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Letter in reply: Glasgow Prognostic Score in heart failure, how can we use it?

Namiuchi, Shigeto; Sugie, Tadashi; Kato, Atsushi

Journal of Cardiovascular Medicine: January 2016 - Volume 17 - Issue 1 - p 70–71
doi: 10.2459/JCM.0000000000000321
Letters to the editor

Department of Cardiology, Sendai City Medical Center, Sendai, Japan

Correspondence to Shigeto Namiuchi, PhD, Sendai City Medical Center, 5-22-1 Tsurugaya, Miyagino-ku, Sendai 983-0824, Japan. Tel: +81 22 252 1111; fax: +81 22 252 9431; e-mail: nami@openhp.or.jp

Received 22 June, 2015

Accepted 26 June, 2015

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To the Editor

We thank Dr Eyuboglu for his interest and important comments on our article The systemic inflammation-based Glasgow Prognostic Score as a prognostic factor in patients with acute failure published by the Journal of Cardiovascular Medicine.

The Glasgow Prognostic Score (GPS) is a simple score combining C-reactive protein and serum albumin concentrations. In our study, we introduced the GPS as a new predictor of the prognoses of patients with acute decompensated failure.1 We focused on C-reactive protein as an inflammatory marker because its concentration is the easiest to determine and is most widely used in general hospitals and/or clinics. However, C-reactive protein level is a ‘rough’ marker to directly determine several conditions, such as a mild-to-moderate elevation of circulating cytokines, infiltration of inflammatory cells in the myocardium, and myocardial fibrosis. Other markers, such as high-sensitivity C-reactive protein, fibrinogen, tumor necrosis factor, or interleukin-6, are more sensitive and useful to directly evaluate myocardial inflammation. C-reactive protein level is a systemic marker that represents the general condition, similarly to serum albumin concentration.

In our study, we included all patients who had been admitted to our hospital owing to acute decompensated heart failure, and we did not exclude heart failure patients with infectious or collagen diseases or cancers. Accordingly, our population included patients with acute heart failure due to inflammation. Surprisingly, one-third of all patients had more than 1.0 mg/dl C-reactive protein. Many patients with acute decompensated heart failure have complications related to systemic inflammation. This indicates that acute heart failure in daily clinical practice cannot be treated independently from other inflammation-related causes such as bronchitis, pneumonia, and urinary tract infection. We believe that patients should be treated comprehensively.

Systemic inflammation worsens prognoses of patients even if the inflammation is related to infection, collagen disease, or cancer. Naturally, the cause of inflammation and/or the inflammation itself may not be fatal, although these factors strongly influence the status of patients with heart failure. In fact, cardiac death occurred in 55% patients in this study, and there was no difference in the cause of death across the three groups. Moreover, GPS significantly predicted all-cause death, as indicated by the Cox proportional hazards model including variables that had been previously reported to be useful prognostic predictors.2 Based on these findings, we are further convinced that GPS may be useful for predicting the prognosis of hospitalized patients with acute decompensated heart failure, regardless of the origin of systemic inflammation.

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Acknowledgements

The authors have no conflicts of interest.

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References

1. Namiuchi S, Sugie T, Saji K, Takii T, Suda A, Kato A. The systemic inflammation-based Glasgow Prognostic Score as a prognostic factor in patients with acute heart failure. J Cardiovasc Med 2015; 16:409–415.
2. Cleland JG, Chiswell K, Teerlink JR, et al. Predictors of postdischarge outcomes from information acquired shortly after admission for acute heart failure: a report from the Placebo-Controlled Randomized Study of the Selective A1 Adenosine Receptor Antagonist Rolofylline for Patients Hospitalized With Acute Decompensated Heart Failure and Volume Overload to Assess Treatment Effect on Congestion and Renal Function (PROTECT) Study. Circ Heart Fail 2014; 7:76–87.
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