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Recently, we evaluated patients who had received a dual chamber pacemaker implant due to sinus node disease or 3rd/2nd degree type 2 atrioventricular block in chronic kidney disease (CKD) stages 2, 3 and 4. We observed that the sustained ventricular tachycardia episodes only occurred in patients with CKD stage 4, suggesting that the most advanced the stage of CKD, greater the incidence of malignant arrhythmias [1].Kidney disease induces cardiac remodeling including left ventricular hypertrophy (LVH) and heart fibrosis. Several clinical studies, including those who recruited participants with mild-to-moderate reduction in estimated glomerular filtration rate (eGFR), showed an independent association between CKD and LVH [2-5]. Specifically, there is a progressive increase in the prevalence of LVH, and left ventricular mass increased when the eGFR decreases. In addition, among participants with more advanced kidney disease on dialysis, magnetic resonance imaging (MRI) with contrast demonstrates a diffuse pattern image with gadolinium uptake suggestive of fibrosis and non-ischemic cardiomyopathy [6]. The pathogenesis of these conditions is considered multifactorial, and the presence of commonly associated comorbidities, such as hypertension, diabetes mellitus, and anemia, explain only part of the left ventricular remodeling [7-9]. The molecular basis for these changes includes activation of growth factors, protooncogenes, plasma norepinephrine, cytokines, and angiotensin II. These factors regulate intracellular processes that accelerate cardiac hypertrophy, myocardial fibrosis, and apoptosis [10,11]. Any LVH and cardiac fibrosis have been linked to increased risk of sustained ventricular arrhythmias and predisposition to SCD [12-16]. Structural changes can alter the electrophysiological properties of the myocardium. The myocardial fibrosis disrupts the normal architecture and results in a decrease in conduction velocity through the diseased tissue [17]. This condition can form heterogeneous areas of conduction and depolarization that can sustain a re-entrant arrhythmia, such as ventricular tachycardia [14,15,18]. These structural changes in cardiac conduction delay ventricular activation and create late potentials in the terminal portion of the QRS complex. Furthermore, these low amplitude signals, which may be detected using a high-resolution electrocardiogram, were identified in 25% of patients on dialysis [19].

Electrical Left Ventricular Mapping in Patients without CKD and with different stages of CKD