Page 202 - Read Online

Page 6 of 10 Berezin. Vessel Plus 2018;2:22 I http://dx.doi.org/10.20517/2574-1209.2018.23

decreased EPC levels may contribute to the pathophysiology of albuminuria or proteinuria in hypertensive
patients with nephropathy. In patients with essential hypertension with ECG evidence of left ventricular
[81]
hypertrophy (LVH), the circulating levels of EPCs were lowered to those who did not have LVH . In hyper-
tensive individuals with end-stage renal disease, EPC number and function were significantly reduced and
[82]
inversely associated with CV risk . Moreover, the levels of EPCs in the peripheral blood of women with
pregnancy-induced hypertension were significantly lower compared with those of control pregnant women
[83]
with normal BP level . Numerous investigators reported that a lowered number of EPC and an altered EPC
function related strongly not only with brachial BP levels, but the increased central aortic systolic pressure,
aortic augmentation index, and pulse wave velocity as a marker of arterial stiffness. It altered brachial artery
flow-mediated dilatation as a marker of endothelial dysfunction and left ventricular (LV) twisting [77,84-87] .
Additionally, patients with newly diagnosed essential hypertension had increased proportions of various
[88]
CD34(+) populations of EPCs and CD34(+)VEGFR2(+) c-Kit(+) EPCs . Moreover, CD34(+) EPCs seem to be
influenced by angiotensin II and KLOTHO encoding gene polymorphism [88,89] . It has been suggested that the
increased proportions of CD34 EPCs in the circulation may be a compensatory mechanism for increased
+
[88]
endothelial damage and microvasculature inflammation in hypertension .

However, the predictive role of EPC dysfunction in hypertensive individuals remains controversial.
Although there is a relation between both lowered level of circulating EPCs and weak EPC function in vitro
and an increased CV risk, there is not quite enough evidence regarding independent prognostication of EPC
[90]
dysfunction in the hypertensive population . In contrast, in patients with established CAD, myocardial
infarction, heart failure, cardiomyopathies, the EPC dysfunction was determined to be a predictor of fatal
clinical outcomes [91,92] . In fact, EPC dysfunction associates with CV risk and frequently associates with a
number of CV risk factors including hypertension, dyslipidemia, abdominal obesity, prediabetes/diabetes
mellitus. Whether EPC dysfunction appears prior to hypertension or it shapes the hypertensive phenotype
[93]
without corresponding to other CV risk factors is not fully clear . In this context, the independent
predictive value of EPC dysfunction in hypertensive patients requires to be investigated in details in large
clinical controlled trials.

CONCLUSION
The altered endothelial function in hypertensive patients is strongly associated with a decreased number
and a reduced function of EPCs and may be determined even at a pre-hypertensive stage of the evolution of
the disease. There is much evidence that EPCs play a pivotal role in maintaining the vascular integrity and
reparation preventing alteration of the endothelium and manifestation of endothelial dysfunction. The EPCs
dysfunction is established independent of CV risk factors in the general population and in patients with
known CV disease. In this context, a number of circulating EPCs can be recognized as potential diagnostic
and prognostic biomarkers in hypertensive individuals, while there is not quite enough evidence from large
clinical trials.

DECLARATIONS
Authors’ contributions
Berezin AE solely responsible for the paper

Availability of data and materials
Not applicable.

Financial support and sponsorship
None.