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NDT Advance Access originally published online on July 31, 2006
Nephrology Dialysis Transplantation 2006 21(12):3609-3610; doi:10.1093/ndt/gfl417
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Progression of vascular calcification increases QT interval in haemodialysis patients

Email: b.diiorio{at}tiscali.it

Sir,

Vascular calcifications are now recognized as an important determinant of cardiovascular mortality in patients on dialysis [1], and are independent predictors of all-cause and cardiovascular mortality in chronic kidney disease (CKD) [2]. Few data are currently available comparing vascular calcifications and their attendant functional cardiovascular consequences between CKD stage-4 patients and both peritoneal dialysis (PD) and haemodialysis (HD) patients. NDT recently published several articles on vascular calcification and associated cardiovascular dysfunction [1–3]. The authors show that older age, male gender, presence of diabetes and high Ca x P product contribute to the presence of vascular calcification [2,3].

We would like to present herein our experience and preliminary data on cardiac calcification (TC score) and QT interval (and QT dispersion) correlation in uraemia [4]. The score calcification >400 was found to be highly prevalent in CKD-4 and HD patients: significantly more HD patients (62.5%) demonstrated calcifications than CKD-4 patients (33%; P = 0.01). QT interval was higher with higher TC scores in HD and CKD-4 patients (~11%), but QT dispersion is significantly higher in TC scores >400. QT dispersion shows a linear correlation with the TC score (R = 0.899; P < 0.0001 and R = 0.901; P < 0.0001 in CKD-4 and HD patients, respectively). In order to identify the possible determinants of QT dispersion, a multivariate regression analysis was performed, which showed that male gender, age, months of uraemia, low-density lipoprotein (LDL) cholesterol, albumin, Ca–P product and parathyroid hormone (PTH) and cardiac calcifications are important determinants of QT dispersion [4].

Concern has been raised that hypercalcaemia, hyperzphosphoraemia and hyperlipidaemia may be associated with arterial calcifications. Today there is evidence that sevelamer is associated with significantly greater reductions in calcification scores [5,6].

We studied 14 new haemodialysis patients with follow-up for 1 year after starting dialysis, and evaluated the TC score changes and QT dispersion. Seven patients used sevelamer during follow-up, while the remaining seven used the other hypophosphataemic therapy (no sevelamer). All patients presented normal phosphorus values using their assigned therapy. Figure 1 shows that TC score changes correlate with QT dispersion changes (R = 0.992; P < 0.000001), but in the sevelamer group the TC score increased 1.0 ± 3.2% while in the no-sevelamer patients, an increase of 16.7 ± 3.9% (P < 0.001) was observed. QT dispersion increases from 0.42 ± 3.2% in sevelamer to 13.7 ± 3.8% in the no-sevelamer group (P < 0.0001).


Figure 1
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Fig. 1. Percentage TC score changes after 1 year follow-up in correlation with QT dispersion changes in new HD patients in therapy with sevelamer (closed diamonds) and with no-sevelamer (open diamonds).

 
These data confirm the conclusions of our previous work [4]: cardiac calcifications are an independent determinant of QT interval, and both correlate also in patients starting haemodialysis; sevelamer attenuates cardiac calcification and reduces QT dispersion increases. This study shows a preliminary data, and we recognize that its primary limitation is the small number of patients studied. This study, however, was conducted in the course of usual patient care and therefore represents a ‘real life'situation.

Conflict of interest statement. None declared.

Biagio Raffaele Di Iorio1, Ernesto D'Avanzo2, Carmine Piscopo3, Pellegrino Grimaldi3, Emanuele Cucciniello1, Nicola Cillo1 and Vincenzo Bellizzi1

1UO di Nefrologia e Dialisi
2UO Diagnostica per Immagini and
3UO Medicina, PO ‘A. Landolfi’
Solofra (AV)
Italy

References

  1. Shanahan CM. (2006) Vascular calcification: a matter of damage limitation? Nephrol Dial Transplant 21:1166–1169.[Free Full Text]
  2. Sigrist M, Bungay P, Taal MW, McIntyre CW. (2006) Vascukar calcification and cardiovascular function in chronic kidney disease. Nephrol Dial Transplant 21:707–714.[Abstract/Free Full Text]
  3. Sigrist MK, Devlin L, Taal MW, et al. (2005) Length of interdialytic interval influences serum calcium and phosphorus concentrations. Nephrol Dial Transplant 20:1643–1646.[Abstract/Free Full Text]
  4. Di Iorio B, Bortone S, Piscopo C. (2006) Cardiac vascular calcification and Q-T interval in ESRD patients: is there a link? Blood Purif (in press).
  5. Chertow GM, Burke SK, Raggi P. (2002) Sevelamer attenuates the progression of coronary and aortic calcification in hemodialysis patients. Kidney Int 62:245–252.[CrossRef][Web of Science][Medline]
  6. Block GA, Spiegel DM, Ehrlich H, et al. (2005) Effects of sevelamer and calcium on coronary artery calcification in patients new to hemodialysis. Kidney Int 68:1815–1824.[CrossRef][Web of Science][Medline]

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This Article
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