Alterations In Hypertensive Patients Research Articles

Blood pressure response in exercise is associated with future cardiac structural alterations in hypertensive patients

Abstract Background/Introduction Exaggerated blood pressure response (EBPR) during the exercise treadmill test (ETT) is often observed in individuals without known cardiovascular disease. Although it is generally considered as an abnormal response and a risk factor for hypertension development, its clinical significance remains controversial. On the other hand, regression of left ventricular hypertrophy (LVH) is independently associated with improved cardiovascular outcome. Purpose In this study we aimed to investigate the role of EBPR during exercise in LVH regression in hypertensive subjects over time. Methods 1413 hypertensive subjects, (mean age 57±11 years), 51% males, with baseline office blood pressure (BP) 144/89mmHg were followed for a mean period of 6.4±3.0 years. At baseline and last follow-up visit all patients underwent office BP, laboratory tests and echocardiographical determination of left ventricular mass index (LVMI). At baseline, all subjects underwent treadmill exercise testing (Bruce protocol) in order to identify the presence of EBPR based on the systolic BP elevation at peak exercise (> or =210 mmHg for men and > or =190 mmHg for women). Main outcome variable was LVH Regression/prevention (LVH Regr/prev), defined as: LVH at baseline visit with normal LVMI values at last visit or absence of LVH at baseline and last visit. BP control was considered optimal when the mean of office BP measurements during follow-up was <140/90mmHg. Results 46% of study population presented LVH Regr/prev during follow-up period. Cox-regression analysis, after adjustment for clinical and biochemical variables, revealed that low levels of baseline LVMI (HR=0.98, 95% CI 0.97–0.99, p<0.0001), absence of EBPR (HR=0.81, 95% CI 0.67–0.98, p=0.02) and optimal BP control during follow-up (HR=1.19, 95% CI 1.01–1.56, p=0.03) were independent predictors of LVH Regr/prev during follow-up. Conclusions Beyond optimal BP control, EBPR is a significant predictor of left ventricular mass changes overtime. Hence, ETT can provide clinical relevant information, including EBPR, which may help in the improvement of risk stratification of hypertensive subjects. Funding Acknowledgement Type of funding source: None

Brain MRI fiber-tracking reveals white matter alterations in hypertensive patients without damage at conventional neuroimaging

Hypertension is one of the main risk factor for dementia. The subtle damage provoked by chronic high blood pressure in the brain is usually evidenced by conventional magnetic resonance imaging (MRI), in terms of white matter (WM) hyperintensities or cerebral atrophy. However, it is clear that by the time brain damage is visible, it may be too late hampering neurodegeneration. Aim of this study was to characterize a signature of early brain damage induced by hypertension, before the neurodegenerative injury manifests. This work was conducted on hypertensive and normotensive subjects with no sign of structural damage at conventional neuroimaging and no diagnosis of dementia revealed by neuropsychological assessment. All individuals underwent cardiological clinical examination in order to define the hypertensive status and the related target organ damage. Additionally, patients were subjected to DTI-MRI scan to identify microstructural damage of WM by probabilistic fiber-tracking. To gain insights in the neurocognitive profile of patients a specific battery of tests was administered. As primary outcome of the study we aimed at finding any specific signature of fiber-tracts alterations in hypertensive patients, associated with an impairment of the related cognitive functions. Hypertensive patients showed significant alterations in three specific WM fiber-tracts: the anterior thalamic radiation, the superior longitudinal fasciculus and the forceps minor. Hypertensive patients also scored significantly worse in the cognitive domains ascribable to brain regions connected through those WM fiber-tracts, showing decreased performances in executive functions, processing speed, memory, and paired associative learning tasks. Overall, WM fiber-tracking on MRI evidenced an early signature of damage in hypertensive patients when otherwise undetectable by conventional neuroimaging. In perspective, this approach could allow identifying those patients that are in initial stages of brain damage and could benefit of therapies aimed at limiting the transition to dementia and neurodegeneration.

Urinary exosomes reveal protein signatures in hypertensive patients with albuminuria.

Albuminuria is an indicator of cardiovascular risk and renal damage in hypertensive individuals. Chronic renin–angiotensin system (RAS) suppression facilitates blood pressure control and prevents development of new-onset-albuminuria. A significant number of patients, however, develop albuminuria despite chronic RAS blockade, and the physiopathological mechanisms are underexplored. Urinary exosomes reflect pathological changes taking place in the kidney. The objective of this work was to examine exosomal protein alterations in hypertensive patients with albuminuria in the presence of chronic RAS suppression, to find novel clues underlying its development. Patients were followed-up for three years and were classified as: a) patients with persistent normoalbuminuria; b) patients developing de novo albuminuria; and c) patients with maintained albuminuria. Exosomal protein alterations between groups were identified by isobaric tag quantitation (iTRAQ). Confirmation was approached by target analysis (SRM). In total, 487 proteins were identified with high confidence. Specifically, 48 proteins showed an altered pattern in response to hypertension and/or albuminuria. Out of them, 21 proteins interact together in three main functional clusters: glycosaminoglycan degradation, coagulation and complement system, and oxidative stress. The identified proteins constitute potential targets for drug development and may help to define therapeutic strategies to evade albuminuria progression in hypertensive patients chronically treated.

Abstract 379: Circulating T Regulatory Lymphocytes and Microvascular Structural Alterations in Hypertensive Patients and Normotensive Subjects

Background and Methods. Different components of the immune system, including innate immunity and adaptive immunity (T effector lymphocytes and T regulatory lymphocytes: Tregs) may be involved in the development of hypertension. In addition, it was recently demonstrated that Tregs may prevent angiotensin II-induced vascular injury/inflammation, while Th1, Th2 and Th17 may play a role in the progression of vascular remodeling. However, no data are available in human beings about relationships between T-lymphocyte subtypes and microvascular structure. In the present, preliminary study, we enrolled 7 normotensive subjects and 3 hypertensive patients undergoing an election surgical intervention. No sign of local or systemic inflammation was present in any subjects or patients. All patients underwent a biopsy of subcutaneous fat during surgery. Subcutaneous small resistance arteries were dissected and mounted on a wire myograph, morphological parameter were measured, in particular media to lumen ratio (M/L) was calculated. A peripheral blood sample was obtained before surgery for assessment of T lymphocytes subpopulations by flow cytometry. Results are summarized in the Table. RTE: recent thymus emigrant; naïve: no contact with antigens, TDEM: highly antigen-experienced cells that assume pro-apoptotic properties. Additional significant positive correlations were observed between M/L and Th17 effector lymphocytes: r=0.67, p<0.05). Conclusion Our data suggest that some lymphocytes subpopulations may be related to microvascular remodeling, and open the possibility to regress small artery remodeling in human by specific drug modulation of lymphocyte subtypes.

Hemodynamic alterations in hypertensive patients at rest and during passive head-up tilt

Hypertension is characterized by increased vascular resistance and arterial stiffness, but information about upright hemodynamics is scarce. We compared hemodynamics in hypertensive versus normotensive patients at rest and during passive head-up tilt. Volunteers (n = 387, 19-72 years) without antihypertensive medication were recorded using continuous tonometric pulse wave analysis and whole-body impedance cardiography. Seated office blood pressure was 4/10 mmHg (systolic/diastolic) higher than average supine values during hemodynamic measurements. As there is no accepted cut-off for hypertension during tilt-table tests, supine level at least 135/85 mmHg defined hypertension (n = 155) versus normotension (n = 232). Age, BMI, and proportion of men were higher among hypertensives (49 vs. 42 years, 28 vs. 25, 55 vs. 38%, respectively), and analyses were adjusted for these differences. Both at rest and during head-up tilt radial and aortic blood pressure and pulse pressure, cardiac index (CI) and work, systemic vascular resistance (SVR), and augmentation pressure were higher in hypertensive patients (P < 0.05 for all). Adjusted linear regression analyses showed that during passive head-up tilt aortic SBP and pulse pressure, stroke index, and left cardiac work index decreased less; heart rate increased less; and aortic DBP and SVR increased more in hypertensive patients (P < 0.05 for all); whereas reduction in CI and augmentation index did not differ between the groups. Not only supine hemodynamics, but also responses to head-up tilt differed between normotensive and hypertensive patients, indicating functional alterations beyond increased vascular resistance and higher arterial stiffness in hypertension.

INSULIN RESISTANCE, TUMOR NECROSIS FACTOR-ALPHA IN OBESITY-ASSOCIATED HYPERTENSION: PP.34.367

Objective: It was proposed that adipokines such as tumor necrosis factor-α (TNF-α), in addition to their role in immune response in hypertension, are involved in the development of insulin resistance and obesity. The aim of our clinical study was to assess plasma TNF-α levels, body mass, glucose, insulin, HbA1c levels, and HOMA means in hypertensive patients depend on presence of insulin resistance. Design and Methods: 67 hypertensive patients were examined by anthropometric methods (height, body mass, body mass index (BMI), waist circumference). Plasma TNF-α by ELISA, fasting glucose, insulin, HbA1c, and HOMA were measured. Results: Patients were divided into two groups depend on insulin resistance (IR) presence according to HOMA means: 1group without IR – 25 (37 ± 6%) patients with HOMA<2.77, 2 group with IR – 42 (63 ± 6%) patients with HOMA>2.77. It was found that waist circumference (98.74 ± 1.8 cm) and BMI 35.04 ± 0.88 kg/m2) in insulin resistant patients were statistically higher than in hypertensives without IR (82.0 ± 1.9 cm; 29.71 ± 1.14 kg/m2; p = 0.001, correspondingly). Plasma insulin levels (23.17 ± 2.13 μU/ml) in patients with IR was threefold as compared with patients without IR (7.28 ± 0.67 μU/ml; p = 0.001). ÍbÀñ1, means (7.52 ± 0.43% vs 5.75 ± 0.4%; p = 0.004) and HOMA (8.43 ± 1.23 vs 1.61 ± 0.14; p = 0.001) were also statistically higher in insulin resistance patients. Comparison of TNF-α levels reveals significant its elevation in insulin resistance presence (36.02 ± 3.62 pg/ml) as compared with normal insulin metabolism (17.49 ± 1.51 pg/ml; p = 0.001). In hypertensive patients with IR correlations between TNF-α and insulin r = 0.75, p = 0,001), ÍÎÌÀ (r=0.70, p = 0.001), and ÍbÀñ1 (r = 0.42, p = 0.001) were determined. Conclusions: Our results showed carbohydrates metabolism alterations in hypertensive patients related to obesity presence and TNF-α activity. Insulin resistance that revealed in 63 ± 6% patients with arterial hypertension was associated with increased TNF-α production. In insulin resistant hypertensives close relationships between TNF-α and insulin, HOMA were revealed that can suggest influence of cytokine on insulin resistance development.

1.11 Prevalence of Metabolic Alterations In Hypertensive Patients with Stable vs Unstable Angina

1.11 Prevalence of Metabolic Alterations In Hypertensive Patients with Stable vs Unstable Angina

Retinal microvascular changes and target organ damage in untreated essential hypertensives.

The clinical and prognostic significance of initial retinal alterations in hypertensive patients remains controversial. Therefore, we assessed the relationship of microvascular abnormalities with prognostically validated markers of target organ damage (TOD), such as left ventricular mass (LVM), carotid intima-media thickness (IMT) and microalbuminuria, in early stages of untreated essential hypertension. A total of 437 consecutive, never-treated patients with grade 1 or 2 essential hypertension, referred to our outpatient clinic, underwent the following procedures: (1) clinical and routine laboratory examinations, (2) 24-h ambulatory blood pressure monitoring, (3) 24-h urine collection for microalbuminuria, (4) echocardiography, (5) carotid ultrasonography, (6) non-mydriatic retinography. Patients were divided into group I, with either a normal retinal pattern (n=65, 14.9%) or arteriolar narrowing (n=185, 42.4%) and group II with arteriovenous crossings (n=187, 42.7%). The two groups were similar for gender, body mass index, smoking habit, heart rate, clinic and ambulatory blood pressure (BP) values, while mean age was slightly but significantly higher in group II than in group I (47.6 +/- 10.7 versus 44.5 +/- 12.5 years, P=0.008). No differences occurred between the two groups in LVM index (101.8 +/- 18.5 versus 99.9 +/- 20.4 g/m), carotid IMT (0.67 +/- 0.12 versus 0.66 +/- 0.20 mm), urinary albumin excretion rate (14.4 +/- 27.7 versus 13.3 +/- 27.7 mg/24 h) as well as in the prevalence of LV hypertrophy (14.3 versus 14.0%), IM thickening and/or plaques (26.5 versus 27.2%) (both defined according to 2003 ESH-ESC guidelines) and microalbuminuria (10.1 versus 8.7%). Furthermore, the three different retinal artery patterns were similarly distributed among tertiles of LV mass index, IMT and urinary albumin excretion rate. These results show that: (1) a very large fraction (more than 80%) of untreated, recently diagnosed hypertensive patients have initial retinal microvascular abnormalities detectable by non-mydriatic retinography, (2) the presence of arteriovenous crossings is not associated with more prominent cardiac and extracardiac TOD, (3) fundoscopic examination has a limited clinical value to detect widespread organ involvement in early phases of grade 1 and 2 hypertension.

Prevalence and incidence of urinary sediment alterations in hypertensive patients

P-152 Key Words: Patients Assessment, Haematuria, Sediment Alterations

Carotid hemodynamic alterations in hypertensive patients with insulin resistance

Background Insulin resistance (IR) is implicated in the pathogenesis of atherosclerosis. One mechanism is thought to be the impaired vasodilation, which can lead to a reduction in peripheral blood flow. Hypertensive patients with IR have greater intima–media thickness (IMT) in the common carotid artery (CCA) than those without IR. However, the relationship between IR and hemodynamic alterations of the CCA has not been clarified. Methods Seventy patients with essential hypertension (EHT) and 11 normotensive controls (NT) participated in this study. The IMT, number of plaques, and internal dimensions of the CCA were evaluated by ultrasound imaging. Mean diastolic (Vd) and systolic (Vs) velocity were determined by the Doppler flow method, and other parameters such as Vd/Vs and the cross-sectional distensibility coefficient (CSDC) were further calculated. When the homeostasis model assessment (HOMA) index exceeded 2.0, the subject was considered to have IR. Results: The IMT was positively correlated with the HOMA index in all subjects. The Vd/Vs and CSDC were significantly decreased in EHT patients with IR compared to NT and EHT patients without IR. The Vd/Vs and CSDC were negatively correlated with the HOMA index. A stepwise regression analysis revealed that age, HDL-cholesterol, and the HOMA index were independently associated with IMT in patients with EHT. Age, the HOMA index, and mean blood pressure (MBP) were independently associated with CSDC, and the first two factors were independently associated with Vd/Vs. Conclusions Decreased distensibility of the arterial wall and ensuing low diastolic perfusion are possible mechanisms of atherosclerotic changes in the CCA in EHT patients with IR.

Haemorheologic alterations in hypertensive patients (dipper and no dipper)

Haemorheologic alterations in hypertensive patients (dipper and no dipper)

Hemodynamic alterations in hypertensive patients due to chlorothiazide.

ONLY two studies have been published that detail the changes in cardiac output after chlorothiazide.1 , 2 Other reports3 , 4 have alluded to the changes in cardiac output without tabulating any data. In the studies in which results were reported in detail, cardiac output was performed by the dye-dilution technic. Aleksandrow and his co-workers1 reported variable results in 7 hypertensive patients whereas Dustan and her associates2 demonstrated a consistent decrease. This communication reports on a series of hypertensive patients in whom cardiac output was measured before and after administration of chlorothiazide. In the majority of patients the direct Fick method was used, the . . .