CKD and sudden cardiac death: epidemiology, mechanisms, and therapeutic approaches

Abstract

Multiple studies demonstrate a strong independent association between CKD and cardiovascular events including death, heart failure, and myocardial infarction. This review focuses on recent clinical studies that expand this spectrum of adverse cardiovascular events to include ventricular arrhythmias and sudden cardiac death. In addition, experimental models suggest structural remodeling of the heart and electrophysiologic changes in this population. These processes may explain the increased arrhythmic risk in kidney disease and aid in identifying patients who are at higher risk for sudden cardiac death. Finally, we review here the data to support the use of pharmacologic and device-based therapies for both the primary and secondary prevention of sudden cardiac death.

Figure 1.

Cystatin C–based eGFR and SCD. The SCD rate increased across cystatin C tertiles: 0.10% per year, 0.25% per year, and 0.32% per year.

Figure 2.

Overview of SCD and kidney dysfunction.

Figure 3.

Mortality rates according to kidney function and ICD status. In this subgroup analysis from the MADIT-II study, mortality rates increased across eGFR categories in both the ICD and conventional treatment groups. In addition, mortality was significantly lower in the ICD group compared with the conventional therapy group in patients with an eGFR >35 ml/min per 1.73 m².

Figure 4.

Mortality rates in ESRD patients who had a history of cardiac arrest. “Number at risk” reflects the number of patients who survived to each time interval (i.e., 12, 24, 36, and 48 months). The 1-, 2-, 3-, 4-, and 5-year survival in the ICD group was 71%, 53%, 36%, 25%, and 22%, respectively; in the no-ICD group, it was 49%, 33%, 23%, 16%, and 12% (P<0.001), respectively.