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The effect of candesartan on pentraxin-3 plasma levels as marker of endothelial dysfunction in patients with essential arterial hypertension

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Abstract

Background

In the last decades, the studies performed on the field of endothelial dysfunction confirmed the fact that the starting point of this pathology is the inflammation. Several inflammatory biomarkers had been discovered and studied, ones showing systemic inflammation, and others being more specific biomarkers and showing the local inflammation. Pentraxin-3 (PTX3) is a new inflammatory biomarker, from the same family as high-selectivity C-reactive protein (hs-CRP), but it is a more specific biomarker, due to its local production: the endothelial cells and not the liver like in the case of hs-CRP.

Aims

Several antihypertensive classes of drugs seem to have a positive impact on reducing the local endothelial inflammation, beyond their effect of lowering the blood pressure, so this study aims to analyze the effect of candesartan on the two inflammatory biomarkers: PTX3 and CRP, compared with other antihypertensive drugs, in hypertensive patients with endothelial dysfunction.

Methods

A total of 365 patients were included in the study: 127 hypertensive patients were under treatment with candesartan, 134 patients were under treatment with other hypotensive medication (beta blockers, calcium channel blockers, and diuretics), both groups with controlled values of blood pressure, and 104 were normotensive persons. Classical methods of assessing the endothelial function were correlated with these biochemical markers.

Results

The patients treated with candesartan had a significant lower value of PTX3 and hs-CRP, compared with those under treatment with other antihypertensive medication as follows: PTX3: 0.61 ± 0.49 vs 0.95 ± 1.04 ng/ml, P = 0.006 and hs-CRP: 0.19 ± 0.20 vs 0.20 ± 0.22 mg/dl, P = 0.54.

Conclusions

Candesartan decreases PTX3 and hs-CRP plasma levels more powerful than other classes of antihypertensive drugs (beta blockers, calcium channel blockers, and diuretics), so we may assume that candesartan has a more potent action in reversing endothelial dysfunction and that it offers a higher vascular protection than other classes of antihypertensive drugs. We are suggesting that this new biochemical marker, PTX3, might be better and more specific marker for endothelial dysfunction, than hs-CRP.

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Acknowledgements

This work was supported by the Grant PII-C4-TC-2016-16441-09 offered by the “Victor Babes” University of Medicine and Pharmacy of Timisoara, Romania.

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Authors and Affiliations

  1. Department of Pharmacology and Clinical Pharmacy, Faculty of Pharmacy, “Victor Babes” University of Medicine and Pharmacy Timişoara, 2 Eftimie Murgu Street, 300041, Timisoara, Romania

    V. Buda, C. Cristescu & M. Voicu

  2. Department of Medical Semiotics, Faculty of Medicine, “Victor Babes” University of Medicine and Pharmacy Timişoara, 2 Eftimie Murgu Street, 300041, Timisoara, Romania

    M. Andor, F. Cochera & M. C. Tomescu

  3. Department of Balneophysiotherapy, Rheumatology and Rehabilitation, “Vasile Goldis” Western University, 94 Revolutiei Blvd, Arad, Romania

    P. Tuduce

  4. Cardiovascular Diseases Institute of Timisoara, 13 Gheorghe Adam Street, Timisoara, Romania

    L. Petrescu

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  1. V. Buda
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  2. M. Andor
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  3. C. Cristescu
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  4. M. Voicu
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  6. P. Tuduce
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  8. M. C. Tomescu
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Corresponding author

Correspondence to M. Andor.

Ethics declarations

All procedures performed in this study with human participants were in accordance with the ethical standards of the institutional research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards. This study has been approved by the Ethical Committee of the “Victor Babes” University of Medicine and Pharmacy, Timisoara, Romania (no. 7/2016).

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Buda, V., Andor, M., Cristescu, C. et al. The effect of candesartan on pentraxin-3 plasma levels as marker of endothelial dysfunction in patients with essential arterial hypertension. Ir J Med Sci 186, 621–629 (2017). https://doi.org/10.1007/s11845-017-1580-5

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