endothelin-1 and Carotid-Artery-Diseases

Vascular stiffening is associated with the prognosis of cardiovascular disease (CVD). Endothelial dysfunction, as shown by reduced vasodilation and increased vasoconstriction, not only affects vascular tone, but also accelerates the progression of CVD. However, the precise effect of vascular stiffening on endothelial function and its mechanism is unclear and a possible underlying has not been determined. In this study, we found that increasing substrate stiffness promoted endothelin-1 (ET-1) expression and inhibited endothelial nitric oxide synthase expression in human umbilical vein endothelial cells. Additionally, miR-6740-5p was identified as a stiffness-sensitive microRNA, which was downregulated by a stiff substrate, resulting in increased ET-1 expression. Furthermore, we found that substrate stiffening reduced the expression and activity of the calcium channel TRPV4, which subsequently enhanced ET-1 expression by inhibiting miR-6740-5p. Finally, analysis of clinical plasma samples showed that plasma miR-6740-5p levels in patients with carotid atherosclerosis were significantly lower than those in healthy people. Taken together, our findings show a novel mechanically regulated TRPV4/miR-6740/ET-1 signaling axis by which substrate stiffness affects endothelial function. Our findings indicate that vascular stiffening induces endothelial dysfunction, thereby accelerating progression of CVD. Furthermore, this study indicates that endothelial dysfunction induced by improper biophysical cues from cardiovascular implants may be an important reason for complications arising from the use of cardiovascular implants. STATEMENT OF SIGNIFICANCE: Cardiovascular disease is the leading cause of morbidity and mortality worldwide. The incidence of cardiovascular disease is accompanied by increased vascular stiffness. Our work indicated that increased vascular stiffness accelerates the development of cardiovascular disease by inducing endothelial dysfunction, which is a key contributor to the pathogenesis of cardiovascular disease. In addition, we identified a novel underlying molecular pathophysiological mechanism by which increased stiffness induce endothelial dysfunction. Our work could help determine the pathogenesis of cardiovascular disease induced by biomechanical factors.

Topics: Calcium Signaling; Carotid Artery Diseases; Case-Control Studies; Cell Adhesion; Cytoskeleton; Cytosol; Endothelin-1; Extracellular Matrix; Female; Gene Expression Regulation; HEK293 Cells; Human Umbilical Vein Endothelial Cells; Humans; Male; Mechanotransduction, Cellular; MicroRNAs; Middle Aged; TRPV Cation Channels

There are a lot of convincing evidences about the involvement of endothelin pathway proteins in the pathogenesis of atherosclerosis and its fatal complications. In this study, the analysis of a possible association between

Topics: Aged; Brain Ischemia; Carotid Artery Diseases; Endothelin-1; Female; Humans; Male; Middle Aged; Polymorphism, Single Nucleotide; Receptor, Endothelin A; Stroke; Ukraine

To evaluate the association of obstructive sleep apnea hypopnea syndrome (OSAHS) with carotid atherosclerosis and the efficacy of continuous positive airway pressure (CPAP) treatment.. A total of 93 OSAHS patients diagnosed by polysomnography (PSG) were selected from Sleep Disorders Center at Affiliated Hospital of Xuzhou Medical College between March 2013 and December 2014. Based on the results of apnea-hypopnea index (AHI), they were divided into mild (n=22), moderate (n=37), and severe OSAHS group (n=34). Meanwhile, 28 healthy adult individuals matched for age and body mass index (BMI) were enrolled as the control group. The carotid intima-mesa thickness (IMT) was measured by color Doppler uhrasonography, and plasma levels of tumor necrosis factor-α (TNF-α), endothelin-1 (ET-1) and nitric oxide (NO) were determined by Enzyme-Linked Immunosorbent Assay (ELISA). The correlations between carotid IMT and plasma levels of TNF-α, ET-1 and NO were analyzed. A total of 24 patients with moderate to severe OSAHS underwent CPAP treatment and the carotid IMT, plasma levels of TNF-α, ET-1 and NO were compared before and after CPAP treatment.. OSAHS patients had significant increase of carotid IMT with the increasing disease severity, and the carotid IMT in mild, moderate and severe OSAHS groups were all significantly higher than that in the control group ((0.73 ± 0.31), (0.86 ± 0.07), (1.07 ± 0.14) vs (0.65 ± 0.10) mm, all P<0.05). The plasma levels of TNF-α and ET-1 in mild to severe OSAHS group were significantly higher than those in controls ((17.45 ± 3.02), (23.81 ± 2.91), (35.16 ± 3.43) vs (12.53 ± 3.48) ng/L and (0.81 ± 0.13), (1.06 ± 0.21), (1.66 ± 0.30) vs (0.64 ± 0.12) ng/L, all P<0.05 ), whereas plasma levels of NO in the three OSAHS groups were significantly decreased compared with the control group ((35.46 ± 10.12), (29.32 ± 9.47), (20.16 ± 7.41) vs (45.43 ± 7.92) µmol/L, all P<0.05). Furthermore, there were significant differences in plasma levels of TNF-α, ET-1 and NO among the three OSAHS groups (all P<0.05). Carotid IMT was positively correlated with plasma TNF-α and ET-1 (r=0.56 and 0.51) and negatively correlated with plasma NO (r=-0.46) (all P<0.05). After 3 months of CPAP treatment, plasma levels of TNF-α and ET-1 in OSAHS patients were significantly reduced ((19.64 ± 5.28), (0.94 ± 0.21) vs (28.72 ± 5.36), (1.36 ± 0.36) ng/L), and plasma NO was markedly increased ((33.57 ± 6.32) vs (24.34 ± 4.46) µmol/L, all P<0.05). However, CPAP treatment did not have a significant effect on carotid IMT ((0.91 ± 0.21) vs (0.96 ± 0.14) mm), P>0.05).. Systemic inflammation and vascular endothelial dysfunction may play an important role in pathogenesis and development of carotid artery atherosclerosis in OSAHS. Short-term CPAP therapy alleviates systemic inflammation and improves endothelial function, but does not influence the increased carotid IMT in OSAHS patients.

Topics: Atherosclerosis; Body Mass Index; Carotid Artery Diseases; Continuous Positive Airway Pressure; Endothelin-1; Enzyme-Linked Immunosorbent Assay; Humans; Inflammation; Nitric Oxide; Polysomnography; Sleep Apnea, Obstructive; Tumor Necrosis Factor-alpha; Tunica Intima

The purpose of this study was to determine endothelin (ET)-1 and nitric oxide (NO) serum concentration levels at baseline and after 1 year of peritoneal dialysis (PD) treatment. A further aim was to evaluate the association between ET-1 and NO with parameters of echocardiography and the common carotid artery (CCA) ultrasound, and to assess their impact on cardiovascular remodeling. We also aimed to evaluate the influence of dialysis adequacy and residual renal function (RRF) on cardiovascular remodeling.. This study included 40 PD patients in whom we measured serum ET-1 and NO concentrations, echocardiography and CCA ultrasound parameters.. ET-1 decreased and NO serum concentration levels increased (p < 0.01) after 12 months of PD treatment compared to baseline values. Left ventricular (LV) hypertrophy was observed in 77.5% of patients at baseline with significant reduction in LV mass index (LVMI), CCA intima media thickness (IMT) and plaque score after 12 months of PD treatment (p < 0.001). The dialysis adequacy and RRF were significantly associated with LVMI and CCA IMT after 12 months on PD.. In our study, ET-1 significantly decreased while NO increased during PD treatment and both were independently related to the cardiovascular remodeling parameters in PD patients.

Topics: Adult; Aged; Biomarkers; Carotid Artery Diseases; Diabetes Mellitus, Type 2; Endothelin-1; Female; Follow-Up Studies; Humans; Hypertrophy, Left Ventricular; Kidney Failure, Chronic; Male; Middle Aged; Nitric Oxide; Peritoneal Dialysis; Prospective Studies; Ultrasonography; Ventricular Remodeling

Clinical and experimental evidence suggests that endothelin-1 (ET-1) plays a role in cardiac and vascular disease. In the present study, we investigated the prognostic significance of ET-1 for cerebrovascular and cardiovascular outcome, in a 20-year follow-up.. We studied 82 originally healthy individuals, referred to our Unit of Cardiovascular Prevention, to evaluate the presence of asymptomatic carotid lesions. We subdivided these individuals into two groups, according to the plasma values of ET-1 (respectively ≤ or >2.7 pg/ml). Traditional cardiovascular risk factors were investigated, and by carotid ultrasound examination, we distinguished between normal individuals and those with intima-media thickening or asymptomatic carotid plaque.. Major cardiac and cerebral events (all-cause death, myocardial infarction, revascularization procedures, fatal and nonfatal stroke) were registered in 41 individuals and significantly more in those with high vs. low ET-1 levels (95 vs. 5%; P < 0.0001). Furthermore, by logistic multivariate regression analysis, we found that among all evaluated baseline clinical and laboratory variables, hypertension [odds ratio (OR): 20.4 (3.3-127), P = 0.001], high ET-1 concentrations [OR: 1.4 (1.0-1.8), P = 0.02] and the presence of intima-media thickness or asymptomatic carotid plaque [OR: 3.7 (1.14-12.1), P = 0.02] were independent predictors of future events. Finally, integrating technical and laboratory data, high levels of ET-1 have defined a high risk of major cardiac and cerebral event and stroke at follow-up, which increased in relation to the progression of carotid atherosclerosis (P < 0.05).. ET-1 plasmatic levels significantly influence the cardiovascular and cerebrovascular risk profile, beyond traditional cardiovascular risk factors and preclinical carotid atherosclerosis.

Topics: Adult; Aged; Asymptomatic Diseases; Biomarkers; Cardiovascular Diseases; Carotid Artery Diseases; Carotid Intima-Media Thickness; Cerebrovascular Disorders; Endothelin-1; Female; Follow-Up Studies; Humans; Male; Middle Aged; Plaque, Atherosclerotic; Predictive Value of Tests; Prognosis; Prospective Studies; Risk Factors

To investigate variability in self-measured home blood pressure (HBP) and its effects on carotid artery atherosclerosis and endothelial function in normotensive and mild-moderate hypertensive individuals.. This is a cross-sectional study. HBP monitoring over 7 consecutive days, carotid artery ultrasound, and brachial artery flow-mediated dilation (FMD) were performed in 314 normotensive, prehypertensive, and mild-moderate hypertensive volunteers. Variability in HBP was assessed by the SDs of the daily BP average of the last 6 consecutive days. The plasma endothelin-1 (ET-1) level was tested using an enzyme-linked immunosorbent assay.. The tendency of SD of systolic HBP increased significantly from the normotension to the moderate hypertension group. SD of systolic HBP was significantly correlated with carotid intima-media thickness (IMT) (r=0.569, P<0.001), stiffness parameter β (r=0.447, P<0.001), FMD (r=-0.636, P<0.001), and ET-1 (r=0.649, P<0.001). SD of diastolic HBP was also correlated with carotid IMT, stiffness parameter β, FMD, and ET-1, but the strength of the correlation was weaker than SD of systolic HBP (all P<0.001). After adjustment of all covariants, SD of systolic HBP was always significantly associated with carotid IMT, stiffness parameter β, FMD, and ET-1.. Day-by-day variability in HBP increased with increasing BP level. This was significantly associated with carotid artery atherosclerosis and endothelial function in normotensive and mild-moderate hypertensive individuals. Day-by-day variability in HBP may serve as an important prognostic factor for atherosclerosis and endothelial dysfunction.

Topics: Adult; Blood Pressure; Brachial Artery; Carotid Arteries; Carotid Artery Diseases; Carotid Intima-Media Thickness; Cross-Sectional Studies; Endothelin-1; Female; Humans; Hypertension; Male; Middle Aged; Vascular Stiffness; Vasodilation

Endothelin-1 (ET-1) and oxidative stress are involved in the development of hypertension-induced cardiovascular complications. The aim of this study was to evaluate the relationship between plasma ET-1 level and plasma antioxidant capacity and carotid atherosclerosis. In 61 treated patients with hypertension (44 women, 35 diabetics, mean age 72.4+/-7.2 years) medical histories, ambulatory blood pressure, blood tests (glucose, creatinine, cholesterol, haemoglobin A1c (HbA1c), ET-1) and common carotid artery intima-media thickness (CCA-IMT) measurement were carried out. Plasma antioxidant capacity was assessed by the ferric-reducing ability of plasma (FRAP). Subjects with diabetes presented with higher concentrations of glucose (7.01+/-2.3 vs 5.14+/-0.6 mmol l(-1), P<0.001), HbA1c (7.75+/-2.1 vs 6.1+/-1.2%, P<0.001) and ET-1 (1.36+/-0.53 vs 1.01+/-0.4 pg ml(-1), P<0.01), and lower cholesterol level (5.02+/-0.8 vs 5.86+/-1.3 mmol l(-1), P<0.01). A significant positive correlation between CCA-IMT and ET-1 plasma concentration (r=0.40, P<0.001) and reverse relationship between CCA-IMT and FRAP (r=-0.36, P<0.01) was observed. In a stepwise regression analysis, after adjustment for all confounders, CCA-IMT was independently influenced by age, systolic blood pressure (SBP), HbA1c and ET-1. When FRAP was included in the regression model, CCA-IMT was significantly influenced by age, FRAP, HbA1c and SBP. ET-1 promotes the increase in CCA-IMT contributing to the development of end-organ damage. Plasma antioxidant capacity may modulate this deleterious effect, but whether better antioxidant defence may prevent against the development of atherosclerosis remains to be elucidated.

Topics: Aged; Antioxidants; Carotid Artery Diseases; Carotid Artery, Common; Diabetic Angiopathies; Endothelin-1; Female; Humans; Hypertension; Male; Multivariate Analysis; Oxidative Stress; Regression Analysis; Signal Transduction; Tunica Intima; Tunica Media; Ultrasonography

Recent studies indicated that migraine is associated with specific vascular risk profile. However, the functional and structural vascular abnormalities in migraine are rarely addressed. We evaluated the vascular risk factors, endothelial function, and carotid artery (CA)-intima-media thickness (IMT), segregators of preclinical atherosclerosis, in migraineurs. This preliminary study included 63 adults with headache (migraine with aura [n=14], migraine without aura [n=24], transformed migraine [n=6], and tension headache [n=19]) and 35 matched healthy subjects. The following vascular risks were assessed: body mass index (BMI), systolic blood pressure (SBP) and diastolic blood pressures (DBP), serum levels of C-reactive protein, fasting glucose, fasting insulin, total cholesterol, and triglycerides. Plasma endothelin (ET)-1, a vasoactive peptide produced by vascular smooth muscle cells and marker for endothelial injury and atherosclerosis, was measured. Endothelial-dependent vasoreactivity was assessed using brachial artery flow-mediated dilatation (FMD) in response to hyperemia. CA-IMT, structural marker of early atherosclerosis, was measured. Compared with control subjects, SBP, DBP, glucose, insulin, ET-1, and CA-IMT were elevated with migraine. FMD% was inversely correlated with SBP (P < .001), DBP (P < .01), glucose (P < .001), and insulin levels (P < .01). CA-IMT was correlated with BMI (P < .05), SBP (P < .01), total cholesterol (P < .01), triglycerides (P < .001), glucose (P < .001), insulin (P < .01), and FMD% (P < .05). In multivariate analysis, ET-1 was correlated with duration of illness, SBP, DBP, glucose, insulin, IMT, and FMD%. We conclude that endothelial injury, impaired endothelial vasoreactivity, and increased CA-IMT occur with migraine and are associated with vascular risk factors that strongly suggest that migraine could be a risk for atherosclerosis.

Topics: Adult; Biomarkers; Blood Glucose; Blood Pressure; Body Mass Index; C-Reactive Protein; Carotid Arteries; Carotid Artery Diseases; Case-Control Studies; Cholesterol; Comorbidity; Diabetes Complications; Endothelial Cells; Endothelin-1; Female; Humans; Hypertension; Male; Migraine Disorders; Multivariate Analysis; Risk Factors; Triglycerides; Tunica Intima; Vasoconstriction

Intracerebral injection of the vasoconstrictor peptide, endothelin-1 (ET-1), has been used as a method to induce focal ischemia in rats. The relative technical simplicity of this model makes it attractive for use in mice. However, the effect of ET-1 on mouse brains has not been firmly established. In this study, we determined the ability of ET-1 to induce focal cerebral ischemia in four different mouse strains (CD1, C57/BL6, NOD/SCID, and FVB). In contrast to rats, intracerebral injection of ET-1 did not produce a lesion in any mouse strain tested. A combination of ET-1 injection with either CCA occlusion or N(G)-nitro-l-arginine methyl ester (l-NAME) injection produced only a small infarct and its size was strain-dependent. A triple combination of CCA occlusion with co-injection of ET-1 and l-NAME produced a lesion in all mouse strains tested, and this resulted in a significant motor deficit. However, lesion size was still relatively small and strain-dependent. This study shows that ET-1 has a much less potent effect for producing an infarct in mice than rats.

Topics: Animals; Brain Infarction; Brain Ischemia; Carotid Artery Diseases; Cerebral Arteries; Disease Models, Animal; Endothelin-1; Enzyme Inhibitors; Male; Mice; Mice, Inbred C57BL; Mice, SCID; NG-Nitroarginine Methyl Ester; Nitric Oxide Synthase Type III; Rats; Rats, Sprague-Dawley; Species Specificity; Vasoconstriction; Vasoconstrictor Agents

We studied the association of endothelin (ET)-1 with carotid atherosclerosis and asymptomatic cerebrovascular lesions in patients with essential hypertension. Neurologically normal patients with essential hypertension (n=293; 138 male, 155 female; mean age, 65 years) and age-matched control subjects (n=242) were studied with B-mode ultrasonography of the common and internal carotid arteries and magnetic resonance imaging of the brain. Plasma ET-1 was measured by enzyme immunoassay. Hypertensive patients were divided into groups with carotid plaques and low ET-1 concentrations (< 0.75 pg/ml; PL group); carotid plaques and mid-range ET-1 (0.75 to 1.55 pg/ml; PM group); carotid plaques and high ET-1 (> or = 1.55 pg/ml; PH group); no plaques and low ET-1 (NPL); no plaques and mid-range ET-1 (NPM); and no plaques and high ET-1 (NPH). Overall, ET-1 concentrations were significantly higher in patients than in control subjects. Carotid plaque prevalence was significantly related to ET-1 in hypertensive patients. ET-1 showed a significant positive relationship with the number of asymptomatic lacunar infarcts of the brain in hypertensive patients with carotid plaques (rho=0.48, p<0.001). No significant relationship was seen between ET-1 and periventricular hyperintensity scores in patients with plaques. ET-1 did not show a relationship to either brain lesion type in patients without carotid plaques. Thus, ET-1 may foster asymptomatic lacunar cerebral infarcts by promoting carotid atherosclerosis in patients with essential hypertension.

Topics: Adult; Aged; Carotid Artery Diseases; Cerebral Infarction; Cerebrovascular Disorders; Endothelin-1; Female; Humans; Hypertension; Intracranial Arteriosclerosis; Magnetic Resonance Imaging; Male; Middle Aged; Osmolar Concentration; Reference Values; Ultrasonography

The aim of this study was to investigate the behaviour of circulating ET-1 in patients with carotid atherosclerosis, before and after carotid thromboendarterectomy (TEA), to test the hypothesis that plasma ET-1 decreases after removal of atherosclerotic lesion. Plasma immunoreactive ET-1 levels were determined in 17 patients with symptomatic and/or hemodynamically significant carotid atherosclerosis on the day before TEA, 48 h and 72 h after surgery and, in 11 of them, also after 8 h and 24 h. Compared to controls, ET-1 levels were significantly higher both before and after TEA; after carotid revascularisation (8 h) ET-1 increased; then, from the 24th h, ET-1 gradually decreased and at the 48th h and 72th h the decrease was significant in front of basal values. The increase of plasma ET-1 in the acute postoperative phase may reflect the degree of surgical stress and manipulation in diseased blood vessels; the following decrease may indicate the improvement of vascular dysfunction in the involved carotid site; the persistence of high ET-1 levels 72 h after surgery could suggest the presence of residual ischemia in the involved district and/or the involvement of other sites in ET-1 production.

Topics: Aged; Arteriosclerosis; Carotid Artery Diseases; Endarterectomy, Carotid; Endothelin-1; Female; Humans; Male

Antibodies to endothelial cells (aECs) and to cardiolipin (aCLs) are implicated in autoimmune diseases like systemic lupus erythematosus vasculitis. Beta2-Glycoprotein 1 (beta2GP1) is a cofactor for aCLs. The present study investigated the possible role of aECs, aCLs, and abeta2GP1 in borderline hypertension.. Seventy-three men with borderline hypertension (BHT) and 73 age-matched normotensive (NT) men (diastolic blood pressure, 85 to 94 and <80 mm Hg, respectively) were recruited from a population screening program. Antibody levels were determined by ELISA. Presence of carotid atherosclerosis was determined by B-mode ultrasonography, and 29 individuals had atherosclerotic plaques. BHT men had significantly higher aEC and abeta2GP1 levels of IgG class than NT control subjects (P=0.029 and P=0.0001, respectively). aEC levels of IgM class were higher in BHT (P=0.012), but not abeta2GP1 levels. There was no correlation between aCL levels and BHT. Individuals with atherosclerotic plaques had significantly higher aEC levels of both IgG (P=0.042) and IgM subclasses (P=0.018) than those without plaques, but no difference was found in aCL and abeta2GP1 levels. Endothelin and aECs of IgM class were significantly associated.. We demonstrate the first evidence of a significant elevation of aEC and abeta2GP1 levels in borderline hypertension. These findings provide a new link between hypertension and atherosclerosis and indicate that humoral immune reactions to the endothelium may play an important role in both conditions.

Topics: Adult; Apolipoproteins; Arteriosclerosis; beta 2-Glycoprotein I; Blood Pressure; Carotid Artery Diseases; Cross Reactions; Endothelin-1; Endothelium, Vascular; Glycoproteins; Humans; Hypertension; Immunoglobulin G; Immunoglobulin M; Insulin-Like Growth Factor Binding Protein 1; Male; Middle Aged; Ultrasonography

The role of endothelium-related factors in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH) has gained interest since the discovery of EDRF and of endothelin-1 (ET-1). The effect of SAH and both treatment of deferoxamine (DFO) and sympathectomy on endothelium-dependent vasodilation and ET-1-induced vasoconstriction of isolated rabbit carotid artery was examined using an isometric tension recording method. Thirty-five rabbits were divided into four groups: control animals, 7 days after SAH, treatment with DFO after SAH for 7 days and sympathectomy after SAH. Acetylcholine (10(-8) to 10(-5) M) was used to evoke concentration-dependent vasodilation of isolated arterial rings previously contracted by 10(-6) M phenylephrine. In the animals killed 7 days after SAH, acetylcholine-induced relaxation was suppressed and the degree of relaxation of this group was 50% of the initial contractile tone in response to the 10(-5) M acetylcholine. These relaxant responses did not return to control values in carotid arteries obtained from animals treated with DFO and subjected to sympathectomy. In isolated carotid arteries, ET-1 (10(-10) to 10(-8) M) produced concentration-dependent contractions. These contractile responses were significantly enhanced in animals 7 days after SAH compared with controls and did not return to control values in carotid arteries obtained from animals both treated with DFO and sympathectomized for 7 days after SAH. The present experiments suggest that impairment of endothelium-dependent vasodilation and the hyperreactivity of ET-1 of the carotid artery as well as cerebral arteries may be involved in the pathogenesis of cerebral vasospasm. Both treatment with DFO and sympathectomy during the chronic stage for vasospasm after SAH did not affect these vascular responses of the extradural part of the carotid artery to ET-1 and acetylcholine.

Topics: Acetylcholine; Animals; Carotid Artery Diseases; Carotid Artery, Common; Deferoxamine; Endothelin-1; Endothelium, Vascular; Female; Ischemic Attack, Transient; Male; Muscle Contraction; Muscle Relaxation; Rabbits; Siderophores; Subarachnoid Hemorrhage; Sympathectomy

The relationship between carotid atherosclerosis and plasma endothelin-1 (ET-1) concentration was studied in senile patients with essential hypertension. A total of 212 patients (83 M, 129 F; mean age, 63 years) with essential hypertension (WHO stage I-II), and 109 age-matched control subjects (mean age, 61 years) were enrolled in the study. The maximum thicknesses of the intima-media complex (IMTmax) in the right common carotid artery (CCA) and the right internal carotid artery (ICA) was measured by B-mode ultrasonography, and ET-1 was measured by enzyme immunoassay. ET-1 levels were significantly higher in the hypertensive patients than in the control subjects. In middle-aged patients (35-64 years old), IMTmax values of the ICA in patients with high ET-1 concentrations (ET-1 > or = 1.71 pg/ml) were significantly higher than in patients with normal ET-1 concentrations (ET-1 < 1.71 pg/ml). However, the IMTmax of the CCA did not show a similar correlation. In senile patients (65-83 years old), both the CCA and ICA IMTmax values were significantly higher in patients with high ET-1 concentrations than in those with normal ET-1 concentrations. These results indicate that high ET-1 levels in middle-aged patients with essential hypertension may play a role in the progression of ICA atherosclerosis. High ET-1 levels in senile patients with essential hypertension may cause progression of atherosclerosis in both the ICA and CCA.

Topics: Adult; Aged; Aged, 80 and over; Arteriosclerosis; Carotid Artery Diseases; Endothelin-1; Female; Humans; Hypertension; Male; Middle Aged