The effect of the physical activity on polymorphic premature ventricular complexes in chronic kidney disease

BACKGROUND: Polymorphic premature ventricular complexes (PVCs) are very common, appearing most frequently in patients with hypertension, obesity, sleep apnea, and structural heart disease. Sympathetic hyperactivity plays a critical role in the development, maintenance, and aggravation of ventricular arrhythmias. Endurance exercise training clearly lowers sympathetic activity in sympatho-excitatory disease states and may be tolerated by patients with chronic kidney disease (CKD). METHODS: We assessed 40 CKD patients with hypertension with polymorphic PVCs. Patients underwent a complete medical history and physical examination. We evaluated the effectiveness of β blocker only or β blocker + exercise during 12 months of follow-up regarding the changes of the numbers of PVCs and mean heart rate (HR) by 24-hour-Holter. RESULTS: We observed in the β blocker group a significant decrease in the number of polymorphic PVCs from baseline 36,515 ± 3,518 to 3, 6, 9 and 12 months of follow-up, 28,314 ± 2,938, 23,709 ± 1,846, 22,564 ± 1,673, and 22,725 ± 1,415, respectively (P < 0.001). In the β blocker + exercise group a significant decrease in the number of polymorphic PVCs also occurred from baseline 36,091 ± 3,327 to 3, 6, 9 and 12 months of follow-up, 29,252 ± 3,211, 20,948 ± 2,386, 14,238 ± 3,338, and 6,225 ± 2,319, respectively (P < 0.001). Comparisons between the two groups at the same time point showed differences from the sixth month onwards: the 6th (Δ = −2,761, P = 0.045), 9th (Δ = −8,325, P < 0.001) and 12th (Δ = −16,500, P < 0.001) months. There was an improvement during the 12 months of follow-up vs. baseline, after the β blocker or β blocker + exercise in mean 24-hour HR Holter monitoring, creatinine values, eGFR, and ACR. CONCLUSION: Polymorphic PVCs may be modifiable by physical activity in CKD patients with hypertension without structural heart disease.

Chronic kidney disease and risk factors responsible for sudden cardiac death: a whiff of hope?

Several studies have shown a strong independent association between chronic kidney disease (CKD) and cardiovascular events, including death, heart failure, and myocardial infarction. Recent clinical trials extend this range of adverse cardiovascular events, also including ventricular arrhythmias and sudden cardiac death. Furthermore, other studies suggest structural remodeling of the heart and electrophysiological alterations in this population. These processes may explain the increased risk of arrhythmia in kidney disease and help to identify patients who are at increased risk of sudden cardiac death. Sympathetic hyperactivity is well known to increase cardiovascular risk in CKD patients and is a hallmark of essential hypertensive state that occurs early in the clinical course of the disease. In CKD, the sympathetic hyperactivity seems to be expressed at the earliest clinical stage of the disease, showing a direct relationship with the severity of the condition of renal failure, being more pronounced in the terminal stage of CKD. The sympathetic efferent and afferent neural activity in kidney failure is a key mediator for the maintenance and progression of the disease. The aim of this review was to show that the feedback loop of this cycle, due to adrenergic hyperactivity, also aggravates many of the risk factors responsible for causing sudden cardiac death and may be a potential target modifiable by percutaneous renal sympathetic denervation. If it is feasible and effective in end-stage renal disease, little is known.

Pulmonary vein isolation alone and combined with renal sympathetic denervation in chronic kidney disease patients with refractory atrial fibrillation

BACKGROUND: Atrial fibrillation (AF) commonly occurs in association with chronic kidney disease (CKD), resulting in adverse outcomes. Combining pulmonary vein isolation (PVI) and renal sympathetic denervation (RSD) may reduce the recurrence of AF in patients with CKD and hypertension. We considered that RSD could reduce the recurrence of AF in patients with CKD by modulating sympathetic hyperactivity. Our goal was to compare the impact of PVI + RSD with that of PVI alone in patients with concurrent AF and CKD. METHODS: This was a single-center, prospective, longitudinal, randomized, double-blind study. Forty-five patients with controlled hypertension, symptomatic paroxysmal AF and/or persistent AF, stage 2 or 3 CKD, and a dual-chamber pacemaker were enrolled from January 2014 to January 2015. We assessed the 30-second recurrence of AF recorded by the pacemaker, 24-hour ambulatory blood pressure measurements, estimated glomerular filtration rate, albuminuria, echocardiographic parameters, and safety of RSD. RESULTS: No patient developed procedural or other complications. The ambulatory blood pressure measurements did not differ within the PVI + RSD group or between the PVI + RSD and PVI groups throughout the study. Significantly more patients in the PVI + RSD group than in the PVI group were free of AF at the 12-month follow-up evaluation. The PVI group had an unacceptable response to ablation with respect to changes in echocardiographic parameters, whereas these parameters improved in the PVI + RSD group. CONCLUSION: PVI + RSD were associated with a lower AF recurrence rate than PVI alone; it also improved renal function and some echocardiographic parameters. These encouraging data will serve as baseline information for further long-term studies on larger patient populations.