Maria Selima

Association of obstructive sleep apnea with urinary albumin excretion in essential hypertension: a cross-sectional study.

BACKGROUND Microalbuminuria reflects a state of widespread vascular dysfunction, whereas obstructive sleep apnea (OSA) further promotes atherosclerotic damage in hypertension. STUDY DESIGN Cross-sectional. SETTING & PARTICIPANTS In an outpatient hypertensive unit, 62 untreated hypertensive patients (aged 48 +/- 7 years; office blood pressure [BP], 151 +/- 8/97 +/- 7 mm Hg) with OSA and 70 hypertensive patients without OSA (apnea hypopnea index [AHI] < or = 5) matched for age, sex, smoking status, body mass index, and 24-hour pulse pressure were studied. PREDICTOR VARIABLE Hypertension and OSA compared with hypertension without OSA. OSA defined as AHI greater than 5, documented by polysomnography. OUTCOME VARIABLE Albuminuria assessed by urinary albumin-creatinine ratio (ACR). MEASUREMENTS Participants underwent polysomnography, ambulatory BP monitoring, echocardiography, routine metabolic profile assessment, and glomerular filtration rate estimation, whereas ACR was measured from 2 nonconsecutive morning spot urine samples. RESULTS Hypertensive patients with OSA compared with those without OSA showed increased 24-hour diastolic BP (87 +/- 7 versus 85 +/- 7 mm Hg; P = 0.03) and nighttime pulse pressure (50 +/- 10 versus 45 +/- 10 mm Hg; P = 0.008), but did not differ regarding metabolic profile and estimated glomerular filtration rate. Albuminuria was greater by 57% in patients with OSA compared with those without OSA: log(10)ACR, 1.1 +/- 0.2 versus 0.7 +/- 0.4 mg/g; P < 0.001). In the entire study population, log10(ACR) correlated with log10(AHI) (r = 0.35; P < 0.001), minimum oxygen saturation during sleep (r = -0.33; P < 0.001), 24-hour pulse pressure (r = 0.38; P < 0.001), and nighttime pulse pressure (r = 0.21; P =0 .01). In a multivariable linear regression model, independent predictors of ACR were AHI (beta = 0.36; P < 0.001) and 24-hour pulse pressure (beta = 0.25; P = 0.01). LIMITATIONS Cross-sectional study. CONCLUSIONS Albuminuria increases within the normal range in hypertensive individuals with OSA compared with those without OSA proportionally to OSA severity independently of confounders. The association of upper-airway dysfunction with albuminuria and pulsatile hemodynamic load may provide an explanatory mechanism for the OSA-related risk in hypertension.

Exercise Blood Pressure Response, Albuminuria and Arterial Stiffness in Hypertension

BACKGROUND A hypertensive response to exercise is associated with high cardiovascular risk, whereas the data about its relation to surrogates of subclinical atherosclerosis are scarce. We investigated the relationships of a hypertensive response to exercise with urinary albumin excretion and arterial stiffness in hypertensives. METHODS There were 171 untreated males (mean age 52 years, all Caucasian) with stage I-II essential hypertension and a negative treadmill exercise test divided into those with a hypertensive response to exercise (n=48) (peak exercise systolic blood pressure > or =210 mm Hg) and to those with normal blood pressure response (n=123). Albumin-to-creatinine ratio values were determined as the mean of 3 nonconsecutive morning spot urine samples, and arterial stiffness was evaluated on the basis of carotid-to-femoral pulse wave velocity. RESULTS Patients with a hypertensive response to exercise compared with those with normal blood pressure response exhibited greater log albumin-to-creatinine ratio (1.52+/-0.59 vs 0.97+/-0.33 mg/g) and higher pulse wave velocity (8.7+/-1.6 vs 7.7+/-1.2 m/s), independent of potentially confounding demographic and clinical factors. Resting systolic blood pressure (odds ratio [OR] 1.11, 95% confidence interval [CI], 1.06-1.16), body mass index (OR 1.12, 95% CI, 1.02-1.23), resting heart rate (OR 0.96, 95% CI, 0.93-0.99), and albumin-to-creatinine ratio (OR 7.45, 95% CI, 2.54-21.83) were independently associated with a hypertensive response to exercise. CONCLUSION A hypertensive response to exercise is related to augmented albumin-to-creatinine ratio and arterial stiffness, reflecting accelerated subclinical atherosclerosis. The association of albumin excretion with exercise blood pressure response suggests that albuminuria constitutes an important factor in the interpretation of the hypertensive response to exercise-associated risk.

Impact of waist circumference on cardiac phenotype in hypertensives according to gender.

Our aim was to assess the differential effect of waist circumference on left‐ventricular (LV) structural and functional alterations, in hypertensive males and females. One thousand seven hundred and eighty nine consecutive, nondiabetic, essential hypertensives (aged 55.8 ± 13.5 years, 966 females), included in the 3H Study, an ongoing registry of hypertension‐related‐target‐organ damage, were classified to obese and nonobese groups according to Adult Treatment Panel III criteria. All participants underwent complete echocardiographic study including LV diastolic function evaluation by means of conventional and tissue Doppler imaging (TDI) methods, averaging early and late diastolic mitral annular peak velocities (Em, Am, Em/Am) from four separate sites of measurement. Hypertensive obese women compared with nonobese exhibited significantly greater LV mass index and prevalence of LV hypertrophy (by 5.5 g/m2, P = 0.003, and 8.8%, P = 0.005, respectively), while such differences were not present among men. Obese women compared to nonobese ones were accompanied by lower transmitral E/A (by 0.08, P < 0.001), TDI‐derived Em/Am (by 0.12, P < 0.001), and higher E/Em ratio (by 0.8, P = 0.016). In contrast, hypertensive obese men compared to nonobese ones exhibited lower E and Em (by 0.04 m/s and 0.6 cm/s, both P < 0.05). A significant interaction between sex and abdominal obesity was observed only regarding TDI‐derived Am and Em/Am. Furthermore, waist circumference was a predictor of E/A (β = −0.097, P = 0.002) and Em/Am (β = −0.116, P = 0.001), independently of body size, in females but not in males. The adverse effect of abdominal obesity on LV alterations is more pronounced among female hypertensives, suggesting that routine measurement of waist circumference provides additional information on cardiac phenotype especially in women.

Evidence for no global effect of metabolic syndrome per se on early hypertensive sequelae.

Objective In the present study we assessed the impact of metabolic syndrome (MS) and its components on markers of cardiovascular and renal damage in a population of essential hypertensives. Methods A total of 651 consecutive, untreated and non-diabetic hypertensives (age 54 ± 12 years, 340 males) who were included in the 3H Study, an ongoing registry of hypertension-related target organ damage, were considered for analysis. Left ventricular mass was indexed both for body surface area (LVMBSA) and for height2.7 (LVMheight2.7). Diastolic function was estimated by means of both conventional and tissue Doppler imaging (TDI) methods. Arterial stiffness was evaluated on the basis of carotid to femoral pulse wave velocity (c-f PWV) and microalbuminuria (MA) as albumin to creatinine ratio (ACR) 22–300 mg/g in men and 31–300 mg/g in women in two non-consecutive morning spot urine samples. Results MS (Adult Treatment Panel III criteria) was present in 201 hypertensives (30.9%). Hypertensives with MS had increased logACR (by 10%, P = 0.01) and higher prevalence of MA (17 versus 8%, P < 0.001). Both groups exhibited similar values of LVMBSA, transmitral and TDI-derived indexes and c-f PWV (NS for all) while LVMheight2.7 was significantly higher in hypertensives with MS (by 2.6 g/m2.7, P = 0.023). Multiple regression analysis revealed that MS was an independent predictor only of logACR (β = 0.110, P = 0.007) and MA (odds ratio = 2.577, P < 0.001), while components of blood pressure affected all studied indices of organ damage. Conclusions MS per se does not deteriorate cardiac adaptations and aortic stiffness beyond haemodynamic load in hypertension. The MS-related unfavourable effect is limited to the level of the glomerulus.

Association of resistin with urinary albumin excretion in nondiabetic patients with essential hypertension.

BACKGROUND Evidence suggests that resistin, a recently described protein, is associated with subclinical atherosclerosis in different clinical settings. In this study, we investigated the relationship of increased resistin levels with urinary albumin excretion, expressed as the albumin-to-creatinine ratio (ACR), an established index of diffuse vascular damage, in hypertensives. METHODS Our population consisted of 132 untreated nondiabetic subjects with stage I-II essential hypertension (49 males, mean age = 54 years, mean office blood pressure (BP) = 159/100 mm Hg). In all patients, ACR was determined as the average of three nonconsecutive morning spot urine samples, and venous blood sampling was performed for estimation of resistin concentrations. The distribution of resistin was split by the median (4.63 ng/ml), and accordingly, subjects were stratified into those with high and low values. RESULTS Hypertensive patients with high (n = 66) compared to those with low resistin (n = 66) exhibited higher ACR values (21.8 + or - 15.3 vs. 10.3 + or - 3.8 mg/g, P < 0.01), even after adjustment for confounders. In the total population, resistin was associated with 24-h systolic BP (r = 0.244, P < 0.05), serum creatinine (r = 0.311, P = 0.007), and ACR (r = 0.499, P < 0.01). Multiple regression analysis revealed that age (b = 0.193, P = 0.02), body mass index (b = 0.237, P = 0.02), 24-h systolic BP (b = 0.338, P < 0.0001), 24-h heart rate (b = 0.169, P = 0.04), and resistin (b = 0.77, P < 0.01) were independently associated with ACR (R(2) = 0.471, P < 0.01). CONCLUSIONS Hypertensive subjects with augmented resistin levels exhibit higher albuminuria, independently of established risk factors. Moreover, the association of resistin with ACR suggests a link between resistin and microvascular disease in the early stages of essential hypertension.

CHRONIC PERIODONTAL DISEASE AND SYSTEMIC INFLAMMATION ON ENDOTHELIAL DYSFUNCTION IN UNTREATED HYPERTENSIVE PATIENTS: PP.2.53

Objectives: To investigate the relationship between periodontal disease indexes (PDI) and endothelial dysfunction by means of asymmetric dimethyl-arginine (ADMA) in conditions of both increased and decreased systemic inflammation in the setting of hypertension. Design and Methods: We studied 108 - aged 52 ± 9 years - untreated hypertensive subjects (24 h systolic/diastolic blood pressure [BP] 131 ± 11/83 ± 9mmHg) with diverse severity of periodontal disease (i.e. mean clinical loss of attachment [CLA], maximum probe depth [MPD] and gingival index [GI]). Subjects underwent office and ambulatory BP measurements, echocardiography, and periodontal examination; while from fasting venous blood samples we assessed metabolic profile, and we measured ADMA and high sensitivity C reactive protein (hsCRP) levels. With respect to the median of hsCRP and ADMA (1.79 mg/l and 0.81 ìmol/l, respectively) the study population was divided in four groups: low-ADMA/low-hsCRP (n = 30), low-ADMA/high-hsCRP (n = 27), high-ADMA /low-hsCRP (n=21) and high-ADMA/high-hsCRP (n = 30). Results: High-ADMA/high-hsCRP group resulted significantly older compared with both low-ADMA/low-hsCRP and high-ADMA/high-hsCRP groups, while high compared with low-ADMA groups demonstrated increased low-density lipoprotein cholesterol. PDIs were increased in those with high compared with those with low-hsCRP, while the addition of high-ADMA contributed significantly to that comparison. Log(10)(hsCRP) and log(10)(ADMA) were correlated with CLA (β=0.35, p = 0.01 and β=0.25, p = 0.012, respectively), MPD (β=0.25, p = 0.002 and β=0.32, p = 0.008, respectively) and GI (β=0.34, p < 0.001 and β=0.36, p < 0.001, respectively). After adjustment for confounders, high-ADMA/high-hsCRP was significantly associated - by means of adjusted z-scores - with mean clinical loss of attachment, maximum probe depth and gingival index by 10.33, 8.84 and 2.74 times more often with respect to the low-ADMA/low-hsCRP pattern. Conclusion: PDI are associated in a dose-dependent manner with ADMA in untreated hypertensives and increased systemic inflammation further contributes to that phenomenon.