Carotid Diameter Research Articles

Carotid integrated backscatter analysis in patients with subclinical hypothyroidism

The aim of the present study was to determine whether integrated backscatter (IBS) analysis combined with conventional ultrasonography could differentiate the tissue characteristics of carotid artery intimal hyperplasia in patients with subclinical hypothyroidism (SH). Forty-one patients with SH, as judged by elevated serum TSH levels and free thyroid hormones within the normal range, and 31 sex- and age-matched euthyroid volunteers underwent two-dimensional conventional ultrasonography and IBS analysis of the carotid wall. Carotid intima-media thickness (IMT) and corrected IBS (C-IBS), an index of arterial wall degeneration and fibrosis, were evaluated. Mean IMT as well C-IBS values were higher in SH than in controls (P < 0.0001 for both), whereas the carotid diameter was not significantly different between the two groups. The distribution of C-IBS values in each group showed that regions with higher C-IBS values were found more frequently in SH patients than in control subjects. The percentage of regions that could be considered as fibromatous (C-IBS value from -18 to -21 dB) was 28% in SH and 9% in euthyroid subjects (P < 0.0001). In the SH group, C-IBS values were significantly and positively associated with plasma TSH (r = 0.32, P < 0.05 and r = 0.59, P < 0.0001, respectively) and with both total cholesterol (r = 0.46, P = 0.01) and low density lipoprotein (LDL)-cholesterol (r = 0.55, P = 0.001). Carotid IMT in subclinically hypothyroid patients is higher than that in euthyroid controls. This is characterized by increased IBS values, which are related to the collagen content of the arterial wall. The severity of this remodelling process seems to be related to TSH and cholesterol levels.

Risk for the development of atherosclerosis in women with a high level of dental plaque and severe gingival inflammation

Chronic infection and inflammation are considered to be risk factors in the development of cardiovascular diseases; the chronic inflammatory and microbial burden caused by the dental plaque in these individuals may predispose them to atherosclerotic process. The aims were to study the involvement of a high level of dental plaque, severe gingival inflammation and periodontitis in the development of early atherosclerotic process in women. Forty-six randomly chosen women with periodontitis and 21 periodontally healthy women were subjected to a comprehensive clinical oral examination, including oral hygiene status and level of gingival inflammation. Atherosclerotic risk factor analysis and carotid ultrasonography were performed. Common carotid artery intima-media thickness (IMT) and lumen diameter were measured and intima-media area (cIMA) was calculated. The following statistical methods were used: analysis of variance, chi-squared tests and multiple logistic regression analysis. There were highly significant differences between the patients and controls in the amount of dental plaque, gingival inflammation as well as bleeding on probing and pocket depth. The mean values of IMT and cIMA were significantly higher in women with periodontal disease than in controls. Multiple logistic regression analysis identified periodontitis as a principal-independent predictor of both the common carotid artery cIMA and IMT. The present results indicate that a high amount of dental plaque, severe gingival inflammation as well as periodontitis seem to be associated with the development of atherosclerotic lesions in women already at its early and subclinical stages.

Effects of Continuous Positive Airway Pressure on Early Signs of Atherosclerosis in Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) is associated with adverse cardiovascular outcomes, including myocardial infarction and stroke. Atherosclerosis is a key mechanism for these cardiovascular events. Recent cross-sectional studies showed the presence of early signs of atherosclerosis in patients with OSA who were free of comorbidities. To determine the impact of treatment with continuous positive airway pressure (CPAP) on atherosclerosis. We randomly assigned 24 patients with severe OSA (age, 46 +/- 6 yr) who were free of comorbidities to receive no treatment (control, n = 12) or CPAP (n = 12) for 4 months. Carotid intima-media thickness, arterial stiffness (evaluated by pulse-wave velocity), carotid diameter, 24-hour blood pressure monitoring, C-reactive protein, and catecholamines were determined at baseline and after 4 months. At baseline, all measurements were similar in both groups and did not change in the control group after 4 months. In contrast, a significant decrease occurred in carotid intima-media thickness (707 +/- 105 vs. 645 +/- 95 microm, P = 0.04), pulse-wave velocity (10.4 +/- 1.0 vs. 9.3 +/- 0.9 m/s, P < 0.001), C-reactive protein (3.7 +/- 1.8 vs. 2.0 +/- 1.2 mg/L, P = 0.001), and catecholamines (365 +/- 125 vs. 205 +/- 51 ng/ml, P < 0.001) after 4 months of CPAP. Carotid diameter did not change significantly. Regarding the whole group, changes in carotid intima-media thickness were correlated with changes in catecholamines (r = 0.41, P < 0.05). Changes in pulse-wave velocity were correlated with changes in C-reactive protein (r = 0.58, P < 0.01) and catecholamines (r = 0.54, P < 0.01). The treatment of OSA significantly improves early signs of atherosclerosis, supporting the concept that OSA is an independent risk factor for atherosclerosis. Clinical trial registered with www.clinicaltrials.gov (NCT 00400543).

Adaptation of baroreflex function to increased carotid artery stiffening in patients with transposition of great arteries

We have shown previously that TGA (transposition of great arteries) is associated with increased carotid artery stiffness. It has been established that stiffening of the barosensory vessel wall results in reduced baroreceptor activation and impaired BRS (baroreflex sensitivity). In the present study we tested the hypothesis that the increased carotid artery stiffness in TGA patients was associated with reduced cardiovagal BRS. We studied 32 TGA patients aged 9-19 years, 12+/-3 years after surgical repair and 32 age-matched healthy control subjects. Carotid artery diastolic diameter and pulsatile distension was determined by echo wall tracking; carotid blood pressure was measured by tonometry. BRS was measured using spontaneous techniques [BRS(seq) and LF(gain) (low-frequency transfer function gain)] and by the phenylephrine method (BRS(phe)). Carotid artery distensibility was markedly reduced in patients as compared with controls (5.6+/-1.9 x 10(-3) compared with 8.7+/-2.7 x 10(-3)/mmHg P<0.05, as determined using an unpaired Student's t test), but BRS was not different in patients and controls (20.3+/-14.7 compared with 21.7+/-12.7 for BRS(seq); 13.1+/-9.2 compared with 10.6+/-4.5 for LF(gain); and 19.1+/-8.6 compared with 24.8+/-7.2 for BRS(phe) respectively). Carotid artery elastic function was markedly impaired in patients with TGA, but the increased stiffness of the barosensory vessel wall was not associated with reduced BRS. It appears that attenuation of baroreceptor stimulus due to arterial stiffening may be compensated by other, possibly neural, mechanisms when it exists as a congenital abnormality.

Carotid intima–media thickness, carotid distensibility and mitral, aortic valve calcification: a useful diagnostic parameter of systemic atherosclerotic disease

Mitral (MAC) and aortic (AVC) calcification are observed more frequently in the elderly and are associated with coronary artery disease, aortic atheroma and peripheral arterial atherosclerotic disease. Common carotid intima-media thickness (cIMT) and distensibility (cDIST) are also independent predictors of adverse cardiovascular outcomes. We examined the relationship between the degree of MAC-AVC and cIMT and cDIST. One hundred and forty-three patients referred for transthoracic echocardiography and carotid artery echo-Doppler were evaluated; the variables measured were: systemic blood pressure, pulse pressure; body mass index, traditional risk factors, cIMT, cDIST (cDIST = [(csD - cdD)/PP]/csD; where csD and cdD were systolic and diastolic carotid diameters, respectively). MAC and AVC score, based on acoustic densitometry, were: 1 = absence of annular/valvular (av) sclerosis/calcification; 2 = av sclerosis; 3 = av calcification; 4 = av calcification; 5 = av calcification with no recognition of the leaflets; the resulting score was the highest for either valvular annulus. Mean cIMT increased linearly with increasing valvular calcification score (P < 0.0001) whereas cDIST decreased for scores 1 to 5 (P < 0.0001). Distribution of cIMT quartiles showed that 75% of the patients in the lowest quartile had a score of 1 and 70% of patients in the highest quartile had a score of 5; 47% of the patients in the highest quartile of cDIST had a score of 1, whereas 60% of patients in the lowest quartile of cDIST had a score of 4. The MAC and AVC score identifies subgroups of patients with different cIMT and cDIST. These data may confirm MAC-AVC as a useful important diagnostic parameter of systemic atherosclerotic disease.

Maternal nutrition during gestation and carotid arterial compliance in the adult offspring: the Dutch famine birth cohort

Experimental evidence indicates that maternal undernutrition during gestation may program hypertension in the offspring. We investigated whether maternal undernutrition leads to increased arterial stiffness. We measured carotid artery lumen diameter (LD), distensibility (DC), stiffness (beta), and compliance (CC) by M-mode ultrasound in 673 individuals, aged 56-61 years, who had been born as term singletons around the time of the 1944-45 Dutch famine. Maternal famine exposure had no effect on any of the measures of carotid size or stiffness in the offspring. Low maternal weight at the end of pregnancy and low birth weight were associated with decreased LD (0.01 mm/kg maternal weight, sex-adjusted P < 0.001; 0.1 mm/kg birth weight, sex-adjusted P = 0.08) and CC (0.002 mm2/kPa per kg maternal weight, sex-adjusted P = 0.001; 0.03 mm2/kPa per kg birth weight, sex-adjusted P = 0.03), but neither was associated with increased beta, or decreased DC. These effects were not attenuated by adjusting for maternal protein/carbohydrate ratio in the third trimester. The association of low birth weight with increased CC diminished after adjusting for maternal weight. The association of maternal weight with CC was smaller when adjusted for LD. Our findings suggest that small maternal size, not poor maternal diet, in late gestation programs decreased arterial compliance in the adult offspring by affecting vessel size rather than vessel wall stiffness.

Large brachial and common carotid artery diameter in postmenopausal women with carotid atherosclerosis

Background and purposeIt is recognized that arteries can enlarge to compensate atherosclerosis. The role of diameter enlargement of unaffected arteries is not well known. We hypothesized that brachial and common carotid arteries diameters were larger in subjects with carotid atherosclerosis compared to subjects without these lesions. MethodsWe measured diameters in the common carotid and brachial arteries. Intimal medial thickness (IMT) of carotid arteries and carotid atherosclerosis were also evaluated using ultrasound in 83 cases and 83 disease-free control subjects. ResultsCommon carotid and brachial diameter was greater in cases (subjects with carotid atherosclerosis) than controls (subjects without carotid atherosclerosis) after adjustment for confounding variables (P<0.02). Common carotid diameter was also larger in individuals with greater IMT (P<0.0001), whereas brachial artery diameter was not. Subjects with more than one carotid plaque had larger arterial diameters than those with one or without plaques. ConclusionsCommon carotid and brachial artery diameters are both larger in cases than controls. This result suggests that vascular remodeling is a systemic process and not only a local response to atherosclerosis. The relationship between diameters and burden of disease could also suggest a link between vascular remodeling and severity of disease. Finally, if confirmed in prospective studies, brachial artery diameter could help to identify subjects at high cardiovascular risk, at least in postmenopausal women.

Association of clinic and ambulatory blood pressure with vascular damage in the elderly: the EPICARDIAN study

In middle-aged adults, vascular damage correlates better with ambulatory than with clinic blood pressure. This study aimed to determine whether vascular damage evaluated by carotid ultrasonography in the elderly is also more closely related to ambulatory than to clinic blood pressure, and which blood pressure variables are better associated with vascular damage. Cross-sectional study of 292 randomly selected >65 years old participants who underwent 24-h noninvasive ambulatory blood pressure monitoring. Blood pressure variables analyzed were (a) clinic blood pressure: systolic and diastolic blood pressure, pulse pressure; (b) ambulatory blood pressure monitoring: mean values of systolic and diastolic blood pressure, systolic and diastolic blood pressure load, pulse pressure, as well as variability, evaluated within 24 h, diurnal and nocturnal periods; and day-night blood pressure difference. A clinical history, physical examination, carotid ultrasonography and laboratory tests were performed. To estimate the relationship between blood pressure and vascular damage, univariate and multivariate analyses were performed. Mean age: 73+/-6 years, 45% men, 76.7% hypertensive patients. In the simple regression analysis, the best significant correlations (P<0.05) were common carotid intima-media thickness with 24-h and nocturnal pulse pressure (r=0.32), and common carotid diameter with 24-h systolic blood pressure load (r=0.47). In the multivariate analysis, the significant associations (P<0.05) were (a) linear regression: nocturnal pulse pressure with common carotid intima-media thickness, and diurnal pulse pressure as well as 24-h systolic blood pressure load with common carotid diameter; (b) logistic regression, adjusted odds ratio: nocturnal pulse pressure and nocturnal diastolic blood pressure load with the presence of carotid atherosclerotic plaques 1.03 and 0.98, respectively. In the elderly, ambulatory blood pressure monitoring is better associated with carotid damage than clinic blood pressure. Systolic blood pressure variables are the best associated, blood pressure load and pulse pressure being better associated with carotid damage than the mean levels of ambulatory blood pressure.

Inhibitory Effects of Micronized Fenofibrate on Carotid Atherosclerosis in Patients with Essential Hypertension

The coexistence of hypertension and dyslipidemia synergistically increases the risk of cardiovascular events. We investigated the effect of the lipid-lowering agent micronized fenofibrate on inhibition of carotid atherosclerosis in patients with essential hypertension and mild hyperlipidemia. We measured serum lipid profiles and inflammatory markers on chemistry or immune analyzers and common or internal carotid intima-media thickness (IMT) and diameter (D) by ultrasonography. Patients receiving micronized fenofibrate for 24 months in addition to antihypertensive treatment had decreased concentrations of total cholesterol, LDL-cholesterol, triglyceride, apolipoprotein B100, oxidized LDL, high-sensitivity C-reactive protein, P-selectin, and cytokines. These patients had increased concentrations of HDL-cholesterol, apolipoprotein A-I, and nitric oxide. Common carotid artery IMT (CCAIMT) and internal carotid artery IMT (ICAIMT) remained unchanged during the 24-month intervention. Moreover, the mean CCAIMT/D ratio and ICAIMT/D ratio were significantly decreased in the fenofibrate intervention group. In contrast, CCAIMT/D and ICAIMT/D ratios were increased in the control group. The incidence rates of carotid artery plaque formation and stroke in the fenofibrate intervention group were significantly lower than those in the control group. The combination of antihypertensive agents with micronized fenofibrate can effectively prevent the progression of carotid atherosclerosis and reduce the incidence of stroke in patients with essential hypertension.

Abstract 4179: The Association of Sex Hormones with Arterial Compliance Differs Between Men and Women in the Multi-Ethnic Study of Atherosclerosis (MESA)

Studies show differences in vascular stiffness between older men and women. However, the relationship between sex hormones (SH) and vascular stiffness has not been studied. We examined the cross sectional association between endogenous SH (bioavailable testosterone, BioT; estradiol, E2; dehydroepiandrostenedione, DHEA; and sex-hormone binding globulin, SHBG) and carotid vascular compliance in men and women in MESA. Methods: We included 2966 men and 1886 postmenopausal women who were not on hormone therapy (45– 84 years, 35% white, 13% Chinese, 27% African-American, 24% Hispanic ethnicity). Baseline systolic and diastolic blood pressure (BP) were measured during carotid ultrasound examination. Carotid strain, a measure of distensibility (fractional change in carotid diameter) was measured from B-mode images. Because men and women differed in the relationship between strain and BP, analyses were performed separately by sex. Log-transformed carotid strain was regressed on log-transformed SH adjusting for log-transformed BP, age, race, glucose, smoking, and BMI. All SH were included in the same model. Differences of coefficients between men and women were evaluated by examining their standard errors. Results: Carotid strain was 6.8±2.7% in men and 7.0±3.2% in women (p=0.027). In regression analysis (Table ), in men, E2 was significantly associated with lesser carotid strain (increased stiffness) while the BioT was associated with borderline significance to higher strain. In women, there was no association between either E2 or T and carotid strain. DHEA and SHBG were not associated with compliance. No race interaction was found with these associations. Conclusion: E2 is associated with greater arterial stiffness in men, while BioT is weakly associated with lesser stiffness. Sex hormones are not associated with arterial stiffness in women. The hyperestro-genic hypoandrogenic state may impair vascular health in older men. Carotid Strain and Sex Hormones

Carotid Atherosclerosis Is Associated with Brain Atrophy in Japanese Elders

Background: The relation between atherosclerosis and brain atrophy remains unclear in patients with risk factors for cardiovascular diseases. Objective: This study was performed to clarify the relation between brain atrophy and carotid atherosclerosis. Methods: A total of 142 patients (78 women and 64 men, mean age 74 years) with no neurologic disturbances were studied. Brain atrophy was evaluated on the basis of the brain atrophy index (BAI, BAI = brain parenchyma/intracranial space A 100%), calculated by means of digitized computed tomographic scans obtained at the level of the basal ganglia. Carotid atherosclerosis was evaluated on the basis of the plaque score (PS), defined as the sum of all plaque heights in both carotid arteries, intima-media thickness (IMT), and vessel diameter (VD) of the common carotid artery as assessed by ultrasonography. Results: Age negatively correlated with BAI in both men (r = –0.587, p < 0.001) and women (r = –0.724, p < 0.001). PS of the carotid artery also negatively correlated with BAI in men (r = –0.502, p < 0.001) as well as women (r = –0.480, p < 0.001). VD and IMT of the right carotid artery negatively correlated with BAI in women (VD; –0.256, p < 0.05, IMT; –0.216, p < 0.05) but not in men. Other characteristics were unrelated to BAI. Multiple regression analysis showed that age and PS were independent predictors of brain atrophy in both sexes. The percentage of variance of BAI values explained by this model in women (51.9%) was much greater than that in men (35.5%). Conclusion: Carotid atherosclerosis may be a useful morphological index of brain atrophy.

Carotid Artery Disease

Carotid arteries are the blood vessels that deliver blood through the neck to the brain. There is one carotid artery on each side of the neck, where its pulsation can be felt with a finger below the jaw bone. Blockages in the carotid artery decrease blood flow to the brain, causing a medical condition known as carotid artery disease. Interruptions in blood flow to the brain (commonly known as stroke) can cause permanent injury. This Cardiology Patient Page describes how blockages resulting from carotid artery disease cause stroke and what you and your doctor can do to prevent it. Stroke, or cerebrovascular accident, is most frequently caused by a sudden stoppage of blood flow to a portion of the brain. Every year in the United States, an estimated 750 000 people become victims of stroke. There are 2 common causes of stroke. First, an irregular heart rhythm, called atrial fibrillation, can cause stroke when small blood clots form as the heart is quivering instead of beating normally. Once a small blood clot is formed, it can be launched by the heart through the carotid arteries, block a blood vessel in the brain, and deprive that part of the brain of blood, resulting in a stroke. The other common cause of stroke is a blockage in the carotid arteries. The carotid arteries carry blood to the brain; like the blood vessels that supply blood to the heart, these arteries can become narrowed or blocked. The blockages are deposits of cholesterol, or atherosclerosis, that narrow the blood flow channel in the carotid arteries (Figure 1). If these cholesterol deposits or blockages break or rupture, small blood clots and cholesterol fragments break off from the plaque, enter the blood flow to the brain, and can get caught in a smaller blood vessel in …

The Chronic Vascular and Haemodynamic Response after Permanent Bilateral Common Carotid Occlusion in Newborn and Adult Rats

Vascular growth and redistribution of flow can compensate for arterial occlusion and possibly reduce the effects of hypoperfusion. As yet there is limited information on the age-dependent nature of vasculature remodelling. In this study, we have monitored the vascular and morphologic changes using magnetic resonance imaging and histology in a chronic bilateral common carotid artery occlusion (BCCAO) model in both newborn and adult rats. Acutely, cerebral blood flow (CBF) decreased immediately after BCCAO, producing a state of oligemic hypoperfusion. At 6 months after BCCAO in both adult and neonatal rats, the CBF had normalised at control values. To investigate the underlying mechanism for the return of CBF to control values, intra- and extracerebral magnetic resonance angiograms (MRAs) were acquired. As expected, signal from the common carotid arteries was present in the sham-operated rats, but was absent in the BCCAO animals. India ink angiograms demonstrated more tortuous basilar arteries in the adult rats post-BCCAO and MRAs demonstrated more extracerebral midline collaterals in the neonatal rats post-BCCAO, indicating different modes of vascular adaptation dependent on the age at onset of the insult. Both groups had collateral vessels arising from the vertebral arteries, and BCCAO was also associated with increased diameter of basilar, posterior cerebral, posterior communicating, internal carotid, middle cerebral and anterior cerebral arteries. Our study suggests that the developing and mature animals exhibit different patterns of vascular remodelling and that the BCCAO hypoperfusion model will be useful for investigating age-dependent vascular events in response to vaso-occlusive disease.

Effects of iodinated contrast media on common carotid and brachial artery blood flow and wall shear stress

The aim of our study was to evaluate the effect of the intravenous contrast media iomeprol on wall shear stress, blood flow and vascular parameters in the common carotid and brachial artery. Thirty outpatients undergoing thoracic or abdominal spiral CT scans were studied. The internal diameter and flow velocity of the common carotid and brachial artery were evaluated by ultrasound, and blood viscosity was measured before and after low osmolality iomeprol (Iomeron 350) injection. The wall shear stress, blood flow and pulsatility index were calculated. To test the differences between groups, the Wilcoxon rank test and Mann Whitney U test were applied. Blood viscosity decreased slightly, but significantly after contrast media (4.6+/-0.7 vs. 4.5+/-0.7 mPa.s, P = 0.02). Contrarily, blood flow and wall shear stress did not change in the common carotid artery, but significantly decreased in the brachial artery (0.9+/-0.4 vs. 0.6+/-0.3 ml/s, P < 0.0001, and 41.5+/-13.9 vs. 35.3+/-11.0 dynes/cm2, P < 0.002, respectively), whereas the pulsatility index significantly increased in the brachial artery (5.0+/-3.3 vs. 7.5+/-5.3, P < 0.001). Iomeprol injection causes blood flow and wall shear stress reduction of the brachial artery; the rise in the pulsatility index suggests an increase in peripheral vascular resistance. Further investigation is needed to evaluate whether these modifications can be clinically relevant.

Vascular Structure and Function in Women: Relationship with Body Mass Index

The purpose of the present study was to compare endothelial function in lean (body mass index [BMI]=18.0-24.9 kg/m2); overweight (BMI=25-29.9 kg/m2); and obese (BMI>30 kg/m2), healthy, eumenorrheic women. Eighteen lean, 22 overweight, and 19 obese eumenorrheic middle-aged women were studied. Vascular structure and function were assessed via non-invasive ultrasound imaging of the carotid and brachial arteries. Body composition, blood pressure, fasting blood lipids, glucose, and insulin also were measured. The groups demonstrated significantly (p<0.001) different mean values for total body, lean body, and fat masses. The obese group demonstrated significantly (p<0.05) elevated fasting glucose and insulin levels and lower high-density lipoprotein levels as compared to the lean group. The overweight group also demonstrated elevated fasting glucose levels as compared to the lean group (p<0.05) with no significant difference from the obese group. Only systolic blood pressure differed among the three groups, being elevated in the obese group compared to the lean group (p<0.05). The obese group demonstrated significantly (p<0.05) elevated carotid artery lumen diameter, carotid artery wall cross-sectional area, and brachial artery lumen diameter with significantly (p<0.05) lower flow-mediated dilation as compared to the lean group. The overweight group demonstrated elevated carotid artery wall cross-sectional area and brachial artery lumen diameter as well as lower flow-mediated dilation as compared to the lean group (p<0.05). The results of this study support the hypothesis that carotid artery wall cross-sectional area is elevated and flow-mediated dilation reduced in overweight and obese eumennorheic women as compared to lean counterparts in relation to BMI classification.

3127: Comparative study on carotid changes of hypertension and coronary artery disease with ultrasonography

Objectives: The aim of this paper is to evaluate the differentiation of the carotid change between the essential hypertension (HT) and coronary artery disease (CAD) with ultrasonography.Methods: Forty-three cases with HT but without CAD and diabetes mellitus (DM) and 41 cases with CAD but without HT and DM, the carotid were examined display the structures of common carotid artery (CCA), measure vascular internal diameter (D), carotid intima-media thickness (IMT), atherosclerotic plague and blood stream parameters.Results: The results showed that carotid diameter, IMT and plague in HT group were significant more than the CAD group. We believe that carotid changes between the HT and CAD is differential at the initial stage of a disease. Carotid IMT, lipoidosis in the vascular internal membrane and plague were shown in HT than CAD earlier, the soft lipid plagues more shown in HT.Conclusions: Using ultrasonography study carotid to understanding HT and CAD was valuable. Objectives: The aim of this paper is to evaluate the differentiation of the carotid change between the essential hypertension (HT) and coronary artery disease (CAD) with ultrasonography. Methods: Forty-three cases with HT but without CAD and diabetes mellitus (DM) and 41 cases with CAD but without HT and DM, the carotid were examined display the structures of common carotid artery (CCA), measure vascular internal diameter (D), carotid intima-media thickness (IMT), atherosclerotic plague and blood stream parameters. Results: The results showed that carotid diameter, IMT and plague in HT group were significant more than the CAD group. We believe that carotid changes between the HT and CAD is differential at the initial stage of a disease. Carotid IMT, lipoidosis in the vascular internal membrane and plague were shown in HT than CAD earlier, the soft lipid plagues more shown in HT. Conclusions: Using ultrasonography study carotid to understanding HT and CAD was valuable.

Effects of smoking on cardiopulmonary baroreceptor activation and peripheral vascular resistance

We studied 16 healthy smokers and 16 nonsmokers acting as controls. We subjected smokers and nonsmokers to cardiopulmonary baroreceptor stimulation by studying forearm and common carotid haemodynamic and sympathovagal balance. Smokers repeated the tests after smoking one cigarette. Smokers and controls were subjected to passive elevation of the legs and the trunk in a horizontal position with pressure monitoring and measurement of the calibre and flow in the brachial and common carotid arteries using a colourDoppler ultrasound. We calculated forearm resistance and carotid wall tension. We also studied R-R variability, calculating the ratio between low frequency (LF) and high frequency (HF) R-R interval variability. During stimulation diastolic blood pressure values decreased in controls and in smokers at rest. After smoking one cigarette, smokers showed an increase in systolic and diastolic blood pressure as well as in the heart rate during stimulation. Humeral artery increased the calibre during stimulation in both groups; after cigarette smoking the calibre declined throughout the study phases. Forearm resistance decreased in both groups during stimulation at rest, but increased after cigarette smoking. The LF/HF ratio decreased during stimulation in both groups, and it increased at rest after smoking. Carotid diameter did not change in either group, and wall tension increased in smokers after smoking one cigarette. Smoking one cigarette increases resistance, impairs baroreflex and increases carotid wall tension in mild smokers. These findings may explain the higher rate of a cardiovascular event in smokers.

Transposition of Great Arteries Is Associated With Increased Carotid Artery Stiffness

Transposition of great arteries is the consequence of abnormal aorticopulmonary septation. Animal embryonic data indicate that septation and elastogenesis are related events, but human and clinical data are not available. We tested the hypothesis that large artery elastic function was impaired in patients with transposition of great arteries. We studied 34 patients aged 9 to 19 years, 12+/-3 years after atrial switch operation; 14 patients aged 7 to 9 years, 8+/-1 years after arterial switch operation; and 108 healthy control subjects matched for age. Carotid artery diastolic diameter and pulsatile distension were determined by echo wall-tracking; carotid blood pressure was measured by tonometry. Systolic pressure was higher and diastolic pressure was lower in patients than in controls. Patients with atrial and arterial switch repair were compared with their respective controls by 2-factor ANOVA. For patients with atrial switch repair versus control, stiffness index beta was 4.9+/-1.5 versus 3.1+/-1.0 (P<0.001); for patients witch arterial switch versus control, stiffness index beta was 3.8+/-1.1 versus 2.1+/-0.6 (P<0.001). Similar differences were observed for carotid compliance, distensibility, and incremental elastic modulus as well. The interaction term was not significant for any of the elastic variables, indicating that carotid stiffening was a characteristic of the condition and not the consequence of different hemodynamics. Carotid artery is markedly stiffer in patients, suggesting that impaired elastogenesis may constitute part of the congenital abnormality. Since carotid artery stiffness has been established as an independent cardiovascular risk factor, this condition may have consequences in the clinical management of these patients.

Variations in carotid arterial compliance during the menstrual cycle in young women

The effect of menstrual cycle phase on arterial elasticity is controversial. In 10 healthy women (20.6+/-1.5 years old, mean+/-s.d.), we investigated the variations in central and peripheral arterial elasticity, blood pressure (carotid and brachial), carotid intima-media thickness (IMT), and serum oestradiol and progesterone concentrations at five points in the menstrual cycle (menstrual, M; follicular, F; ovulatory, O; early luteal, EL; and late luteal, LL). Carotid arterial compliance (simultaneous ultrasound and applanation tonometry) varied cyclically, with significant increases from the values seen in M (0.164+/-0.036 mm2 mmHg-1) and F (0.171+/-0.029 mm2 mmHg-1) to that seen in the O phase (0.184+/-0.029 mm2 mmHg-1). Sharp declines were observed in the EL (0.150+/-0.033 mm2 mmHg-1) and LL phases (0.147+/-0.026 mm2 mmHg-1; F=8.51, P<0.05). Pulse wave velocity in the leg (i.e. peripheral arterial stiffness) did not exhibit any significant changes. Fluctuations in carotid arterial elasticity correlated with the balance between oestradiol and progesterone concentrations. No significant changes were found in carotid and brachial blood pressures, carotid artery lumen diameter, or IMT throughout the menstrual cycle. These data provide evidence that the elastic properties of central, but not peripheral, arteries fluctuate significantly with the phases of the menstrual cycle.

Molecular mechanisms of the vascular responses to haemodynamic forces

Blood vessels are permanently subjected to mechanical forces in the form of stretch, encompassing cyclic mechanical strain due to the pulsatile nature of blood flow and shear stress. Significant variations in mechanical forces, of physiological or physiopathological nature, occur in vivo. These are accompanied by phenotypical modulation of smooth muscle cells and endothelial cells, producing structural modifications of the arterial wall. In all the cases, vascular remodelling can be allotted to a modification of the tensional strain or shear, and underlie a trend to reestablish baseline mechanical conditions. Vascular cells are equipped with numerous receptors that allow them to detect and respond to the mechanical forces generated by pressure and shear stress. The cytoskeleton and other structural components have an established role in mechanotransduction, being able to transmit and modulate tension within the cell via focal adhesion sites, integrins, cellular junctions and the extracellular matrix. Mechanical forces also initiate complex signal transduction cascades, including nuclear factor-kappaB and mitogen-activated protein kinase pathways, leading to functional changes within the cell.