CAROTID ELASTICITY IS IMPAIRED IN STAGE 1 HYPERTENSIVE PATIENTS EVEN IF BLOOD PRESSURE IS WELL CONTROLLED BY TREATMENT

Abstract

Objective: Whether impaired arterial elasticity in stage 1 hypertension can be brought back to normal by antihypertensive treatment is unknown. Aim of this study was to evaluate the impact of long-term well-controlled blood pressure (BP) on carotid artery elasticity and endothelial function in stage 1 hypertensive patients at low cardiovascular risk. Design and method: We studied 40 middle-age hypertensives whose BP had been kept at target by pharmacological treatment and/or lifestyle modifications for a mean of 7.5 years. Carotid compliance coefficient (CC) and distensibility coefficient (DC) were measured by B-mode ultrasound system. Measurement of carotid intima-media thickness (IMT) was performed in each carotid artery segment, bilaterally. Endothelial function was evaluated by post-occlusion flow mediated dilation (FMD). hs-CRP and osteoprotegerin were measured as markers of inflammation. Forty normotensive subjects matched for age and sex served as controls. Results: In the hypertensive subjects, BP levels were well controlled throughout the study period (mean office BP 133.7 ± 9.0/81.2 ± 7.0 mmHg; mean 24 hours BP was 124.2 ± 10.4/78.2 ± 7.5 mmHg). However, compared to controls, significantly higher office BP levels and waist circumference were present. Compared to normotensives, carotid elasticity (DC 24.5 ± 9.0 vs 37.0 ± 8.5 10–3/kPa, and CC 0.92 ± 0.34 vs 1.28 ± 0.36 mm2/kPa, p < 0.0005 for both) as well as endothelial function (FMD 5.7 ± 2.4% vs 9.2 ± 2.9%, p < 0.0005) were significantly impaired in hypertensives. Moreover, hs-CRP and osteoprotegerin were higher in HT than in NT (1.41 ± 1.07 vs 0.97 ± 0.65 mg/L, p = 0.030; 1246 ± 560 vs 936 ± 148 pg/ml p = 0.001). In a logistic regression, hypertensive status was a significant predictor of local carotid vascular stiffness (DC < 30 10–3/kPa) with an odds ratio of 14.98 (95%CI, 2.60–18.55) p < 0.0005 for crude data; when data were adjusted for age, FMD, OPG, and BMI, the odds ratio only slightly decreased (13.04 (2.27–74.96), p = 0.004). Hypertensive status remained a significant predictor also after the adjustment for systolic, diastolic, mean BP. Conclusions: Despite the “pseudo-normalization’’ of BP levels, hypertensive patients with long term well-controlled BP according to current standards exhibited increased local arterial stiffness, endothelial dysfunction and increased markers of inflammation. Whether an earlier and more aggressive intervention could be useful to reduce arterial stiffening and improve endothelial function in hypertension should be explored.