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European Heart Journal Advance Access originally published online on June 15, 2007
European Heart Journal 2007 28(16):2041-2042; doi:10.1093/eurheartj/ehm204
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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Cardiac autonomic dysfunction and inflammation in type 1 diabetic patients: reply

Gaetano A. Lanza

Istituto di Cardiologia
Università Cattolica del Sacro Cuore
Largo A. Gemelli, 8
00168 Roma Italy

Tel: +39 06 3015 4187 Fax: +39 06 3055535 E-mail address: g.a.lanza{at}inwind.it

Yildiz et al. raise three major issues about our study on the relation between cardiac autonomic dysfunction and inflammation in type 1 diabetic patients1: (i) the difference in the changes of C-reactive protein (CRP) serum levels over the study period between atenolol and no-atenolol groups achieved statistical significance (P = 0.04) likely only because, together with the reduction in the atenolol group, there was a comparable increase in CRP in the no-atenolol group; (ii) as no correlation analyses between the changes in heart rate variability (HRV) parameters and in CRP serum levels were done, it cannot be concluded that there was a relation between HRV improvement and reduction of CRP levels in the atenolol group; (iii) without controlling for factors potentially influencing changes in CRP over time, it is inappropriate to link the CRP changes to those in autonomic nervous system or atenolol use.

With regard to the first point, it should be noticed that the true effect of atenolol on CRP levels is not only supported by the significant group–CRP interaction on 2-way analysis of variance, but also by the fact that CRP levels decreased significantly in the atenolol group (P = 0.025), whereas they did not show any significant change (specifically, they did not decrease) in the control group (P = 0.14).

With regard to the second point, Spearman test, performed to address the issue raised by Yildiz et al., shows a significant correlation between the changes in low-frequency (LF) power and in CRP serum levels in the whole group of 21 patients enrolled in the drug trial (r = –0.47; P = 0.029); importantly, the correlation coefficient between the changes in LF power and CRP levels was even higher when considering only the 11 patients treated by atenolol, with P-value being just above statistical significance due to the small number of patients (r = –0.57; P = 0.066; only 54% statistical power to detect a significant correlation at P < 0.05).

Finally, as far as the last observation is concerned, clinical conditions (including diabetic status and body mass index) and medical treatment remained unchanged throughout the whole short study period in the two groups of patients randomized in the drug trial1. Thus, there are no reasons to believe that the reduction in CRP levels observed in the atenolol group could be related to more favourable changes in confounding factors, as compared with the control group. Interestingly, although we did not assess triglyceride levels (a potentially modifiable confounding variable) at follow-up, the latter might be expected to increase only in the beta-blockade group2, which, in contrast with Yildiz et al.'s fears, might have limited the favourable autonomic mediated effect on CRP serum levels shown in atenolol treated patients.

References

  1. Lanza GA, Pitocco D, Navarese EP, Sestito A, Sgueglia GA, Manto A, Infusino F, Musella T, Ghirlanda G, Crea F. Association between cardiac autonomic dysfunction and inflammation in type 1 diabetic patients: effect of beta-blockade. Eur Heart J (2007) 28:814–820.[Abstract/Free Full Text]
  2. Cruickshank JM. Beta-blockers, plasma lipids, and coronary heart disease. Circulation. (1990) 82(Suppl. 3):II60–II65.

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This Article
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28/16/2041-a    most recent
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