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      CARDIAC ARRHYTHMIAS AND SILENT MYOCARDIAL ISCHEMIA DURING HEMODIALYSIS

      , , , ,
      Renal Failure
      Informa UK Limited

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          Electrocardiographic abnormalities in patients receiving hemodialysis.

          We assessed standard 12-lead and Holter electrocardiographic (ECG) abnormalities in maintenance hemodialysis (HD) patients. Of 221 outpatients receiving HD, 143 (65%) had ECG abnormalities. Rates were higher in male, elderly, hypertensive, and diabetic patients than in female, younger, normotensive, and nondiabetic patients. The prevalence of ECG changes correlated inversely with HD duration. Serial ECGs were compared in 87 patients whose average HD duration was 7.5 +/- 2.5 years. Thirty-four patients (39%) showed normal ECGs throughout, 27 (31%) relatively stable abnormalities, 22 (25%) worsening, and 4 (5%) reversion to normal. Age, hypertension, and diabetes are factors related to abnormal ECG findings. Among the 142 Holter recordings from 72 patients, 70 (97%) were basically in sinus rhythm, and 2 (3%) were in atrial fibrillation. The average frequency of supraventricular premature contractions (SVPCs) was 1597 +/- 9725 per 24 hours, and that of ventricular premature contractions (VPCs), 556 +/- 1415. VPCs were multifocal in 9%, in runs in 25%, and early in 1%. In 29 (40%) of recordings, VPCs appeared mainly during and for several hours after HD. ST-T changes were seen in 43 (60%). In 11, ST depression occurred during and a few hours after HD. Patients receiving HD showed diverse ECG abnormalities. Holter ECGs revealed a high incidence of arrhythmias and ST-T changes, which frequently appeared in relation to HD timing.
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            Effect of a new model of hemodialysis potassium removal on the control of ventricular arrhythmias.

            The primary aim of this multicenter, prospective, randomized cross-over study was to clarify whether a new model of hemodialysis (HD) potassium (K) removal using a decreasing intra-HD dialysate K concentration and a constant plasma-dialysate K gradient (treatment B) is capable of reducing the arrhythmogenic effect of standard HD, which has a constant dialysate K concentration and decreasing plasma-dialysate K gradient (treatment A). The secondary aim was to verify whether this new model is clinically safe. In treatment B, the initial dialysate K concentration had to be 1.5 mEq/liter less than the plasma K concentration, and exponentially decrease to 2.5 mEq/liter at the end of HD. Forty-two chronic HD patients with an increase in premature ventricular complexes (PVC) during dialysis were enrolled from 18 participating centers, and randomly assigned to either sequence 1 (ABA) or sequence 2 (BAB). A pool of 333 of 378 expected ECG Holter recordings were checked for signal quality; 269 (71%) from 36 patients (86%) had a satisfactory signal quality and 108 were selected for analysis (1 per patient per period). There was a difference in the natural logarithm of the increase in PVC/hr and PVC couplets/hr during HD between treatments A and B (1.70 +/- 1.59 vs. 1.09 +/- 1.76 and 0.94 +/- 0.86 vs. 0.64 +/- 1.01, a reduction of 36% and 32%, P = 0.011 and 0.047, respectively) without any carry over effect (P = 0.61 and 0.24, respectively). The fact that this decrease of one third is due to a lower plasma-dialysate K gradient is supported by the observation that it was more evident during the first than the last two hours of HD (a reduction in the natural logarithm of the increase in PVC/hr and PVC couplets/hr of 60% and 60%, P 0.002 and 0.009, vs. 26% and 17%, P = 0.098 and 0.332, respectively): the initial plasma-dialysate K gradient was 2.3 times lower during treatment B than during treatment A, without adversely affecting pre-HD plasma K levels. These results could have a considerably clinical impact not only because of the possibility of physiologically decreasing the arrhythmogenic effect of HD, but also because this effect can be considered a "marker" of the electrophysiological derangement induced by the administration of standard HD three times a week for years ("electric disequilibrium syndrome").
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              Effect of Hemodialysis on the Dispersion of the QTc Interval

              The QTc dispersion reflects the underlying regional heterogeneity of the recovery of the ventricular excitability, thereby it is considered as a novel marker of risk of ventricular arrhythmias. Because a higher incidence of ventricular arrhythmias is described during and after hemodialysis, the aim of this study has been to evaluate the QTc dispersion before and after uncomplicated hemodialysis session. Twenty chronic uremics without heart failure, ischemic heart disease or dialysis hypotension were selected. The QTc dispersion was determined as the difference between the longer and the shorter QTc interval measured on a 12-lead electrocardiogram. Following the hemodialysis session, the QTc dispersion increased from 30 ± 9 to 54 ± 17 ms (p < 0.001) associated with the expected reduction of potassium and magnesium and with the increase of extracellular calcium concentration. However, no correlation has been observed between the QTc dispersion increase and the degree of the intradialytic changes of plasma electrolytes, blood pressure or body weight. In summary, the hemodialysis treatment per se does induce an increase of the QTc dispersion, likely due to the rapid changes of electrolyte plasma concentrations. This can potentially contribute to the arrhythmogenic effect of the hemodialysis procedure, reflecting an enhanced regional heterogeneity of ventricular repolarization. The clinical importance of the increase of QTc dispersion as risk factor of ventricular arrhythmias, particularly in hemodialyzed patients suffering from ischemic or hypertrophic heart diseases, should be the matter of further investigations.
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                Author and article information

                Journal
                Renal Failure
                Renal Failure
                Informa UK Limited
                0886-022X
                1525-6049
                July 07 2009
                January 2000
                July 07 2009
                January 2000
                : 22
                : 3
                : 355-368
                Article
                10.1081/JDI-100100879
                e5b6851b-cd87-4b97-90da-d7c3a9350216
                © 2000
                History

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