Arteries Of Subjects Research Articles

Arterial pulse wave velocity in elderly patients with dementia

Background: Cardiovascular events influence the quality of life and mortality of elderly patients. Arterial stiffness measured by aortic pulse wave velocity is a useful means of predicting the presence of cardiovascular diseases, even in subjects over 70 years old. This procedure is non-invasive, but the usefulness and easiness of aortic pulse wave velocity for patients with dementia are still unclear. Therefore, to determine how useful and easy it is to measure aortic pulse wave velocity, we evaluated arterial stiffness in patients with or without dementia who required care and support for their daily life. Methods: Fifty-nine subjects over 70-years-old who suffered from dementia were enrolled in this study. After we excluded arteriosclerosis obliterans (ankle-brachial pressure index < 0.80; n = 10) by arterial pulse wave velocity, we classified these subjects into two groups: subjects with Alzheimer's disease (n = 25) and subjects with vascular dementia (n = 24) who were diagnosed by magnetic resource imaging and mini-mental state examination. Results: The authors of the present paper could easily and precisely evaluate arterial stiffness of all patients. The mean pulse wave velocity of right and left brachial-tibial arteries in subjects with Alzheimer's disease (1740 ± 385 cm/s) was significantly lower than those subjects with vascular dementia (2436 ± 586; P < 0.001). Conclusion: The data included in the present study indicate that subjects with Alzheimer's disease had decreased arterial stiffness and would show a lower risk of cardiovascular diseases compared to subjects with other diseases including vascular dementia.

Advanced atherosclerosis of the aortic arch is uncommon in ischemic stroke: An autopsy study

Aortic and carotid atherosclerosis are known risk factors for stroke. The aim of the study was to determine the frequency of atherosclerotic lesions in the aorta and carotid arteries in subjects dying of ischemic and hemorrhagic stroke and to determine whether aortic atherosclerosis was associated with any specific ischemic stroke subtype. Autopsies were performed in 207 patients who died during hospitalization for stroke from 1993 to 1997. Subjects ranged in age from 37 to 98 years, mean 74.45 years (SD ± 11.84). There were 132 women and 75 men. Stroke was hemorrhagic in 66 and ischemic in 141. Advanced atherosclerotic lesions were less frequent in the aortic arch (1.9%) than in the thoracic aorta (51.7%), abdominal aorta (60.4%), or carotid arteries (23.7%). Moderate atherosclerotic lesions in the aortic arch were observed more frequently in ischemic (75.2%) than hemorrhagic stroke (56.1%, p = 0.026). Advanced or moderate atherosclerotic lesions in any part of the aorta did not predict ischemic stroke subtype. Advanced atherosclerosis of the carotids was more common in ischemic stroke (28.4%) than hemorrhagic stroke (13.6%, p < 0.05). Advanced atherosclerosis of the carotids was more common in stroke due to atherothrombosis (51.4%) than in stroke due to cardiac embolism (22.1%) or stroke of unknown etiology (5.6%). The low frequency of advanced atherosclerotic lesions of the aortic arch suggests that this disease process is not a common mechanism of stroke. [Neurol Res 2002; 24: 491-494]

Anticardiolipin antibody titre and plasma homocysteine level independently predict intima media thickness of carotid arteries in subjects with idiopathic antiphospholipid antibodies.

This study evaluated whether IgG anticardiolipin antibody (aCL) titre and traditional risk factors for atherosclerosis bore any relationship to the intima media thickness (IMT) of carotid arteries of patients with idiopathic antiphospholipid antibodies (aPL). IMT was assessed by high-resolution sonography at the common carotid, carotid bifurcation and internal carotid in 42 (13 male, 29 female, mean age 31+/-10 years) aPL subjects, 29 with primary thrombotic antiphospholipid syndrome and 13 with persistence of aPL in the absence of any underlying disorder. In the same subjects the following were measured: plasma fibrinogen (FNG), von Willebrand factor (vWF), plasminogen activator inhibitor (PAI), homocysteine (HC), total cholesterol (CHO), triglycerides (TG), high density and low density lipoprotein (HDL and LDL), platelet numbers and aCL of IgG and IgM isotype. IMT of the internal carotid was greater in males than females (0.48+/-0.03 vs 0.39+/-0.01 mm, P=0.02). IMT of the carotid bifurcation was greater in thrombotic than nonthrombotic subjects (0.50+/-0.02 vs 0.42+/-0.02 mm, P=0.04). By simple regression, IMT of the common carotids correlated with age (P< 0.0001) IgG aCL titre (P=0.001), FNG (P=0.006), LDL (0.01), CHO (0.02) and PAI (P=0.02). IMT of the carotid bifurcation correlated with age (P=0.002), IgG aCL titre (P=0.0002), FNG (P=0.0001), HC (P=0.009), CHO (P=0.02), vWF (P=0.01) and number of thrombotic events (P=0.03). IMT of the internal carotids correlated with age (P=0.002), IgG aCL titre (P=0.0001), FNG (P=0.0008), PAI (P=0.002) and HC (P=0.01). By stepwise multiple regression analysis, IgG aCL titre independently predicted IMT at all carotid segments examined (P always <0.005). In addition, plasma FNG and HC also resulted independent predictors of IMT at the carotid bifurcation (P=0.001 and P<0.0001, respectively) and internal carotid (P=0.03 and P<0.0001, respectively). These data strongly support an atherogenic role for IgG aCL in patients with aPL. Measurement of plasma HC and FNG may help define aPL subjects at higher vascular risk who may require lowering of HC and FNG by vitamin and/or pharmacologic intervention.

Low wall shear stress in carotid arteries in subjects with left ventricular hypertrophy

Left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular complications including atherosclerosis. The close linkage between LVH and carotid atherosclerosis has been the focus of much research. However, the underlying mechanism linking the two conditions is not fully understood. Low wall shear stress contributes to intimal thickening and atherosclerosis development as a local mechanism. In the present study, we investigated the relationship between wall shear stress and LVH in subjects with risk factors for atherosclerosis. Eighty subjects with at least one risk factor for atherosclerosis; ie, hypertension, diabetes mellitus, hyperlipidemia, or smoking, were enrolled. Intimal-medial thickness (IMT), number of plaques, internal dimensions, and blood flow velocity in the common carotid artery were evaluated. Wall shear stress was calculated using a Poiseuillean parabolic model of velocity distribution: shear stress = 4 × blood viscosity × central flow velocity/internal dimension. Subjects were divided into two groups; LVH( −) (n = 36) and LVH( +) (n = 44), according to their left ventricular mass index (LVMI). Mean shear stress and systolic peak shear stress were significantly lower in subjects with LVH compared with subjects without LVH. Furthermore, mean shear stress (r = −0.42, P < .0001) and peak shear stress (r = −0.31, P < 0.01) were significantly inversely related to LVMI. Stepwise regression analysis revealed that wall shear stress independently correlated with LVMI as well as IMT. These results indicate that low shear stress could function as a local factor in the development of atherosclerosis in subjects with LVH.

Chlamydia pneumoniae in atherosclerotic tissue.

The majority of almost 30 publications from 1992 to 1999 describe Chlamydia pneumoniae organisms in atherosclerotic lesions of various major arteries. In the first study in the United Kingdom, C. pneumoniae was found in the aorta and femoral and iliac arteries. In a subsequent study, the organism was detected in arteries of subjects as young as 15 years. In a collaborative investigation, 71% of atheromatous arteries taken at autopsy from white South African subjects were C. pneumoniae positive compared with 9% of nonatheromatous arteries. Of interest, the organisms were detected in 67% of vessels that showed only early atherosclerotic lesions (fatty streaks). C. pneumoniae was also found in the ruptured coronary artery plaque of a black South African who died of myocardial infarction, a rare event. The presence of C. pneumoniae organisms within foam and smooth muscle cells of atherosclerotic plaques is beyond doubt, but their role in atherosclerosis remains enigmatic.

A T -786→C mutation in the 5′-flanking region of the endothelial nitric oxide synthase gene and coronary arterial vasomotility

In the endothelium, synthesis of nitric oxide (NO) from the amino acid L-arginine is catalyzed by the endothelial NO synthase (eNOS), and the continuously generated NO serves to maintain basal vascular tone. Recently, we discovered a T -786→C mutation in the 5′-flanking region of the eNOS gene; this mutation reduced the promoter activity of the eNOS gene and was associated with coronary spasm. We examined the vasomotility of the epicardial coronary artery in subjects with and without T -786→C mutation. We examined vasomotility in 32 consecutive subjects who were heterozygotes for the T -786→C mutation and in 68 subjects without the T -786→C mutation who had equivalent age, sex, and smoking status at the proximal and distal segments of the left descending coronary artery by performing quantitative coronary angiography. In subjects with the mutant allele (-786C allele), basal diameters of proximal and distal segments before intracoronary injection of acetylcholine (ACh) were less than diameters in subjects without the mutant allele (p <0.05), although there was no difference between subjects with and without the mutant allele in the diameters of coronary arteries after isosorbide dinitrate (ISDN) administration. When we compared the changes in diameters, both ACh-induced vasoconstriction and ISDN-induced vasodilatation in subjects with the mutant allele were significantly increased in the proximal (p <0.01, p <0.001, respectively) and distal segments (p <0.03, p <0.01, respectively). Taken together, these findings strongly suggest that the T -786→C mutation increases the basal tone of the coronary artery, and enhances the response to the constrictor effects of ACh and the dilator effect of ISDN because of reducing the endothelial NO synthesis.

In vivo femoropopliteal arterial wall compliance in subjects with and without lower limb vascular disease

Objective: The purpose of this study was to further the development of a compliant vascular graft with a preliminary assessment of the elastic properties of the femoropopliteal artery in subjects with and without lower limb peripheral vascular disease. Methods: This prospective controlled study was set in a university department of surgery. Using an ultrasound scan wall tracking system with the simultaneous measurement of brachial blood pressure, measurements of femoropopliteal artery wall motion were undertaken in 11 patients with peripheral vascular disease (group 1), in 11 older control subjects who were matched for blood pressure, age, and sex (group 2), and in 12 younger control subjects (group 3). Diametrical compliance and stiffness index were determined for the common femoral artery, the proximal superficial femoral artery, the distal superficial femoral artery (DSFA), and the midgenicular popliteal artery. Results: All the arterial segments in group 1 showed a trend towards increased stiffness and less compliance than the group 2, age-matched control vessels, with significantly lower distensibility noted at the common femoral artery (mean compliance of 6.2% vs 14.1% mm Hg –1 × 10 –2, respectively; P < .05) and the DSFA (mean compliance of 2.2% vs 1.9% mm Hg –1 × 10 –2, respectively; P < .05). The popliteal artery segment in group 3 proved to be more compliant and less stiff than did the same vessel in group 2 (8.5% vs 4.7% mm Hg –1 × 10 –2, respectively; P < .01). In all three study groups, the DSFA was consistently noted to be the least distensible vessel segment. Conclusion: Lower limb peripheral vascular disease is associated with a reduction in femoropopliteal artery elasticity. Age alone appears to have a minimal effect on the compliance of the proximal half of the femoropopliteal segment. The elastic properties of the femoropopliteal vessel are subject to marked variation along its course. To minimize compliance mismatch, the degree of elasticity engineered into a vascular graft must reflect that observed in vivo. (J Vasc Surg 1999;30:936-45.)

脳ドック受診者における椎骨動脈の血流速度

脳ドック受診者における椎骨動脈の血流速度

Impaired Endothelium-dependent Vasomotion of Coronary Artery in Subjects With Type-A Behavior

Impaired Endothelium-dependent Vasomotion of Coronary Artery in Subjects With Type-A Behavior

Impaired endothelium-dependent vasomotion of coronary artery in subjects with type-A behavior

Impaired endothelium-dependent vasomotion of coronary artery in subjects with type-A behavior

Endothelial dysfunction of coronary artery in subjects with impaired glucose tolerance

Endothelial dysfunction of coronary artery in subjects with impaired glucose tolerance

Arterial stiffness in hypertensive subjects with or without end-stage renal disease.

Therapeutic trials have shown that the response to antihypertensive drug treatment is heterogeneous, with substantially higher effects of cardiovascular prevention for the cerebral than for the coronary circulation. This finding suggests that the response of large conduit arteries to elevated blood pressure may vary greatly between the different compartments of the arterial bed. Recent in vivo non-invasive studies in humans suggest that the stiffness of large arteries in subjects with essential hypertension differs greatly according to the vascular territory involved. Operational arterial stiffness, i.e., measured at the mean blood pressure of the hypertensive population by comparison with normotensive subjects, is increased in central arteries (carotid artery, aorta) but normal in peripheral muscular arteries (femoral artery, radial artery). On the other hand, when hypertensive and normotensive subjects are compared for the same blood pressure, arterial stiffness appears to be normal for the radial artery but decreased for the femoral artery and the aorta. In the case of carotid arteries, isobaric arterial stiffness is normal in subjects with uncomplicated essential hypertension but decreased in hypertensive patients with end-stage renal disease. Thus, important differences may be observed according to the territory involved, suggesting that the response to drug treatment of hypertension may be influenced not only by the blood pressure reduction itself but also by the regional properties of each particular vascular bed and the presence of advanced renal disease.

Correlation between visual field and color Doppler parameters in chronic open angle glaucoma.

The authors evaluated, by means of colour Doppler imaging, the blood flow in ophthalmic artery and posterior ciliary arteries in subjects with chronic open angle glaucoma. On the basis of the visual field indices (MD, SF, CPSD) the patients' eyes were divided in two groups: group A with better indices and group B with great damage. At the posterior ciliary arteries they found these values: PSV 10.264 +/- 2.363 cm/s (group A) vs. 7.882 +/- 1.251 cm/s (group B) (p < 0.008); RI 0.615 +/- 0.065 (group A) vs. 0.695 +/- 0.064 (group B) (p < 0.009). These data highlight a correlation between the visual field damage and the reduced supply of optic nerve head.

Smooth muscle-derived nitric oxide is elevated in isolated forearm veins in human alcoholic cirrhosis.

1. Cirrhosis is often complicated by disturbances in the systemic circulation. We have previously demonstrated decreased vascular responses to vasoconstrictors in forearm resistance arteries in subjects with alcoholic cirrhosis. In the current study we investigate the role of the potent endogenous vasodilator nitric oxide in the peripheral circulation of these patients. 2. Ten patients with alcoholic cirrhosis (Pugh grade A) and 10 age-matched control subjects were studied. The effect of blockade of nitric oxide synthesis was studied both in vivo in forearm resistance arteries using forearm venous occlusion plethysmography and in vitro in veins isolated from the forearm. The role of endothelium-derived nitric oxide was studied in vivo using the endothelium-dependent vasodilator acetylcholine. 3. Mean arterial pressure and forearm basal flow in vivo were similar in the two groups. The constrictor response (percentage decrease in forearm blood flow) to noradrenaline (100 ng/min) was 26% smaller in patients with cirrhosis (31.65 +/- 2.64%) than in control subjects (42.75 +/- 3.87%, P = 0.037). Constrictor responses to the nitric oxide synthase inhibitor NG-monomethyl-L-arginine were not different in the two groups. Dilator responses to acetylcholine were significantly attenuated in cirrhotic patients compared with control subjects. 4. To investigate the role of smooth muscle-derived nitric oxide in vitro, all veins were stripped of their endothelium. Responses to noradrenaline were significantly diminished in veins isolated from patients with cirrhosis compared with control subjects. Incubation with the nitric oxide synthase inhibitor N omega-nitro-L-arginine had no effect on responses to noradrenaline in veins from control subjects but significantly enhanced the maximal response to noradrenaline by 23.95% (range 3.77-100%, P = 0.043) in veins from patients with cirrhosis. 5. Responses to noradrenaline were attenuated in vivo in forearm resistance arteries in patients with alcoholic cirrhosis. This impairment was also apparent in forearm isolated veins, stripped of the endothelium. Our data exclude a major role for endothelium-derived nitric oxide but highlight a possible role for smooth muscle-derived nitric oxide.

Alpha-adrenoceptor responses of an isolated human artery and blood pressure.

This cross-sectional study examined responses of the isolated cystic artery to 3 alpha-adrenoceptor agonists and the effects of 2 antagonists in relation to subjects' blood pressures. Potency of the 3 amines studied was: alpha-methylnorepinephrine > norepinephrine > phenylephrine. Responses to clonidine were trivial (< 5% of maximum) and remained < 25% of maximum in the presence of subthreshold concentrations of angiotensin II. A weak trend for increased potency of alpha-methylnorepinephrine was noted in arteries of subjects with higher blood pressures (r = 0.268, p = 0.027). There was no relationship between blood pressure and pA2 for yohimbine. The pA2 for prazosin could not be calculated because of a decline in maximal responses but prazosin was clearly more potent than yohimbine. The decline in maximal responses to norepinephrine and phenylephrine after prazosin treatment was related to subjects' diastolic blood pressures (r = -0.400, p = 0.003). There were no significant relationships between these measurements of vascular responsiveness and a family history of hypertension. There were also no significant relationships between these measurements of vascular responsiveness and plasma norepinephrine levels, alpha 2-adrenoceptor binding or platelets of beta 2-adrenoceptor binding of lymphocytes. The major postjunctional alpha-adrenoceptors in this artery are of the alpha 1 type. The data suggest that differences in potency of alpha-adrenoceptor agonists in relation to blood pressure may be due to differences in the alpha 2-adrenoceptor but are not likely due to a difference in binding to the receptor itself.(ABSTRACT TRUNCATED AT 250 WORDS)

Morphometry of structural preservation of tunica media in aged and hypertensive human intracerebral arteries.

Medial smooth muscle cell necrosis has been reported as a lesion that may precede angionecrosis, which is a major cause of not only hypertensive brain hemorrhage but also lacunar infarct. We morphometrically studied a loss of smooth muscle cells in the media of cerebral arteries in relation to clinical risk factors. The lateral striate, ie, perforating arteries and the medullary arteries in the subcortical white matter of the temporal lobe (100 to 400 microns in diameter) were histologically investigated in 121 autopsied brains. Medial area was measured quantitatively, and the number of nuclei of smooth muscle cells in the area was calculated in 1210 cross-sectional arteries of histological sections. The influence on the structural (ie, smooth muscle cell) preservation of the tunica media (ratio of number of smooth muscle cell nuclei to medial area [N-MA ratio]) of age, blood pressure, serum lipids, and presence of absence of extracerebral severe atherosclerosis was investigated. The N-MA ratio decreased slightly with age in both arteries. A reverse correlation between N-MA ratio and age was seen in groups both with and without hypertension. The mean N-MA ratio in the hypertensive group was significantly lower than that of the nonhypertensive group (P < .001) in all decades of life. The mean N-MA ratio of the perforating arteries was slightly lower than that of the medullary arteries in both groups. Severe atherosclerosis of the internal carotid arteries, even with hypertension, mitigated a decrease of the N-MA ratio, which was as slight as that in the nonhypertensive group. Serum cholesterol in this group was higher than in both the conventional hypertensive group (P < .005) and the nonhypertensive group (P < .001). Although both hypertension and age were significant risk factors for medial smooth muscle cell necrosis, hypertension was relatively more significant. Medial smooth muscle cells of the perforating arteries in the basal ganglia were more vulnerable than those of the medullary arteries. Cerebral small arteries in subjects with severe atherosclerosis of the carotid and major cerebral arteries (hypertension in eight of nine subjects) may have been protected from extensive loss of medial smooth muscles presumably because of both high serum cholesterol and decreased wall tensile stress associated with reduced blood perfusion due to severe atherosclerotic stenosis.

Prevalence of carotid atherosclerosis in diabetic patients. Ultrasound high-resolution B-mode imaging on carotid arteries.

To quantitatively assess atherosclerosis of the carotid artery in subjects with and without diabetes. Ultrasound high resolution B-mode imaging of carotid arteries was conducted on 71 nondiabetic subjects without hyperlipidemia or hypertension and 295 diabetic patients to determine IMT of the arterial wall. IMT was linearly related with age in nondiabetic (IMT = [0.0087 x age] + 0.3318) and diabetic subjects (IMT = [0.0155 x age] + 0.32450). The regression coefficient for age was significantly greater in diabetic than nondiabetic subjects. IMT (mean +/- SD) of diabetic subjects aged 20-29 was significantly greater than that of nondiabetic subjects aged 20-29 (0.73 +/- 0.27 vs. 0.52 +/- 0.07 mm, P less than 0.01). Multivariate regression analysis of 275 NIDDM patients indicated smoking, hyperlipidemia, duration of diabetes, hypertension, and age were factors determining thickness of the carotid arterial wall. Diabetes, along with age, hyperlipidemia, smoking, and hypertension, aggravates carotid atherosclerosis.

Surgical anatomy of the arterial blood-supply of the human rectum.

One of the factors possibly responsible for leakage at a colo-rectal anastomosis is a deficient blood-supply. The rectal circulation was studied in 30 cadavers by injection of colloidal barium sulfate with colored gelatin into the hypogastric and inferior mesenteric arteries. It was noted that there was uniformity of supply to the wall of the organ; the blood-supply derived from the hypogastric arteries in subjects over 50 years of age was minor; the predominant blood-supply was derived from the superior rectal artery. These findings suggest that the hypogastric arteries usually provide only a minor supply in persons over 50 years of age and that obstruction of the inferior mesenteric artery associated with the impaired blood-supply inherent in the rectal dissection must be included in the factors responsible for leakage at the colorectal anastomosis.

Extrarenal arterial connections of the normal renal artery.

An angiographic study in cadavers has demonstrated connections between the renal artery and remote vessels including the intercostal, testicular, and inferior mesenteric arteries in subjects with no known history of renal disease. Such communications are a potential route by which embolic material introduced into the renal artery may inadvertently reach other organs.

Clinical anatomical study of the macroscopic anastomoses of the ophthalmic artery in the periorbital region

Using latex injections we have studied the anastomoses between the ophthalmic artery (a. ophthalmica) and the branches of the external carotid (a. carotis exerna) in the orbital region (regio orbitalis). We have limited this report to the macroscopic anastomoses which have a functional supply and which are accessible to examination by the Doppler technique. After examination of 60 specimen pairs it is clear that most anastomoses were inconstant. We have thus recorded their frequency: for the facial artery (a. facialis) the frequency of anastomoses was 60%, for the superficial temporal artery (a. temporalis superficialis) it was 33%, for the infraorbital artery (a. infraorbitalis) anastomoses were present in 37%. We have furthermore studied the association between the different anastomoses to establish whether their relationship to one another was organized or simply random. We found that the anastomoses between the branches of the opthalmic artery and those of the external carotid artery were much more frequent on the right side. Finally, we have compared our anatomical results with those of a series of Doppler examinations designed to detect reversal of the circulation at the level of different anastomoses of the ophthalmic artery in subjects who presented with unilateral thrombosis of the internal carotid artery (a. carotis interna). This study revealed a good correlation between the anatomical findings and those observed on Doppler examination. There are however differences which can be explained by the small number of subjects examined, by the calibre of the vessels and also by the fact that in certain subjects, the circle of Willis (circulus arteriosus cerebri) was particularly well-developed. In such circumstances the anastomoses were not clinically functional and there was no reversal of blood flow within them.