their blood pressure, Hcy, left atrial diameter (LAD), left atrial function index (LAFI), left atrial volume index (LAVI), diastolic global diastolic strain (Sg), systolic strain rate (SRs), standard deviations of time to peak global diastolic strain rate (TPSRg-SD), and standard deviations of time to peak global diastolic strain rate (TPSRg-SD) before and after treatment were detected. Results There were 106 out of 108 patients who finished the study. After treatment with amlodipine, enalapril or enalapril and folic acid, the occurrence of atrial fibrillation significantly decreased in the three groups, which were statistically different (P<0.01). The enalapril and folic acid group showed better protective effects than the other two groups. Compared with the amlodipine group, the levels of LAD and NT-proBNP in the enalapril group and the enalapril and folic acid group significantly decreased (P<0.01). Furthermore, compared with those in the enalapril group and the amlodipine group, remarkable decreases were found in Hcy, LAVI, TPSRg-SD, and TPSRs-SD in the enalapril and folic acid group, but increases were seen in LAFI, Sg, and SRs in the enalapril group and the amlodipine group (P<0.05). There were no reports concerning cardiac dysfunction, stroke or death in each group. Conclusions Enalapril and folic acid tablets can reduce the occurrence of atrial fibrillation in hypertension patients with hyperhomocysteinemia and paroxysmal atrial fibrillation, which may be associated with the mechanism of inhibiting atrial remodeling.