Anatolian journal of cardiology · 2017
Fluvastatin therapy could not decrease progression of paroxysmal atrial fibrillation in non-valvular disease patients.
СтатьяРандомизированное исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Tan Qiang, Zhang Shuangyue, Zou Xiaoyi, Zhao Jun, Hao Jia, Sun Qian
Аннотация
OBJECTIVE: This study aimed to evaluate whether fluvastatin therapy could decrease the probability of atrial fibrillation (AF) progression from paroxysmal AF to permanent AF and decrease the recurrence frequency of AF.
METHODS: Analyses were performed using two-tailed Student's t test or Mann-Whitney U tests. Categorical variables were compared with the χ2 statistics or Fisher's exact test. Patients with paroxysmal AF were randomized case-control, prospective into either the fluvastatin group (n=61) or control group (n=57). Patients were followed up for 24 months. The primary endpoint event was paroxysmal AF that progressed to permanent AF. Secondary endpoints were AF recurrence, cardiac dysfunction, stroke, or death.
RESULTS: There were no differences in AF progression (fluvastatin group, 8.19% vs. control group, 12.51%; p>0.05) and stroke (fluvastatin group. 6.55% vs.
CONTROL GROUP: 8.77%; p>0.05). Patients in the fluvastatin group had a lower rate of AF recurrence (fluvastatin group, 24.59% vs. control group, 49.12%; p<0.05) and a lower rate of cardiac dysfunction (fluvastatin group, 6.55% vs. control group, 19.29%; p<0.05). Death did not occur in both the groups. After 1 week of fluvastatin therapy, C-reactive protein (CRP) and homocysteine (HCY) levels were lower in the fluvastatin group than in the control group. At 24 months of follow-up, CRP and HCY levels remained lower in the fluvastatin group than in the control group. The number of endothelial progenitor cells (EPCs) increased in the fluvastatin group compared with that in the control group (fluvastatin group, 72.27±12.49 counts/105 vs. control group, 57.45±8.24 counts/105, p=0.001).
CONCLUSION: Fluvastatin therapy could not decrease AF progression. However, it could decrease the recurrence frequency of paroxysmal AF and cardiac dysfunction. This may occur because of depressing inflammation and improving circulating EPCs.
METHODS: Analyses were performed using two-tailed Student's t test or Mann-Whitney U tests. Categorical variables were compared with the χ2 statistics or Fisher's exact test. Patients with paroxysmal AF were randomized case-control, prospective into either the fluvastatin group (n=61) or control group (n=57). Patients were followed up for 24 months. The primary endpoint event was paroxysmal AF that progressed to permanent AF. Secondary endpoints were AF recurrence, cardiac dysfunction, stroke, or death.
RESULTS: There were no differences in AF progression (fluvastatin group, 8.19% vs. control group, 12.51%; p>0.05) and stroke (fluvastatin group. 6.55% vs.
CONTROL GROUP: 8.77%; p>0.05). Patients in the fluvastatin group had a lower rate of AF recurrence (fluvastatin group, 24.59% vs. control group, 49.12%; p<0.05) and a lower rate of cardiac dysfunction (fluvastatin group, 6.55% vs. control group, 19.29%; p<0.05). Death did not occur in both the groups. After 1 week of fluvastatin therapy, C-reactive protein (CRP) and homocysteine (HCY) levels were lower in the fluvastatin group than in the control group. At 24 months of follow-up, CRP and HCY levels remained lower in the fluvastatin group than in the control group. The number of endothelial progenitor cells (EPCs) increased in the fluvastatin group compared with that in the control group (fluvastatin group, 72.27±12.49 counts/105 vs. control group, 57.45±8.24 counts/105, p=0.001).
CONCLUSION: Fluvastatin therapy could not decrease AF progression. However, it could decrease the recurrence frequency of paroxysmal AF and cardiac dysfunction. This may occur because of depressing inflammation and improving circulating EPCs.