NLR is independently related to endothelial dysfunction and could predict composite cardiovascular endpoints independent of traditional confounding factors in patients with moderate to severe CKD.

High levels of circulating Von Willebrand factor (vWf) and increased neutrophil to lymphocyte (N/L) ratio may reflect vascular inflammation in hypertensive patients. In present study, we aimed to investigate the effects of valsartan as an angiotensin II receptor antagonist and amlodipine as a calcium channel blocker on the vWf levels and N/L ratio in patients with essential hypertension. Patients were randomized to one of the following intervention protocols: calcium channel blocker (amlodipine, 5-10 mg/day) as group A (n = 20 mean age = 51.85 ± 11.32 y) and angiotensine II receptor blocker (valsartan, 80-320 mg/day) as group B (n = 26 mean age = 49.12 ± 14.12 y). Endothelial dysfunction and vascular inflammation were evaluated with vWf levels and N/L ratio in hypertensive patients before treatment and after treatment in the 12th week. No statistically significant differences were found among the groups in terms of age, sex, and body mass index (BMI). There was a significant decrease in vWf levels (P < .001) and N/L ratio after treatment (P = .04, P < .001, respectively) in both the groups. Von Willebrand factor levels and N/L ratio are very important markers having a role in vascular inflammation and antihypertensive treatment with amlodipine and valsartan may improve cardiovascular outcomes by decreasing these biomarkers.

Vascular inflammation plays an important role in the pathophysiology of hypertension and high levels of endocan may reflect ongoing vascular inflammation in hypertensive patients. In the present hypothesis-generating study, we aimed at investigating the comparative effects of amlodipine and valsartan on endocan levels in newly diagnosed hypertensive patients. The study population consisted of 37 untreated hypertensive patients who were randomized to the two treatment arms. After baseline assessment, each patient was randomly allocated to either 10 mg daily of amlodipine (n = 18, 7 males) or 160 mg daily of valsartan (n = 19, 3 males) and treated for a 3-month period. Sphygmomanometric blood pressure (BP) and serum endocan were measured before and every 2 weeks during drug treatment. There was no statistically significant difference between the two treatment arms as far as baseline socio-demographic and clinical characteristics are concerned. After a 3-month treatment period, systolic and diastolic BP values significantly reduced by antihypertensive treatment (p < 0.001). Furthermore, endocan levels were significantly decreased in both treatment arms (p < 0.05). However, amlodipine caused a greater percent decrease in circulating endocan levels compared with valsartan at the end of the treatment period. Both drugs reduced high sensitivity C-reactive protein values. However, the statistical significant difference vs baseline was achieved only in the group treated with amlodipine. No correlation was found between endocan plasma levels and BP reduction. The results of this hypothesis-generating study suggest that amlodipine and valsartan decrease endocan levels in newly diagnosed hypertensive patients. The effects, which are more evident with amlodipine, may contribute to the anti-inflammatory effects exerted by the two drugs on the vascular target.

Background/Aims: Subclinical or frank hypothyroidism is causally implicated in endothelial dysfunction. Since the plasma concentration of the active form of thyroid hormone, triiodothyronine (T₃), is reduced in chronic kidney disease (CKD), where endothelial function is frequently altered, low T₃ may be a factor implicated in this disturbance in CKD patients. Methods: We investigated the relationship between flow-mediated vasodilatation (FMD) and thyroid hormones in a series of 217 nondiabetic patients with stage 3–4 CKD. Results: The plasma concentration of free T₃ (fT₃) was closely associated with FMD (r = 0.38; p < 0.001). fT₃ was also inversely associated with hemoglobin (r = –0.41; p < 0.001), systolic pressure (r = –0.28; p < 0.001) and the plasma concentration of the endogenous inhibitor of NO synthase, asymmetric dimethylarginine (ADMA; r = –0.18; p = 0.007). However, adjustment for ADMA markedly attenuated the fT₃-FMD link, a phenomenon suggesting that raised plasma ADMA, possibly driven by low fT₃, at least in part mediates the adverse effects of low T₃ on endothelial function in CKD. Conclusions: Low T₃ in patients with moderate-to-severe CKD is a marker of endothelial dysfunction. This study sets a solid rationale for designing specific intervention studies aimed at clarifying the nature (causal or not causal) of the endothelial function-T₃ link in CKD.

Pentraxin 3 (PTX3) is a new candidate immunoinflammatory marker that has been reported to be associated with cardiometabolic risk factors. We aimed to investigate the effects of valsartan and amlodipine on the PTX3 and C-reactive protein (CRP) levels in patients with essential hypertension. Patients with a newly diagnosed essential hypertension were admitted to our internal medicine outpatient clinic. Patients were randomized to one of the following intervention protocols: calcium channel blocker (amlodipine, 5-10 mg/day) as group A (n = 22; mean age ± standard deviation [SD]: 52 ± 11 year) and angiotensine II receptor blocker (valsartan, 80-320 mg/day) as group B (n = 28; mean age ± SD: 50 ± 14 year). Endothelial dysfunction and systemic inflammation were evaluated with PTX3 and CRP. There was a significant decrease in the level of PTX3 after treatment in two groups (P < .05). Although there was a significant decrease in the level of CRP after treatment in amlodipine group, there was no significant decrease in the levels of PTX3 and CRP after treatment in two groups. There were no significant differences in the systolic and diastolic blood pressure reduction between the two treatment groups. In the treatment of hypertension, prior knowledge of the level of plasma PTX3 could be important in antihypertensive drug choice. C-reactive protein and PTX3 are the markers that have role in vascular inflammation and are found associated with the prognosis of cardiovascular outcomes in many trials. In our study, PTX and CRP levels were decreased when compared to baseline levels.