Sofia Papakatsika

Mechanisms of obesity-induced hypertension

The relationship between obesity and hypertension is well established both in children and adults. The mechanisms through which obesity directly causes hypertension are still an area of research. Activation of the sympathetic nervous system has been considered to have an important function in the pathogenesis of obesity-related hypertension. The arterial-pressure control mechanism of diuresis and natriuresis, according to the principle of infinite feedback gain, seems to be shifted toward higher blood-pressure levels in obese individuals. During the early phases of obesity, primary sodium retention exists as a result of increase in renal tubular reabsorption. Extracellular-fluid volume is expanded and the kidney-fluid apparatus is resetted to a hypertensive level, consistent with a model of hypertension because of volume overload. Plasma renin activity, angiotensinogen, angiotensin II and aldosterone values display significant increase during obesity. Insulin resistance and inflammation may promote an altered profile of vascular function and consequently hypertension. Leptin and other neuropeptides are possible links between obesity and the development of hypertension. Obesity should be considered as a chronic medical condition, which is likely to require long-term treatment. Understanding of the mechanisms associated with obesity-related hypertension is essential for successful treatment strategies.

Arterial stiffness and 24 h ambulatory blood pressure monitoring in young healthy volunteers: The early vascular ageing Aristotle University Thessaloniki Study (EVA-ARIS Study)

Differences in 24 h blood pressure (BP) monitoring parameters such as average 24 h BP, day to night BP ratio and BP variability could have an impact in arterial stiffness. The study hypothesis was that despite similar average BP values in ambulatory blood pressure monitoring subjects with increased 24 h BP variability may have increased arterial stiffness. The study population consisted of 115 consecutive young healthy volunteers. Carotid-femoral PWV was measured in all subjects. Clinic BP was measured and an appropriate cuff was fitted on the non-dominant arm of each subject for a 24 h ambulatory blood pressure monitoring session. Waist to hip ratio as well as BMI was measured. Family history and smoking habits were recorded. In univariate analysis, estimated carotid-femoral PWV showed a significant correlation with age, weight, waist circumference, height, clinic systolic and diastolic BP, 24-h systolic and diastolic BP, 24-h pulse pressure, 24-h systolic and diastolic BP variability, daytime systolic and diastolic BP, daytime pulse pressure, daytime systolic and diastolic BP variability, nighttime systolic BP, nighttime pulse pressure and nighttime systolic BP variability. In multivariate regression analysis, age (B=0.95, P<0.001) and 24 h systolic BP variability (B=0.28, P<0.001) were independent determinanats of arterial stiffness. In conclusions, increased 24 h systolic BP variability is associated with arterial stiffness in young healthy volunteers. Pulse wave velocity in a young healthy population is useful to identify determinants of premature arterial stiffness, thus further elucidating the aspects of early vascular ageing.

The role of obesity, salt and exercise on blood pressure in children and adolescents

The increasing trends of blood pressure (BP) in children and adolescents pose great concern for the burden of hypertension-related cardiovascular disease. Although primary hypertension in childhood is commonly associated with obesity, it seems that other factors, such as dietary sodium and exercise, also influence BP levels in children and adolescents. Several studies support that sympathetic nervous system imbalance, impairment of the physiological mechanism of pressure natriuresis, hyperinsulinemia and early vascular changes are involved in the mechanisms causing elevated BP in obese children and adolescents. Under the current evidence on the association of salt intake and BP, dietary sodium restriction appears to be a rational step in the prevention of hypertension in genetically predisposed children and adolescents. Finally, interventional studies show that regular aerobic exercise can significantly reduce BP and restore vascular changes in obese with hypertensive pediatric patients. This article aims to summarize previous studies on the role of obesity, salt intake and exercise on BP in children and adolescents.

Hypothyroidism and hypertension.

Hypothyroidism has been recognized as a cause of secondary hypertension. Previous studies on the prevalence of hypertension in subjects with hypothyroidism have demonstrated elevated blood pressure values. Increased peripheral vascular resistance and low cardiac output has been suggested to be the possible link between hypothyroidism and diastolic hypertension. The hypothyroid population is characterized by significant volume changes, initiating a volume-dependent, low plasma renin activity mechanism of blood pressure elevation. This article summarizes previous studies on the impact of hypothyroidism on blood pressure and early atherosclerotic process.

Arterial stiffness and SBP variability in children and adolescents.

Background: The aim of this study was to explore the impact of ambulatory blood pressure (ABP) parameters on arterial stiffness measured by carotid–femoral pulse wave velocity (cf-PWV) in children and adolescents. Method: The study population consisted of 138 consecutive young patients (age range 4–20 years) referred to our hypertension center. Office blood pressure (BP), 24-h ABP monitoring and cf-PWV measurements were performed in all patients. Family history and smoking habits were also recorded. Results: Among the study population, 10.6% had cf-PWV values equal to or higher than the 95th percentile of the study population. cf-PWV was higher in the hypertensive compared to the normotensive patients, classified by ABP levels even after adjustment for age and sex. Significant correlations were found between cf-PWV and age, weight, height, estimated central pulse pressure (PP), office SBP and DBP, and ABP parameters including 24-h SBP and DBP, weighted 24-h SBP variability, 24-h SBP and DBP load, 24-h mean arterial pressure (MAP), daytime and night-time SBP, daytime and night-time SBP variability, but not with office and 24-h heart rate, 24-h heart rate variability, 24-h daytime and night-time PP, DBP variability, ambulatory arterial stiffeness index and BMI z-score. In analysis of covariance, only weighted 24-h SBP variability (&bgr; = 0.28, P < 0.05) and daytime SBP variability (&bgr; = 0.15, P < 0.05) were the independent determinants of cf-PWV in children and adolescents. Conclusion: These data may suggest that increased SBP variability is closely associated with arterial stiffness in children and adolescents.

9A.01: HYPERURICEMIA IS AN INDEPENDENT DETERMINANT OF ARTERIAL STIFFNESS.

Objective: The aim of the study was to identify determinants of arterial stiffness in patients with increased uric acid levels. Design and method: 280 consecutive subjects (51.4% male) aged 52.98 ± 22.9 years were included in the study. Subjects were never treated before for hypertension or uric acid. A physician measured office BP three times in each subject using a mercury sphygmomanometer. All subjects underwent 24h-ABPM on a usual working day. Pulse wave velocity (PWV) was measured after 15 min of rest in the supine position. The subject was not speaking or sleeping in a quiet, semi-darkened, temperature-controlled laboratory. Participants had been advised to refrain from eating, smoking and drinking caffeine beverages and alcohol before measurement. PWV was calculated as the transit time of the arterial pulse along the carotid-femoral distance divided with the distance measured directly. Results: Carotid-femoral PWV was independently associated (ANCOVA analysis) with age (B = 0.13, P < 0.001), 24 h average SBP (B = 0.07, P < 0.05) and uric acid (B = 0.72, P < 0.001), but not with office BP values, e-GFR, lipid levels, gender and BMI. Carotid-femoral PWV was found 8.215 ± 0.41 m/sec (SE) in patients with normal uric acid values and 10.252 ± 0.91 m/sec (SE) in patients with hyperuricemia after adjustment for age, gender, office BP, 24 h SBP, 24 h pulse pressure, e-GFR, fasting serum cholesterol, triglycerides and BMI. The difference in carotid-femoral PWV between normal uric acid subjects and hyperuricemic patients was 2.037 ± 1.008 m/sec (SE). This difference was statistically significant at the 0.05 level after Bonferronis adjustment for multiple comparisons. Conclusions: Arterial stiffness was found increased in patients with hyperuricemia suggesting a role for increased uric acid in the pathophysiology of large arteries arteriosclerosis independent of age, gender, obesity, blood pressure levels and kidney function.

Early Vascular Aging: A New Target for Hypertension Treatment.

Vascular aging represents a progressive procedure involving biochemical, enzymatic, and cellular changes of the vascular tree. Early vascular aging (EVA), is defined as the inappropriate for age of vascular damage. Increased for age arterial stiffness is a biomarker that should be considered as a cardiovascular (CV) risk factor that can be manipulated. EVA is a new tool for guidance in everyday clinical praxis for patients at increased CV risk or a positive family history of early onset of cardiovascular events, such as stroke or coronary artery disease. Understanding the mechanisms promoting or protecting from EVA, a process that is in close relationship with CV diseases. The role of hypertension treatment against the development of vascular damage is important and different strategies could have a considerable impact on future vascular health.

[PP.09.12] PREVALENCE OF MASKED AND TRUE HYPERTENSION IN MILDLY DISEASED CHRONIC KIDNEY DISEASE

Objective: The aim of this study was to indentify the prevalence of white coat (WCH) and masked hypertension (MH) in mildly diseased chronic kidney disease (CKD) patients(e-GFR:60–90) in comparison to normal kidney function (NKF) subjects (e-GFR >90). Figure. No caption available. Design and method: 558 consecutive subjects (48.5% male) with age 49.2 ± 19.8 years were included in the study. Subjects were never treated before for hypertension. Clinic BP measured three times in each subject using a mercury sphygmomanometer. All the subjects underwent 24h-ABPM on a usual working day. Patients with both ambulatory and clinic BP values in the hypertensive or normotensive range were defined as true hypertensives and normotensives respectively. WCH was defined as office hypertension with ambulatory normotension and MH as ambulatory hypertension with office normotension. e-GFR was estimated with MDRD equation. Results: Age and average 24SBP was significant higher in CKD patients (P < 0.0001) with no differences in clinic BP and average 24 h DBP compared to NKF subjects. Prevalence of true normotension and hypertension are shown in figure. In nominal regression analysis the four groups of hypertension status were included as dependent variable, factors the stage of kidney disease and the gender (reference category: true normotension). WCH, MH and true hypertension were significantly associated with mildly reduced stage of CKD (B = -0.75, P < 0.01, B = -1.24, P < 0.001,. B = -1.14, P < 0.0001 respectively). Conclusions: 24 h ambulatory BP monitoring is important to identify the real BP status in patients with mildly diseased CKD. Mild reduction in GFR is associated with increase 24 h SBP levels in similar clinic BP values.

7C.01: ARTERIAL STIFFNESS IN ISOLATED OFFICE SYSTOLIC HYPERTENSION.

Objective: The aim of this study was to study arterial stiffness in patients indentified as isolated systolic hypertensives. Design and method: 1056 consecutive subjects (48.6% male) aged 47.26 ± 23.4 years were included in the study. 64.7% of the subjects were never treated before for hypertension. A physician measured office BP three times in each subject using a mercury sphygmomanometer. Pulse wave velocity (PWV) was measured after 15 min of rest in the supine position. Patients were classified as having either normal or elevated systolic and diastolic BP, office isolated systolic (>140mmHg systolic and < 90 mmHg diastolic BP) and diastolic hypertensive (<140mmHg systolic and >90 mmHg diastolic BP) subjects. Results: Carotid-femoral (c-f) PWV was 8.045 ± 4.591 m/sec in patients with both normal office systolic and diastolic BP (n = 438), 11.481 ± 6.356 m/sec in patients with isolated office systolic hypertension (n = 202), 7.421 ± 5.108 m/sec in patients with isolated office diastolic hypertension (n = 60), and 9.192 ± 6.113 m/sec in patients with both elevated office systolic and diastolic BP. The difference between isolated office hypertensive subjects and those with both normal systolic and diastolic BP was 3.446 ± 0.471 (SE) m/sec (P < 0.001). The difference between subjects with both elevated systolic and diastolic blood pressure and those with both normal BP was 1.147 ± 0.389 (SE) m/sec (P < 0.05). In univariate analysis of variance age (B = 0.076, P < 0.001) and isolated office systolic hypertension (B = 1.622, P < 0.001) were independent determinants of c-fPWV. c-fPWV was found 8.688 ± 0.266 (SE) in patients with both normal office systolic and diastolic BP and 10.575 ± 0.386 (SE) m/sec in patients with isolated office systolic hypertension after adjustment for age, gender, and BMI. The difference in c-fPWV between patients with isolated office systolic hypertension and subjects with normal office systolic and diastolic BP was 1.887 ± 0.489 (SE) after adjustment for age, gender, and BMI. This difference was significant at the 0.001 level after Bonferronis adjustment for multiple comparisons. Conclusions: Arterial stiffness was found increased in patients with office isolated systolic hypertension suggesting a role for increased office systolic BP in the pathophysiology of large arteries arteriosclerosis independent of age, gender and obesity or a role of stiffer arteries in the pathogenesis of isolated systolic hypertension.

24H PULSE PRESSURE AND AGEING ARE INDEPENDENT PREDICTORS OF ARTERIAL STIFFNESS: PP.3.105

Objectives: To study factors associated with arterial stiffness and early vascular aging. Methods: 523 consecutive patients who visited our hypertension centre were examined. All subjects underwent 24 h Ambulatory Blood Pressure Monitoring (ABPM) and Carotid-femoral (c-f) pulse wave velocity (PWV) measurements. Subjects were overnight fast and avoided smoking. Clinic BP was measured as the average of 6 measurements in two consecutive days. Home BP was estimated according to the ESH guidelines. Waist circumference and BMI were also measured. Results: C-f PWV was positively associated with age (r = 0.75, P < 0.001), clinic SBP (r = 0.41, P < 0.001), clinic DBP(r = 0.16, P < 0.001), home SBP (r = 0.37, P < 0.001), 24 h SBP (r = 0.59, P < 0.001), 24 h SBP variability (r = 0.20, P < 0.001), 24 h DBP (r = 0.34, P < 0.001), 24 h DBP variability (r = -0.25, P < 0.001), 24 h pulse pressure (PP) (r = 0.58, P < 0.001), waist circumference (r = 0.40, P < 0.001), BMI (r = 0.32, p < 0.001), fasting glucose (r = 0.36, P < 0.001), and total cholesterol (r = 0.12, P < 0.05). Home DBP was not associated with carotid-femoral PWV (r = 0.07, P = 0.42). Univariate analysis of variance revealed that age (B = 0.13, P < 0.001) and 24 h PP (B = 0.06, P < 0.05) were independently associated with PWV (models adjusted R2 = 0.66, intercept = 5.11). Clinic and home BP, glucose, cholesterol, waist circumference, and BMI were not predictors in the model. Conclusions: Factors independently associated with c-f PWV were ageing and 24 h pulse pressure. 24 h ABPM seems to be superior to clinic and home blood pressure values to predict arterial stiffness.