European Heart Journal Advance Access originally published online on June 15, 2007
European Heart Journal 2007 28(16):2041; doi:10.1093/eurheartj/ehm206
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Cardiac autonomic dysfunction and inflammation in type 1 diabetic patients
Department of Cardiology
Harran University School of Medicine
P.K:112
63100 Sanliurfa
Turkey
Department of Cardiology
Harran University School of Medicine
P.K:112
63100 Sanliurfa
Turkey
Department of Cardiology
Harran University School of Medicine
P.K:112
63100 Sanliurfa
Turkey
Department of Cardiology
Harran University School of Medicine
P.K:112
63100 Sanliurfa
Turkey
Tel: +90 505 327 42 65 Fax: +90 414 315 11 81 E-mail address: ghcayildiz{at}yahoo.com
We read the article by Lanza et al.1 dealing with the association between cardiac autonomic dysfunction and inflammation in type 1 diabetic patients with great interest. The authors revealed an inverse correlation between C-reactive protein levels and heart rate variability (HRV) parameters, especially with low-frequency (LF) power. Authors have also revealed significantly higher C-reactive protein serum levels in patients with bottom quartile values of LF power that improved significantly with atenolol parallel to improvement in LF power. In our opinion, some points of this work are not sufficiently clear.
Authors reported significant difference (P = 0.04) in the alterations of serum high-sensitive C-reactive protein level over the study period between atenolol and no atenolol groups by using two-way ANOVA test (Table 5, Figure 3). The difference between the two groups, with regard to change in serum high-sensitive C-reactive protein level, is partly due to a decrease in atenolol group (from 3.02 ± 2.9 to 2.01 ± 1.9 mg/L) and is partly due to a comparable increase in no atenolol group (from 2.89 ± 2.9 to 3.88 ± 3.8 mg/L) over study period. If serum high-sensitive C-reactive protein level was not changed over the study period in no atenolol group, then the difference of alterations in serum high-sensitive C-reactive protein level between the two groups would probably not reach statistical significance. Therefore, the statistically significant difference in the alterations in serum high-sensitive C-reactive protein level over the study period between the two groups may not be attributed to atenolol use with the findings of this study.
Authors revealed improved HRV parameters and decreased serum high-sensitive C-reactive protein level in atenolol group without assessing the correlation between the changes in HRV parameters and serum high-sensitive C-reactive protein level. Consequently, they discussed the relationship between autonomic nervous system and inflammatory reactions. However, in order to report such a relationship with data of this study, correlation analysis should have been performed for evaluation of the association between the alterations in HRV parameters and the alterations in serum high-sensitive C-reactive protein levels over the study period.
As stated in the limitations of the study, serum high-sensitive C-reactive protein is a reliable marker of inflammation, but also is a multivariate, non-specific marker of inflammation. Without controlling the influencing factors over time, linking the change in serum high-sensitive C-reactive protein level with atenolol use or autonomic nervous system functions is not appropriate. Evaluation of body mass index, serum triglyceride levels, and microalbuminuria during the follow-up concomitantly with serum high-sensitive C-reactive protein level would add value of this article since these factors were correlated with serum high-sensitive C-reactive protein level at baseline.
Reference
- 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. Published online ahead of print March 19, 2007.
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