https://www.heartrhythmjournal.com/pb/assets/raw/Health%20Advance/journals/hrthm/hrt00912001524.pdf

2012 EHRA/HRS expert consensus statement on cardiac resynchronization therapy in heart failure : implant and follow-up recommendations and management

Characteristics of sudden death in hemodialysis patients

PVCs and Left Ventricular Dysfunction. Background: Frequent premature ventricular complexes (PVCs) can cause a decline in left ventricular ejection fraction (LVEF). We investigated whether the site of origin and other PVC characteristics are associated with LVEF.

Methods: We retrospectively studied 70 consecutive patients (mean age 42 ± 17 years, 40 [57%] female) with no other cause of cardiomyopathy undergoing ablation of PVCs. We analyzed the association of a reduced LVEF, defined by LVEF <50% on echocardiography, with features of PVCs obtained from electrocardiography, 24- or 48-hour Holter monitor and electrophysiology study.

Results: Patients with reduced LVEF (n = 17) as compared to normal LVEF (n = 53) had an increased burden of PVCs (29.3 ± 14.6% vs 16.7 ± 13.7%, P = 0.004), higher prevalence of nonsustained ventricular tachycardia (VT) [13 (76%) vs 21 (40%), P = 0.01], longer PVC duration (154.3 ± 22.9 vs 145.6 ± 20.8 ms, P = 0.03) and higher prevalence of multiform PVCs [15 (88%) vs 31 (58%), P = 0.04]. There was no significant difference in prevalence of sustained VT, QRS duration of normally conducted complexes, PVC coupling interval, or delay in PVC intrinsicoid deflection. Patients with fascicular PVCs (n = 5) had higher mean LVEF compared to others (66.2 ± 4.0% vs 53.0 ± 10.0%, P = 0.002). There was no association of LVEF with other PVC foci or with left-bundle versus right-bundle branch block morphologies. The threshold burden of PVCs associated with reduced LVEF was lower for right as compared to left ventricular PVCs.

Conclusion: In addition to the PVC burden, other characteristics like a longer PVC duration, presence of nonsustained VT, multiform PVCs and right ventricular PVCs might be associated with cardiomyopathy. (J Cardiovasc Electrophysiol, Vol. 22, pp. 791-798, July 2011)

Characteristics of premature ventricular complexes as correlates of reduced left ventricular systolic function: study of the burden, duration, coupling interval, morphology and site of origin of PVCs.

Electrocardiographic abnormalities and uremic cardiomyopathy

Hyperkalemia is a potentially life-threatening electrolyte disorder appreciated with greater frequency in patients with renal disease, heart failure, and with use of certain medications such as renin angiotensin aldosterone inhibitors. The traditional views that hyperkalemia can be reliably diagnosed by electrocardiogram and that particular levels of hyperkalemia confer cardiotoxic risk have been challenged by several reports of patients with atypic presentations. Epidemiologic data demonstrate strong associations of morbidity and mortality in patients with hyperkalemia but these associations appear disconnected in certain patient populations and in differing clinical presentations. Physiologic adaptation, structural cardiac disease, medication use, and degree of concurrent illness might predispose certain patients presenting with hyperkalemia to a lower or higher threshold for toxicity. These factors are often overlooked; yet data suggest that the clinical context in which hyperkalemia develops is at least as important as the degree of hyperkalemia is in determining patient outcome. This review summarizes the clinical data linking hyperkalemia with poor outcomes and discusses how the efficacy of certain treatments might depend on the clinical presentation.

How Dangerous Is Hyperkalemia

BACKGROUND Analysing a 12-lead surface electrocardiogram (ECG), the inter-lead variability of the P wave interval, i.e. P wave dispersion, is defined as the difference between the maximum and the minimum P wave duration. Our aim was to assess the effect of haemodialysis on P wave duration and dispersion in non-diabetic patients with end-stage renal failure on chronic haemodialysis. METHODS Twenty-eight patients (14 men and 14 women, mean age 58+/-16 years, average duration of dialysis 4.5+/-2.8 years) were examined. Prior to haemodialysis, echocardiography (M-mode and two-dimensional) was performed. Haemodialysis sessions were carried out with polysulfone dialysers and bicarbonate dialysate fluids. Twelve-lead ECGs were recorded at the beginning, 15 and 30 min after starting dialysis, at the end, and 2 h after completion of each session. Ionic parameters were checked during the study. P wave durations were measured with calipers in three consecutive complexes of each lead by one observer. RESULTS P maximum was 58+/-16 ms at the beginning, and showed an increase by the end of dialysis to 98+/-8.9 ms (P<0.0001). Pre-dialysis P dispersion was 23+/-10 ms and increased to 41+/-16 ms by the end of the sessions (P<0.0001). In patients with a left atrial diameter larger than 45 mm, P dispersion increased from 23+/-11 to 53+/-10 ms (P<0.0003) by the end of the sessions. CONCLUSIONS According to our results, ionic imbalance and dialysis itself may cause changes in P duration and dispersion simultaneously.

/pdf/effects-of-haemodialysis-on-maximum-p-wave-duration-and-p-4wzzaxwzrp.pdf

Effects of haemodialysis on maximum P wave duration and P wave dispersion

Background
QT interval (QT) and QT dispersion (QTd) are electrocardiograph (ECG) parameters for the evaluation of myocardial repolarization. The inhomogeneity of ventricular repolarization is associated with ventricular arrhythmias. An increased QT, QTd, and increased incidence of nocturnal cardiac rhythm disturbances have been described in patients with obstructive sleep apnea (OSA), while other investigators did not find a relationship between ventricular arrhythmias and OSA.

Hypothesis
The aim of this study was to examine the occurrence of ventricular arrhythmias and to measure QT parameters in patients with untreated OSA using an ambulatory Holter-ECG.

Methods
A total of 25 patients with untreated OSA were studied. After routine biochemical investigation and 2-dimensional, M-mode echocardiography, a 24-hour Holter-ECG was recorded to detect cardiac arrhythmias and QT parameters. QT parameters were measured by the QT Guard system.

Results
Only the QT interval increased significantly during the nighttime period (nocturnal QT interval: 423.1 ± 34.6 ms, daytime QT interval: 381.6 ± 33.8 ms, 24-hour QT interval: 394.7 ± 31.1 ms). However, during the nighttime QT interval (422.8 ± 14.9 ms), QTd (31.2 ± 11.0 ms) and QT dispersion (30.5 ± 10.2 ms) did not show any change compared to 24-hour (QTc interval: 423.7 ± 14.2 ms, QTd: 28.8 ± 9.4 ms, QTcd: 30.5 ± 9.43 ms) and daytime levels (QTc interval: 423.9 ± 14.3 ms, QTd: 27.3 ± 10.7 ms, QTcd: 29.9 ± 11.1 ms). None of the patients had ventricular arrhythmias.

Conclusions
QTd and QTcd did not increase during the nighttime period. Our study did not show an increased risk of ventricular arrhythmias in this population during the monitoring period. Copyright © 2010 Wiley Periodicals, Inc.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/clc.20619

The effect of sleep apnea on QT interval, QT dispersion, and arrhythmias.

Frequent premature ventricular complexes (PVCs) have been demonstrated to cause tachycardiomyopathy in some individuals with a structurally normal heart. We report a patient with severe congestive cardiomyopathy which did not respond to cardiac resynchronization therapy (CRT). Ambulatory monitoring and interrogation of the device memory revealed frequent monomorphic PVCs that were considered a potential cause of the failure of CRT. Radiofrequency ablation of the focus at the postero-inferior left ventricle eliminated the arrhythmia, with a resultant rapid improvement in the clinical status and echo parameters. As PVCs are often associated with severe heart failure, the presence of frequent extrasystoles may be an underrecognized cause of a non-response to resynchronization therapy.

Radiofrequency catheter ablation of premature ventricular complexes improved left ventricular function in a non-responder to cardiac resynchronization therapy

ECG abnormalities in hemodialysis.

The incidence of atrial fibrillation is increased during hemodialysis (HD); however, the effects of hemodiafiltration (HDF) on atrial arrhythmias have not been evaluated. The prolongation of the P wave and P dispersion (Pd) can predict atrial arrhythmias. Data from 30 patients receiving HDF over a period of 3 months were collected; the same group of patients was then evaluated during treatment with conventional HD for at least another 3 months. Electrolyte values were obtained, and surface electrocardiograms (ECG), echocardiography, and Holter ECGs were performed. The duration of the P wave and Pd increased significantly during HD. The left atrial diameter decreased significantly only during HDF. During HDF, the left atrial cross diameter measured at the beginning of the session was positively correlated with the incidence of supraventricular premature beats (p = 0.011, r = 0.4556). The decrease in left atrial diameter during HDF was negatively correlated with the incidence of supraventricular premature beats (p = 0.016, r = −0.43). During HDF, the changes in sodium and Pd were significantly positively correlated (p < 0.05, r = 0.478). During HD, the changes in ionized calcium levels and Pd were positively correlated (p < 0.05, r = 0.377). Our results suggest that HDF has a more beneficial effect on P wave duration and Pd than HD. The alterations in the ECG markers may be the result of the simultaneous occurrence of certain electrolyte imbalances and renal replacement methods.

Hemodiafiltration and hemodialysis differently affect P wave duration and dispersion on the surface electrocardiogram

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