Abstract

IntroductionRecent studies have shown that in chronic kidney disease (CKD) 25(OH)D deficiency or insufficiency is a significant risk factor for cardiovascular diseases (CVDs), sudden cardiac death (SCD) and mortality. Premature ventricular complexes (PVCs) are very common in patients with CKD, hypertension, obesity, sleep apnea, and structural heart disease. Often PVCs in the structurally normal heart are considered benign, although they seem to be associated with a more than two-fold higher risk of cardiovascular complications, including stroke disease and death. AimIn the present study we aimed to evaluate the influence of different 25(OH)D levels on the changes of the numbers of PVCs in all patients, assessed by 24-hour-Holter monitoring 3months after β-blocker onset. Methods and resultsWe conducted a prospective, longitudinal study of 824 patients with PVCs and CKD (estimated glomerular filtration rate measured by MDRD equation, between 16 and 59mL/min/1.73m2). All patients were treated with a β-blocker (bisoprolol 10mg daily). We observed that the 3 groups presented a significant decrease in the number of PVCs from baseline 26,091±3327 (25(OH)D deficiency group), 25,902±3501 (25(OH)D insufficiency group), and 25,554±3637 (25(OH)D sufficiency group) to 20,554±3782, 19,885±3945 and 15,433±4059, respectively, after 3months of β-blocker therapy (P<0.0001 for the comparisons between time points in the same group). However at the 3rd month after bisoprolol onset, comparisons between 25(OH)D deficiency vs. 25(OH)D sufficiency groups showed a mean difference of 5121 PVCs (P<0.0001), and comparisons between 25(OH)D insufficiency vs. 25(OH)D sufficiency groups showed a mean difference of 4452 PVCs (P<0.0001). No difference was observed between 25(OH)D deficiency vs. 25(OH)D insufficiency groups (P=0.3181). ConclusionsWe suggest that the effectiveness of β-blocker treatment for PVCs in CKD patients was observed in all 25(OH)D levels. However, the responsiveness was higher in patients with a normal range of 25(OH)D in comparison to patients with deficiency or insufficiency in 25(OH)D levels. Whether vitamin D supplementation increases the efficacy of beta-blocker mediated suppression of PVCs requires further evaluation.

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