A meta-analysis of 15 RCTs undertaken in patients with cardiomyopathy in the general population[15] (all but one trial was for primary prevention and one was an implantable cardioverter defibrillator (ICD) trial) reported that amiodarone led to reduced SCD risk (7.1% vs 9.7%, OR 0.71, P < 0.001). Serious side effects were present, in particular pulmonary (2.9% in treatment vs 1.5% control; OR = 1.97, P = 0.002) and thyroid toxicity (3.6% vs 0.4%; OR = 5.68, P < 0.001). As a result, amiodarone is no longer the first-line agent for arrhythmia control in the general

population. No RCT data exist for its use in CKD-5D specifically. Consequently, amiodarone is used in line with current guidelines for use in the general population. Prolonged QT, QTc, QT dispersion (difference between maximum and minimum QT interval) and torsade de pointes FK866 price may contribute to SCD. Medications such as typical and atypical antipsychotics, sotalol or substances inhibiting

the metabolism/excretion of QT prolonging medications such as grapefruit juice, can prolong QT interval. Data are limited on the association of these medications and SCD, possibly related to low overall use. In DOPPS, only amiodarone was associated with SCD (likely due to confounding by indication), with HR = 1.44, 95% CI = 1.16–1.81; P = 0.001. Prescriptions of other QT prolonging medications did not show any association with SCD (HR = 1.10; 95% CI = 0.94–1.28, P = 0.22).[6] CAD is common in patients with CKD-5D. In one cohort, 64% of haemodialysis find more patients who suffered SCD had CAD.[16] Haemodialysis patients with ≥75% coronary stenosis have a higher frequency of induction and persistence of Lown Class 4 ventricular arrhythmia during and after dialysis compared mafosfamide with those without coronary stenosis.[17] Individual RCTs have failed to show benefit of lipid-lowering

therapy (LLT) in CKD-5D. A recent meta-analysis assessed LLT compared with placebo in dialysis patients. There were 7051 patients from three RCs: 4D (the German Diabetes and Dialysis Study), AURORA (A Study to Evaluate the Use of Rosuvastatin in Subjects on Regular Hemodialysis: An Assessment of Survival and Cardiovascular Events) and SHARP (the Study of Heart and Renal Protection).[18] OR for atherosclerotic cardiovascular event was 0.89 (95% CI = 0.80–0.99, P = 0.04), stroke was 1.11 (95% CI = 0.85–1.46, P = 0.45) and all-cause mortality was 0.97 (95% CI = 0.88–1.06, P = 0.49) when treated with LLT. Therefore, LLT may be useful in dialysis patients to reduce the risk of atherosclerotic events; however, as the authors note, this risk reduction is lower than that quoted in general population studies (relative risk, RR = 0.80) or non-dialysis-dependent CKD (RR = 0.83). This may reflect the increased prevalence of non-atherosclerotic cardiovascular disease such as LVH and vascular stiffness/calcification in CKD-5D (Fig. 1). The latter may also explain why there was no survival difference between arms in the meta-analysis.