Hypertension, especially non-dipper hypertension is a risk factor for adverse cardiovascular events. Lack of nocturnal BP fall (nondipping) is more closely associated with target organ damage and worsened cardiovascular outcomes
7,8. In a meta analysis including data of 3468 patients from four prospective studies, the dipping pattern and the night-day BP ratio significantly and independently predicted mortality and cardiovascular disease
9. The present study carried out in a treated dipper and non-dipper essential hypertensive patients showed that inflammatory activity and platelet activation were higher in non-dipper hypertensives. There was strong and independent association of RDW level with risk of all-cause and cardiovascular (CV) mortality in patients with cardiovascular disease (CVD)
10 and in the general population
11. High RDW indicate the presence of anisocytosis which is related to impairment of erythropoiesis and degradation of erythrocytes, reflecting chronic inflammation and increased level of oxidative stress
12. However the underlying biological mechanism remains unclear. RDW is recognized as a global marker of chronic inflammation and oxidative stress
13. The relation of RDW to hypertension has been investigated in several studies. Tanindi et al reported that RDW is higher in prehypertensive and hypertensive patients compared with healthy controls. They found a positive correlation between RDW and both systolic and diastolic blood pressures
14. Gunebakmaz et al reported not only higher RDW levels in hypertensive patients compared to controls but also elevated RDW levels in the non-dippers compared to dippers
15. Another study showed that RDW is significantly increased in patients with non-dipper hypertension compared with the dipper Hypertension and inflammatory activity was closely related to RDW in non-dipper hypertensives
16. We showed that the sensitivity and specificity of RDW with a cut-off value of 13.85 for nondipper hypertensive patients was 61.3 % and 57.4 %, respectively.
Platelets are known to have a major effect on the formation of atherosclerotic plaques and therefore play an essential role in the pathogenesis of atherothrombosis. Mean platelet volume (MPV), a determinant of platelet function, is a newly emerging risk factor for atherothrombosis. Several studies indicate that high MPV levels and high platelet reactivity are associated with overall vascular mortality, including myocardial infarction17-21. MPV has been reported to increase in HT. MPV was found to be higher in patients with hypertension22. MPV, has a positive correlation with blood pressure and is elevated in non-dippers compared with dipper hypertensives23. Non-dipper hypertensives have increased platelet activation6,24.
NLR, is a cost-effective, easily applicable, and reproducible inflammatory marker used in our clinical practice. The relationship between neutrophil count, cardiovascular risk and development of HT is known25,26. We have found that non-dipper hypertensive patients have significantly higher NLR values compared to dipper hypertensives. This result indicates that non-dipper hypertensive patients tend to have increased inflammatory status. Non-dipper hypertensive patients have reduced availability of endothelium-dependent vasodilation, mediated by a decrease in nitric oxide release5. Inflammation modifies endothelial function and an inability of the endotehlium to produce nitric oxide and prostacyclin can result in the depletion of vasodilator, antithrombotic and anti-atherogenic properties of the vascular endothelium. In addition, stimulated leukocytes alter rheological properites with an increased capacity to adhere to vascular endothelium and may result in capillary leukocytosis and subsequent increased vascular resistance27. All these changes determine a worse long-term prognosis of those hypertensives with absence of nocturnal dip in BP.
Our results suggest that MPV, RDW and NLR levels are higher in nondipper hypertensives than dipper hypertensives. Nondipping status in ABP monitoring is independently associated with early atherosclerosis28. Increased platelet activation and inflammatory activity could contribute to increase the atherosclerotic risk in non-dipper patients compared with dippers.
Study limitations: The sample size was small and it was conductud in a single center. The relation between RDW, MPV, NLR and clinical outcomes were not assessed.
Conclusion: Our results suggest that RDW, MPV and NLR levels, which are indicators of platelet activation and inflammatory response are significantly higher in non-dippler hypertensive patients compared to dipper hyperensives. This may be one of the reasons for higher mortality in patients with blunted nighttime BP decrease.
Conflict of interest: None declared.