Introduction: Pentraxin-3 (PTX3) is a new inflamma-tory biomarker, more specific than high-selectivity C reactive protein (hsCRP), due to its local production in the endothelial cells.
Objective: To investigate the correlation of PTX3 with other well known markers of endothelial dysfunction (hsCRP, flow mediated vasodilation –FMD and intima media thickening – IMT) in a group of hypertensive patients and as compared with a normotensive group. Methods: We examined a group of 363 hypertensi-ve patients, divided in 3 groups (117 patients – group B – under chronic treatment with other hypertensive drugs: beta-blockers, calcium channel blockers, diu-retics, 129 patients – group C – under chronic treat-ment with ACE inhibitors and 117 patients – group D – under chronic treatment with angiotension II recep-tor blockers) and a control group A of 105 normoten-sive patients, without any treatment. The groups were homogenous in terms of age and gender. All the hyper-tensive patients had controlled values of blood pressure under medication. All the patients recruited had been diagnosed with endothelial dysfunction, confirmed ei-ther by FMD or IMT, either by both. We correlated the degree of the endothelial dysfunction with the duration of the hypertension and the degree of the control.
Results: Patients treated with ACE inhibitors and ARBs had a significantly lower value of PTX3 but not hs-CRP compared to those treated with other antihypertensive agents as follows: PTX3: 0.61±0.49 vs. 0.95±1.04 ng / ml, p=0.001 and hs-CRP: 0.40±0.20 vs. 0.48±0.22 mg / dl, p=0.54. Analyzing correlations of plasma levels of PTX3 with other parameters, we found positive corre-lations (r>0.3) with age, duration of hypertension and common carotid IMT (CC) in groups C and D. Assays of plasma PTX3 concentrations in groups of patients treated with various medications showed that these concentrations were lowest in patients treated with ACE inhibitors and ARBs than with the other agents. These results show that endothelium inflammation is better controlled by inhibitors of ACE and BRA than other hypotensive drugs.
Conclusions: Both ACE inhibitors and ARBs decre-ase the level of PTX3 in hypertensive patients on a lower level than in control group, but not decrease the hs-CRP levels. The explanation could be the fact that PTX3 is produced in the endothelial cells in response to inflammatory stimuli: IL-1 and TNFs and hs-CRP is produced in hepatocites, especially after stimulation of IL-6. In this idea, PTX3 could be a better inflammatory marker than hs-CRP to evaluate the vascular damage and it may be more directly involved in the pathogene-sis of endothelial dysfunction.