Artery In Hypertensive Patients Research Articles

The Difference of Mean WSS Value on The Carotid Bifurcation and The Medial Segment of Common Carotid Artery Using Vector Flow Ultrasonography in Hypertensive Patients at Prof Dr. I.G.N.G Ngoerah General Hospital February-April 2022

Background : Hypertension is a risk factor for atherosclerosis which increases the risk of stroke. Transitions in blood vessels such as bifurcations are associated with changes in the velocity and pattern of blood flow that decrease wall shear stress (WSS) and is believed to be a risk factor for atherosclerosis. Shear stress on the common carotid artery also decreased with increasing blood pressure. This study aims to determine the difference of mean WSS value on the carotid bifurcation and the medial segment of common carotid artery using vector flow ultrasonography in hypertensive patients. Methods: This study used a cross-sectional design with the research location at the Radiology Installation of Prof. Dr. I.G.N.G Ngoerah Hospital Denpasar in February-April 2022. The sample of this study was hypertensive patients who came to the Radiology Installation of Prof. Dr. I.G.N.G Ngoerah Hospital and met the inclusion criteria as many as 32 people. The examination was carried out by a consultant of head and neck radiology, using an ultrasound device with a linear transducer probe that has a probe frequency range of 3-9 Mhz. Results: The average age of the sample in this study was 50 years, with 9 males (28.1%), 23 females (71.9%). The results showed that the average maximum WSS value on the carotid bifurcation (3.37±0.96) Pa, the mean value (1.15±0.45) Pa, while the average maximum WSS value on the medial segment of the common carotid artery (4 ,41±1.45)Pa, the mean value (1.78±0.54)Pa. The average maximal and mean WSS value on carotid bifurcation were lower than the medial segment of the common carotid artery in hypertensive patients (p<0,05). The results of multivariate analysis on WSS values after controlling for confounding variables, obtained the average maximal and mean WSS value on carotid bifurcation, remained lower than the medial segment of the common carotid artery (p<0,05). Conclusion: there were significant differences in the mean wall shear stress (WSS) of the carotid bifurcation and the medial segment of the common carotid artery in hypertensive patients. Suggestions that can be done next are in facilities that have vector flow ultrasonography facilities, it is recommended to measure the WSS value in hypertensive patients as additional information as a predictor of atherosclerosis

Evaluation of renal arteries in hypertensive patients by multi-detector computed tomography

Introduction: Among various causes of hypertension, only 1 to 2% is renovascular hypertension which may be characterized by the various reasons in renal vascular supply. Multi-detector computed tomography is used to know about the details of the vascular structures in patients. This study aims to evaluate the renal arteries in hypertensive patients. Methods: A prospective observational study was conducted among 93 hypertensive patients. Contrastenhanced computed tomography of the abdomen and pelvis was conducted, and measurements were obtained from the axial section of the maximum intensity projection image. Data were analyzed using SPSS version 23.0. Independent t-test and Pearson’s Correlation were used. The level of statistical significance was set at p<0.05. Results: The study found mean lengths for the right and left main renal arteries to be 40.33±10.26 mm and 32.36±9.55 mm, and diameters were 4.31±0.86 mm and 4.16±0.81 mm. No significant sex-based differences were observed. However, a significant age-related difference was noted in the length (p=0.012) and diameter (p=0.036) of the right main artery within the 20 to 29 and 80 to 89 years age groups. Weak correlations were observed between left renal artery length and age (r=0.221, p=0.33) and mean right renal artery diameter and age (r=-0.218, p=0.036). Prevalence of accessory renal arteries and early branches was 19.35% and 16.10% respectively. Conclusions: This study found that there were no statistically significant differences in renal arteries dimensions of hypertensive patients with different age groups and genders. Although the proportion of early renal artery branching and accessory arteries are found to be similar to previous studies there may be other associated factors for all hypertensive patients who don’t have early renal branches or accessory arteries.

Association of dipping pattern of blood pressure and atherosclerotic burden of coronary arteries in hypertensive patients.

Aim The aim of this study was to determine the association between the dipping pattern of BP and coronary artery disease in hypertensive patients.Material and methods A total of 356 hypertensive patients were included in the study. The results of ambulatory BP monitoring, echocardiography, and coronary computerised tomographic angiography were evaluated retrospectively. The patients were divided into two groups on the basis of their ambulatory BP monitoring: 1) patients with the dipping pattern of BP; 2) patients with the non-dipping pattern (NDP).Results Among the 356 patients, 145 were male (40.7 %). The smoking status was higher in patients with NDP (p=0.023). The statin usage in patients with the dipping pattern was higher in patients with NDP (p=0.027). There were no significant differences in the echocardiographic findings. 58.6 % of the patients without plaque formation had the dipping pattern of BP (p<0.05), however 84.4 % of patients with >50 % plaque formation had the NDP of BP (p<0.001).Conclusion The NDP of BP might be related to the increased atherosclerotic process in coronary arteries, and pa-tients with NDP might have an increased atherosclerotic burden for coronary arteries when compared with patients with a dipping pattern.

Abstract MP60: Down-regulated Mir-338-3p In Subcutaneous Small Arteries Of Hypertensive Patients With Chronic Kidney Disease Targets Protein Tyrosine Phosphatase Receptor Type S And Glutathione Peroxidase 3

Background: Hypertension (HTN) causes vascular injury identified by endothelial dysfunction, vascular stiffening, and remodeling, which contributes to kidney damage leading to chronic kidney disease (CKD). MicroRNAs (miRNAs) repress/degrade target mRNAs. Their role in vascular injury in HTN remains unclear. We aimed to identify differentially expressed (DE) miRNAs in gluteal subcutaneous arteries of patients with HTN associated or not with CKD to shed light on the pathophysiological molecular mechanisms. Methods: Normotensive subjects and patients with HTN associated or not with CKD grades 3-4 were studied (n=15-16). Small arteries were isolated from gluteal subcutaneous biopsies, RNA extracted and small and total RNA sequencing performed by Illumina HiSeq-2500. DE genes were identified with a P <0.05 and fold change (FC) >1.3. Top 3 DE miRNAs ( P <0.001, FC>2, mean read count number (MRCN) >3,000 in all groups and having predicted mRNA targets) were selected for validation by reverse transcription-quantitative PCR (RT-qPCR). The mRNA targets of the top selected miRNA were predicted by TargetScan with P <0.01, FC>1.5 and MRCN>150 and the top 9 targets were validated by RT-qPCR using gain- and loss-of-function in human aortic endothelial cells (HAECs). Gene ontology enrichment analysis (GOEA) was done in Cytoscape. Results: DE miRNAs and mRNAs were identified uniquely associated with HTN (miRNAs: 10, mRNAs: 68), CKD (miRNAs: 68, mRNAs: 395), and in both groups (miRNAs: 2, mRNAs: 32). miR-338-3p presented the best correlation between RNA sequencing and RT-qPCR (R 2 =0.328, P <0.001) among the top 3 DE miRNAs. Two of the selected top 9 miR-338-3p predicted targets were validated in HAECs. Protein tyrosine phosphatase receptor type S ( PTPRS , FC: 0.80±0.08 vs 1.00±0.00) and glutathione peroxidase 3 ( GPX3 , FC: 0.88±0.04 vs 1.00±0.00) were down-regulated in HAECs transfected with miR-338-3p mimics ( P <0.05). GOEA showed association of GPX3 with oxidative stress detoxification ( q <0.05), and of PTPRS with the immune system, neuronal system and developmental process ( q <0.001). Conclusion: Down-regulated miR-338-3p in gluteal subcutaneous small arteries of hypertensive patients with CKD targets PTPRS and GPX3 that may play a role in vascular injury in HTN.

One-stop assessment of renal function and renal artery in hypertensive patients with suspected renal dysfunction: non-enhanced MRI using spatial labeling with multiple inversion pulses.

To assess whether spatial labeling with multiple inversion pulses (SLEEK) sequence can be employed as a one-stop assessment method for evaluating renal function and displaying renal artery in hypertensive patients with suspected renal dysfunction. A total of 78 patients with suspected hypertensive renal damage were enrolled in this retrospective study. All patients underwent MRI examinations, and both SLEEK and DWI sequences were performed simultaneously. According to estimated glomerular filtration rate (eGFR), patients were divided into three groups (Group 1, eGFR> 90; Group 2, eGFR = 60-90; Group 3, eGFR< 60). Twenty-two of these patients also underwent CT angiography (CTA) examination. Comparison between CTA, DWI, and eGFR was performed to assess the value of SLEEK in evaluating renal function and displaying renal artery. The performance of SLEEK to display renal artery was highly consistent with the results of CTA (kappa = 0.713). The corticomedullary contrast ratio positively correlated with eGFR (p = 0.004, r = 0.322) and was significantly higher in SLEEK images than in DWI images in all three groups (p < 0.001). There was no significant difference in corticomedullary contrast ratio in SLEEK images between Group 1 and Group 2 (p = 0.285). However, the minimal renal cortical thickness, which significantly correlated with eGFR (p < 0.001, r = 0.866), was significantly different between Group 1 and Group 2 (p < 0.001). ROC analysis showed good diagnostic performance when differentiating patients with eGFR> 60 from those with eGFR< 60. The SLEEK sequence could evaluate simultaneously renal function through corticomedullary differentiation and renal arteries, enabling one-stop assessment in hypertensive patients with suspected renal dysfunction. • Spatial labeling with multiple inversion pulses (SLEEK) improves renal corticomedullary differentiation in hypertensive patients with renal dysfunction compared with DWI. • SLEEK clearly displays renal artery in hypertensive patients with renal dysfunction. • SLEEK could be utilized as a one-stop assessment method for evaluating renal function and renal artery in hypertensive patients.

Impact of Diabetes Mellitus and Ischemic Heart Disease on the Blood Resistivity Index of Renal Arteries in Hypertensive Patients

Impact of Diabetes Mellitus and Ischemic Heart Disease on the Blood Resistivity Index of Renal Arteries in Hypertensive Patients

Abstract P3003: miR-338-3p Down-Regulation Caused Up-Regulation of Alkaline Ceramidase 2 and Glutathione Peroxidase 3 mRNAs in Subcutaneous Small Arteries of Hypertensive Patients With Chronic Kidney Disease

Background: Hypertension (HTN) and chronic kidney disease (CKD) are associated with vascular damage characterized by vascular remodeling and stiffening and endothelial dysfunction. miRNAs are small non-coding RNA that regulate gene expression by binding to their target messenger RNAs (mRNAs), leading to mRNA degradation or translational repression. Their implication in vascular injury remains unclear. We aimed to identify differentially expressed (DE) miRs in small arteries of HTN and CKD human subjects to gain insight into pathophysiological molecular mechanisms in these conditions. Methods: Normotensive, HTN [systolic blood pressure (BP) &gt;135 mmHg or diastolic BP of 85-115 mmHg with BpTRU] and CKD subjects (estimated glomerular filtration rate &lt;60mL/min/m 2 ) (n=15-16) were studied. Small arteries were isolated from subcutaneous gluteal biopsies and RNA extracted for small and total RNA sequencing using Illumina HiSeq-2500 and further studied using a systems biology approach. Differentially expressed (DE) genes were identified with fold change &gt;1.5 and fold discovery rate &lt;0.1. Results: DE miRs were identified ( P &lt;0.05) uniquely associated with HTN (3↑ and 6↓) or CKD (42↑ and 39↓) or both groups (2↓). Correlation between RNA-sequencing and RT-qPCR data was demonstrated for 3 of 14 tested miRs. Among them, the first-ranked, miR-338-3p ( r =0.91, P &lt;10 -16 ), uniquely associated with CKD, was studied further. miR-338-3p and some of its predicted targets were highly expressed in human aortic endothelial cells (HAECs). Two of them, alkaline ceramidase 2 ( ACER2 ) and glutathione peroxidase 3 (GPX3), were up-regulated by ~36% and ~60% in HAECs transfected with anti-miR-338-3p, respectively ( P &lt;0.05). miR-338-3p mimic co-transfection decreased by 30% luciferase activity of reporter vectors containing the conserved wild-type but not mutated ACER2 or GPX3 3’ untranslated transcribed region miR-338-3p-5p binding sites ( P &lt;0.05). Conclusion: miR-338-3p was down-regulated in small arteries, which was uniquely associated with CKD. ACER2 and GPX3 , identified as miR-338-3p targets, may play a role in vascular injury in CKD.

A3978 miR-338–3p down-regulation was identified in small arteries of hypertensive patients with chronic kidney disease

A3978 miR-338–3p down-regulation was identified in small arteries of hypertensive patients with chronic kidney disease

Abstract P120: Mir-338-3p is Down-regulated in Subcutaneous Small Arteries of Hypertensive Patients With Chronic Kidney Disease

Background: Hypertension (HTN) and chronic kidney disease (CKD) are among the most prevalent global health conditions that cause millions of deaths per year. They are associated with vascular damage characterized by vascular remodeling, stiffening and endothelial dysfunction. miRNAs (miRs) are a class of small non-coding RNA that regulate gene expression by binding to their target messenger RNAs (mRNAs), thereby leading to mRNA degradation or translational repression. Their implication in vascular injury remains unclear. We aimed to identify differentially expressed (DE) miRs in small arteries of HTN and CKD human subjects to gather insight into pathophysiological molecular mechanisms in these conditions. Methods and Results: Normotensive, HTN [systolic blood pressure (BP) &gt;135 mmHg or diastolic BP of 85-115 mmHg with BpTRU] and CKD subjects (eGFR&lt;60mL/min/m 2 ) (n=15-16) were studied. Small arteries were isolated from subcutaneous gluteal biopsies and RNA extracted for small and total RNA sequencing using Illumina HiSeq-2500. EdgeR identified DE miRs ( P &lt;0.05) uniquely associated with HTN (3 up and 6 down) or CKD (42 up and 39 down) or with both groups (2 down). Reverse transcription-quantitative PCR (RT-qPCR) was used to confirm miRNA differential expression. Correlation between RNA sequencing and RT-qPCR data was demonstrated for 3 miRs from 14 tested: mir-146a-5p (r=0.56, P &lt;10 -4 ), miR-338-3p (r=0.91, P &lt;10 -16 ) and mir-374a-3p (r=0.57, P &lt;10 -4 ). The best correlated DE miRNA, miR-338-3p was down-regulated by 76% ( P &lt;10 -4 ) and uniquely associated with CKD. TargetScan predicted that the up-regulated mRNA encoding glutathione peroxidase 3 ( GPX3 , 1.57 fold, P &lt;0.001) to be a miR-338-3p target. Both miR-338-3p and GPX3 were found to be highly expressed in human aortic endothelial cells (HAECs) by RT-qPCR. Target prediction was validated by showing using RT-qPCR that GPX3 expression was up-regulated 1.73±0.28 fold in HAECs transfected with anti-miR-338-3p ( P &lt;0.05). Conclusion: miR-338-3p down-regulation was found in small arteries, uniquely associated with CKD. GPX3 , which may be important for preservation of endothelial function, is a miR-338-3p potential target. miR-338-3p and associated target may play a role in vascular remodeling in CKD.

ВЗАИМОСВЯЗЬ МЕЖДУ СУБКЛИНИЧЕСКИМИ СТРУКТУРНЫМИ ИЗМЕНЕНИЯМИ СОННОЙ АРТЕРИИ И КОГНИТИВНЫМИ ФУНКЦИЯМИ У ПАЦИЕНТОВ С ГИПЕРТОНИЧЕСКОЙ БОЛЕЗНЬЮ

Introduction. At present, a number of clinical studies have confirmed the relationship between blood pressure and cognitive impairment. Objective. The aim of the study was to analyze the relationship between cognitive impairment and subclinical changes in carotid arteries in hypertensive patients. Material and methods. 69 patients with hypertensive disease of the II stage, average age of 51.38 ± 0.94 years, were examined. Patients were divided into 2 groups with absence and presence of cognitive impairment. The examination of the right common carotid artery was carried out using an ultrasound multifunction scanner. To study cognitive impairment used a number of MoCA test. Results. The average thickness of the intima-media complex in the patients of the first and second groups was not significantly different. The proportion of people with intima-media complex thickness exceeding normal values was significantly higher in persons with cognitive impairment (71%) than in persons without them (39.5%). Сonclusions. In patients with stage II of hypertensive disease, the thickness of the intima-media complex of the carotid artery was increased. A positive correlation of increased thickness of the intoma-media complex with hypertensive crises was found only in persons with cognitive impairment.

Abstract 064: Transactivation of Egfr by Tgfβ Induces Hypertension by Increasing Arteriolar Myogenic Response

Emilin1 (E1) is a protein of the extracellular matrix regulating TGFβ bioavailability through proTGFβ proteolysis. E1 KO mice are hypertensive with increased TGFβ activation. As E1 is expressed in vessels from embryonic life to adulthood, is still unknown whether the E1 KO phenotype results from a developmental defect or lack of homeostatic role in the adult. To dissect this issue, we used a conditional gene targeting inactivating E1 in smooth muscle cells (SMCs) of adult mice, by the use of E1flox/flox and tamoxifen (TAM) inducible Cre recombinase specific for SMCs. When E1fl/fl mice carrying the Smmhc-CreERT2 were given TAM blood pressure significantly increased (SBP: 123±2 vs basal condition 104±3;***p&lt; 0.001) as well as myogenic tone (MT) of resistance arteries (16.3±0.7 vs basal condition 11.4±0.1 % at 125 mmHg). How increased TGFβ signaling in SMCs could determine an increased MT is still unknown. Relevant to this, we found that the higher TGFβ signaling in E1 KO SMCs stimulates heparin binding epidermal growth factor (HB-EGF) and subsequent transactivation of the EGF receptor, a mechanism typically implied in potentiating MT. When mesenteric resistance arteries from E1 were subjected to step-increases in intraluminal pressure, EGFR inhibition rescued the increased MT. At the molecular level, TGFβ-induced EGFR transactivation resulted into the activation of transient receptor potential classical type 6 (TRPC6) and melastatin type 4 (TRPM4) channels. To put our data into translational perspective, we measured MT of resistance arteries isolated from hypertensive patients and normotensive subjects, finding increased MT (HT 16.4±0.7; NT 11±0.4;***p&lt; 0.001) and TGFβ signaling in the former group. By using a neutralizing anti-TGFβ or an anti-EGFR we found a normalization of the increased MT (HT+anti-TGFβ 11±1.3; NT+anti-TGFβ 11.2±1.2;***p&lt; 0.001 and HT+anti-EGFR 9±0.6; NT+anti-EGFR 10.8±1.1;***p&lt; 0.001), thus confirming the relevance of TGFβ-EGFR pathway in humans. Taken together these data suggest that primary increase of MT induced by TGFβ-EGFR transactivation can cause hypertension and that higher TGFβ signaling and MT are common alterations of resistance arteries of hypertensive patients.

Abstract P159: MicroRNA Profiling in Small Resistance Arteries of Hypertensive Patients With or Without Chronic Kidney Disease

Background: Hypertension (HTN) and chronic kidney disease (CKD) are global health disorders that are epidemiologically associated. Vascular injury is an early manifestation in HTN and contributes to CKD. It is characterized by endothelial dysfunction and vascular remodeling that are accompanied by gene expression changes. MicroRNAs (miRs) are important non-coding RNA regulators of gene expression. Dysregulation of miRs has been shown in HTN and CKD, but their implication in vascular injury remains unclear. We aimed to identify differentially expressed (DE) miRs in small arteries of HTN and CKD human subjects to get further insight into pathophysiological molecular mechanisms in these conditions. Methods and Results: Normotensive, HTN (systolic blood pressure (BP) &gt; 135 mm Hg or diastolic BP of 85-115 mm Hg with BpTRU) and CKD subjects (estimated glomerular filtration rate &lt;60mL/min/m 2 ) (n=15-16) were studied. Small arteries were dissected from a subcutaneous gluteal biopsy under RNAse free condition and used for total RNA extraction with the mirVana miR isolation kit. cDNA libraries were prepared using the TruSeq small RNA prep kit and the TruSeq stranded total RNA prep kit, and sequenced by Illumina HiSeq 2500. DE miRs and DE mRNAs ( P &lt;0.05) were identified using EdgeR, which found 3 up- and 6 down-regulated miRs, as well as 134 up- and 149 down-regulated mRNAs uniquely associated with HTN, 42 up- and 39 down-regulated miRs, as well as 743 up- and 348 down-regulated mRNAs uniquely associated with CKD, while 2 up-regulated miRs and 101 up- and 75 down-regulated mRNAs were found in both groups. Target Scan was used to predict DE miR targets in the DE mRNAs. Enrichment analysis showed that the HTN-associated DE miR-targeting DE mRNAs were highly enriched in gene ontology (GO) terms involved in peptidase activity, mitochondrial activity and immune response ( q &lt;0.01), while the CKD-associated DE miR-targeting DE genes were highly enriched in GO terms involved in tube formation, fibroblast proliferation and EGF response ( q &lt;0.001). Conclusions: DE miRs were identified in small arteries of HTN and CKD patients. Enrichment analysis in DE miR-targeting DE mRNAs revealed GO terms that could be linked to different degrees of vascular changes in HTN and CKD.

Abstract 615: Transactivation of EGFR by TGFβ Induces Hypertension by Increasing Arteriolar Myogenic Response

Myogenic tone (MT) is an intrinsic property of arteriolar smooth muscle cells (SMCs) that contract when intraluminal pressure is increased. MT is a relevant physiological mechanism to maintain stable blood flow through important organs like kidney and brain, thus preventing organ damage that could derive from increase in blood pressure (BP). On the other hand, enhancement of the basal MT could raise BP by increasing systemic vascular resistance, thus further contributing to hypertension. Several studies in animal models suggest that primary dysfunctions in SMCs can directly cause abnormalities in BP. However, in hypertensive animal models investigated so far, the increment of MT is accompanied by a stronger response to G protein coupled receptor (GPCR) agonists, thus making it difficult to distinguish whether increased vascular resistance and BP are primary effects of a more robust MT or the consequence of increased reactivity to agonists. Here we show an increased MT in mice deficient of Emilin1 , an extracellular inhibitor of TGFβ signaling, displaying a phenotype of spontaneous hypertension. We also found that the higher TGFβ signaling in Emilin1 deficient SMCs stimulates heparin binding epidermal growth factor (HB-EGF) expression and subsequent transactivation of the EGF receptor. When step-increases in intraluminal pressure are applied to mesenteric resistance arteries (MRA), the combined stimulation of mechanosensor and EGF transactivation results into activation of transient receptor potential classical type 6 (TRPC6) and melastatin type 4 (TRPM4) channels, stimulation of voltage dependent calcium channels (VDCC). To put our data into translational perspective, we measured MT on resistance arteries isolated from hypertensive patients and untreated normotensives, finding increased MT and TGFβ signaling in the former group. In addition, by using an antibody neutralizing EGFR signaling we found a normalization of the increased MT, thus confirming the relevance of TGFβ-EGFR pathway in humans. Overall our results suggest that primary increase of MT induced by TGFβ-EGFR transactivation can cause hypertension and that higher TGFβ-EGFR signaling and MT are common alterations of resistance arteries of hypertensive patients.

Characteristics of changes and clinical and instrumental predictors of the severity of structural remodelling of carotid arteries in hypertensive patients

Background. Mechanisms of activation of the process of vascular wall remodelling in patients affected by arterial hypertension have not been studied in depth and require clarification. Materials and methods. The study included 381 patients with hypertension — 212 men and 169 women of the average age 53.0 (47; 60) years. The structural-functional vessel status was determined by the method of duplex scanning and colour duplex mapping of blood flow with the Logiq 500 MO apparatus (GE, USA). Statistical analyses were made using Microsoft Excel software kit, Statistica for Windows 6.0. Results. The patients with hypertension presented some left-right asymmetry of remodelling extracranial carotid arteries. Unlike the impact of remodelling of the right carotid artery, the most essential effect on the left carotid artery was the impact of daytime pulse arterial pressure and variability of the nocturnal systolic arterial pressure (the strength of impact 25.0 and 13.9%, respectively. The processes of remodelling of the right carotid artery are more sensible to the impact of high values of nocturnal diastolic arterial pressure (the strength of impact 16.4%). The beginning of some brain complication is associated with the significant increase in atherosclerotic affection not only of the left, but also of the right carotid artery. Conclusions. Remarkable remodelling of the right carotid artery is often associated with the severity of the disease and to some extent reflects the severity of the flow of the disease and can be regarded as an additional unfavourable feature.

Aging and structural alterations of subcutaneous small resistance arteries in hypertensive patients

Aging and structural alterations of subcutaneous small resistance arteries in hypertensive patients

Abstract P255: Age and Structural Alterations in Subcutaneous Small Resistance Arteries of Hypertensive Patients

Background: It was proposed that early vascular ageing may be an important mechanism of vascular damage in large conductance arteries. However it is not known whether aging may also affect small resistance artery morphology. Patients and Methods: For this reason, we investigated 100 patients with essential hypertension. Secondary forms of hypertension were excluded according to standard clinical evaluations and biochemical or instrumental assessments. In all patients, an evaluation of small resistance arteries morphology was performed by a wire micromyographic approach (Mulvany’s technique). A small amount of subcutaneous tissue was obtained by local biopsy or during election surgery and subcutaneous small resistance arteries were dissected and mounted on a myograph; the media to lumen ratio (M/L) was then measured. Results: The age range of our populaton was 22-81 years, with a mean value of 57±12 years; 14% of them were current smokers, 32% had alterations in lipid patterns, none of them had diabetes mellitus, 58 were males and average blood pressure values were 156/95±19/12 mmHg. We found a significant correlation between M/L and age (r=0.30, p=0.002): the statistical significance of the correlation persisted after correction for counfounding variables (gender, serum cholesterol, smoking status, serum glucose, systolic or diastolic blood pressure values). A statistically significant inverse correlation was also observed between internal diameter and age (r=-0.20, p=0.046), while the correlation beween age and media thickness did not reach statistical significance (r=0.09, p=0.37). Conclusion: Our data suggest that age may affect microvascular structure in hypertensive patients. It is also possible that hypertension may anticipate the effects of physiological aging, and this should be explored in a relatively large population of normotensive subjects.

Abstract 024: The Direct Renin Inhibitor Aliskiren Improves Vasodilation and Endothelial Function in Resistance Arteries from Diabetic and Hypertensive Patients

We previously demonstrated that the direct renin inhibitor aliskiren (ALK) significantly reduced the remodeling of subcutaneous resistance arteries of hypertensive patients as compared to the angiotensin-converting enzyme inhibitor ramipril (RAM). Here we questioned whether endothelial function of resistance arteries would improve after 1 year of blood pressure (BP) control with ALK or RAM. Sixteen diabetic patients with mild essential hypertension were randomized to ALK (150-300 mg once daily, n=9) or RAM (5-10 mg once daily, n=7). Subcutaneous resistance arteries were dissected from gluteal biopsy and mounted on a pressurized micromyograph. Endothelium-dependent and -independent relaxations were assessed by concentration-response curves to acetylcholine (1 nM to 100 μM) and sodium nitroprusside (10 nM to 1 mM) respectively, in arteries pre-contracted with norepinephrine (10 μM). Carotid-femoral pulse wave velocity (PWV) was assessed by applantion tonometry. Forearm flow mediated dilation (FMD) was assessed by ultrasounds. The expression of P-eNOS/e-NOS and the markers of oxidative stress nitrotyrosine and LOX-1 were assessed by immunohistochemistry in resistance arteries. Patients were similar for age, sex, BMI and glycemic and metabolic control. Systolic BP was significantly and equally reduced by both ALK and RAM (153±8.9 mmHg reduced to 128±7.3 mmHg and 151±10.6 mmHg reduced to 121±12.1, respectively, P&lt;0.01) whereas diastolic BP was significantly reduced only in ALK-treated but not in RAM-treated patients (94.2±7.17 mmHg reduced to 81.4±6.31 mmHg, P&lt;0.01; and 84.7±12.22 reduced to 78.6±7.48, NS, respectively). PWV and FMD were similar in both groups before and after treatment. Endothelium-dependent vasodilation was improved only by ALK (max dilation 92.5±3.8% vs 50.5±14%, P&lt;0.05) but not by RAM (max dilation 72.9±5.6% vs 61.8±14.5%, NS). Endothelium-independent vasodilation was similar in all the groups. Only ALK increased P-eNOS/eNOS expression (+44% vs before treatment, p&lt;0.05). The markers of oxidative stress were similar in both groups before and after treatment. In conclusion ALK improved endothelial function and induced vasodilation in resistance arteries from diabetic and hypertensive patients.

Interrelation between ambulatory blood pressure indices and the lesions of the common carotid arteries in hypertensive patients at early post-stroke period

Objective. To study the variability of blood pressure (BP) based on ambulatory BP monitoring and its correlation with the state of the walls of the carotid arteries in hypertensive post-stroke patients. Design and methods. Anthropometry, fasting blood glucose tests and lipid profile, BP monitoring, doppler ultrasound of the carotid arteries were performed in 90 subjects. Results. There is a positive correlation between indicators of ambulatory BP monitoring and the state of the walls of the carotid arteries, in particular, between daytime variability of systolic BP (SBP) and the diameter of the common carotid arteries (R = 0,5; p < 0,05). A negative correlation between nocturnal SBP variability and blood flow velocity in the common carotid arteries (R = –0,5; p < 0,05) and a positive relation between daytime time index of SBP and resistivity index in external carotid arteries (R = 0,61; p < 0,05) were determined. Mean ambulatory SBP level is directly correlated with the resistivity index of the internal carotid arteries and blood flow velocity in the common carotid arteries (R = 0,52; p < 0,05). There is a correlation between the degree of nocturnal SBP reduction and intima-media thickness (R = –0,62; p < 0,001). Correlation was determined between the degree of nocturnal diastolic BP reduction and blood flow velocity in the common carotid arteries (R = 0,65; p < 0,05). Conclusions. There is a violation of circadian BP profile in all hypertensive patients after stroke, despite achieved target levels of BP. There is a correlation between the severity of atherosclerotic lesions of common carotid arteries and lipid metabolism, age, as well as with ambulatory BP indices. Thus, 24-hour BP parameters should be considered when evaluating the effectiveness of antihypertensive therapy in hypertensive post-stroke patients.

Myocardial bridge and proximal stenosis in hypertensive patients

Dear Editor: A myocardial bridge is an abnormality in which the artery is covered by a superficial membranous bridge, or a deep muscular bridge[1]. It is most commonly found in the left anterior descending coronary artery (LAD). The affected artery is stenosed by the surrounding myocardium, especially in the deep bridge as the artery is situated deep in the myocardium[2]. Atherosclerosis is usually present in the artery proximal to the bridge while the bridge, or tunnel, and the distal artery are free of atherosclerosis[3]. This study intended to examine whether myocardial bridge correlated with the development of atherosclerosis in hypertensive patients. We retrospectively analyzed the clinical and radiological data of 107 hypertensive patients with myocardial bridge and stenosed coronary arteries. The study protocol was approved by the ethics committee of the authors’ affiliated institution. Stenosis was categorized as follows: type 1, 75% stenosis. Sixty-eight (63.5%) were males and the mean age was 63.9±13.0 years. Fiftytwo (48.5%) patients had stage 1 hypertension, and 55 (51.4%) patients had stage 2 hypertension. Thirtytwo (35.5%) patients had type 2 stenosis. LAD was the most common branch with a myocardial bridge. Sixty-nine (64.4%) had superficial bridge with a mean length of 10.26 mm. Thirty-eight patients (35.5%) had deep bridge. Pearson correlation analysis found no significant correlation between superficial bridge and proximal stenosis in hypertensive patients (P>0.993). There was also no significant correlation between deep bridges and proximal stenosis in hypertensive patients (P>0.580). In a Chinese study of 179 patients, 40.8% were found to have stenosis in the proximal part of the bridge[4], but in our study, 76.4% (107 out of 140) of patients had stenosis in the proximal part of the bridge. The difference may be due to the presence of hypertension in and a higher mean age of our patients. The arterial pressure is increased in the artery proximal to the bridge and the blood flow pattern also changes. These factors, in turn, could cause tension on the arterial intima and may cause or worsen preexisting atherosclerosis[5]. Though hypertension is one of the factors for the formation of atherosclerosis, it is not the direct cause for stenosis in patients with myocardial bridge. We found no correlation between myocardial bridge and stenosis of the proximal artery in hypertensive patients. This finding, however, needs to be further confirmed by additional studies involving more patients. Yours Sincerely,

GW25-e5193 The remodeling of gallbladder artery and altered expression of calcium handling genes in hypertensive patients

The remodeling of gallbladder artery in hypertensive patients and its underlying mechanisms are poorly understood. The present study observed the morphological and histological changes of gallbladder arteries and investigated the mechanisms of calcium handling genes involved in remodeling. A total