Aims: We investigated the association of endothelial glycocalyx damage with arterial stiffness, coronary microcirculatory impairment and LV myocardial deformation deterioration in newly diagnosed untreated hypertensive patients.

Methods: In 320 newly-diagnosed untreated hypertensive patients and 160 controls, we measured a) perfused boundary region (PBR) of the sublingual arterial microvessel, an index of glycocalyx thickness, using Sidestream Darkfield Imaging c) coronary flow reserve (CFR) by Doppler echocardiography d) Global Longitudinal strain (GLS) and strain rate (GLSR) by speckle tracking echocardiography, d) carotid to femoral pulse wave velocity (PWV) and central systolic blood pressure (cSBP)

Results: Compared to controls, hypertensives had higher PBR (2.049±0.27 vs 1.769±0.30,p=0.037) PWV, cSPB, and lower GLS and GLSR values (p<0.05, Table 1). In hypertensives, there was a close association of reduced endothelial glycocalyx thickness, as assessed by increased PBR, with increased cSBP, PWV and decreased CFR (p<0.05) as well as a borderline relation of PBR with office SBP (p=0.06) after adjustment for age, sex, BMI, smoking LV mass, heart rate, hyperlipidemia and office SBP. PBR had an additive value to multivariable model including PWV, CFR, and office SBP for the prediction of abnormal GLS (χ2=2.4 to 3.8 after addition of PBR5–25, p for change=0.03).


Table 1. Comparison of vascular and echocardiographic markers between hypertensive patients and healthy controls

Variable  Hypertensive patients (n=320)  Healthy Controls (n=160) 
SBP, mmHg  147±17  120±10  <0.001 
DBP, mmHg  89±10  78±9  <0.001 
PP, mmHg  52.85±11.93  43.21±12.74  0.003 
PBR 5–25 μm  2.049±0.276  1.769±0.306  0.037 
AI, %  27.23±17.23  23.58±16.37  0.012 
PWV, m/s  11.73±2.415  10.21±5.770  0.007 
CFR  2.583±0.880  3.311±0.518  0.002 
GLS, %  -16.97±3.639  -21.91±1.543  0.005 


Conclusions: Endothelial glycocalyx is damaged in newly diagnosed untreated hypertensive patients. This damage is related to abnormal aortic elastic properties and to impaired coronary microcirculatory function and contributes to impairment of LV longitudinal deformation.