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PubMed2006

Effects of local arteriosclerosis on carotid baroreflex sensitivity and on heart rate and arterial pressure variability in humans.

The study examined whether the alterations in heart rate variability (HRV) and baroreflex sensitivity (BRS) observed in patients with coronary artery disease can also be discerned in otherwise healthy subjects with mild-to-moderate arteriosclerosis in the carotid artery bifurcation. Based on the results of carotid duplex ultrasonography, subjects were designated as either having no arteriosclerotic lesions (n = 18), unilateral (n = 19) or bilateral lesions (n = 18) in the bifurcation. Electrocardiograms were recorded and simultaneous and continuous records of arterial pressure were obtained. Resting HRV was determined by calculating the spectral power density in three frequency bands: 0-0.05 Hz [very low frequency (VLF) band], 0.05-0.15 [low frequency (LF) band] and 0.15-2 Hz (high frequency band), whereas the arterial pressure variability (APV) was determined from spectral power density of the VLF and LF bands. Carotid BRS was evaluated by measuring R-R intervals during application of pulse-synchronous graded pressures (40 to -65 mmHg) in a neck-chamber device. Analysis of variance revealed no effect of mild-to-moderate carotid arteriosclerosis on the spectral components of HRV and APV or on BRS. It thus appears that mild-to-moderate asymptomatic carotid arteriosclerosis does not affect carotid BRS, APV or HRV at rest.

Adult↗
PubMed1997

The relationship between endothelin-1, event-related P300 potentials, and prognosis in cerebral arteriosclerosis.

OBJECTIVES: To search for a potential role of endothelin-1 (ET-1), a potent vasoconstrictor and presumably neurotoxic 21-amino acid peptide, for dysfunction of brain signal processing and cerebrovascular morbidity in nondemented patients with cerebral arteriosclerosis. DESIGN: Cross-sectional study with longitudinal follow-up. SETTING: University-affiliated teaching hospital. PARTICIPANTS: A total of 106 nondemented patients with significant stenosis of either the internal carotid (cAD, cases; n = 63, mean age +/- SD, 62 +/- 7 years) or peripheral arteries (pAD, disease controls; n = 43, 60 +/- 11 years) were investigated before carotid endarterectomy and bypass surgery, respectively. After a mean follow-up of about 19 months, cerebrovascular morbidity of the cAD and pAD patients was evaluated by phone. MEASUREMENTS: Brain signal processing functions by event-related visual P300 potentials; cerebrovascular events by a structured telephone interview; the extent of arteriosclerosis by venous ET-1 concentration. RESULTS: Venous ET-1 levels were elevated in both cAD and pAD patient groups, but to the same degree. In these patients, ET-1 concentration was correlated slightly with diastolic blood pressure (r = .334, P = .0326, stepwise regression). Only in cAD patients with ET-1 levels above the 75th percentile were P300 latencies markedly prolonged compared with their lower ET-1 level counterparts. Furthermore, the P300 latencies of the cAD patients, but not of the pAD patients, correlated positively with venous ET-1 concentration and inversely with pack years of smoking (r = .728, P = .0002; stepwise regression). In contrast to base-line P300 abnormalities and classical risk factors (e.g., hypertension), high ET-1 levels predicted an increased cerebrovascular morbidity of cAD, but not of pAD, patients (P = .0044; Mantel Cox test). CONCLUSIONS: In nondemented patients with cerebral arteriosclerosis, endothelin-1 is associated with P300 abnormalities reflecting subclinical dysfunction of brain signal processing. In the long-term, high venous ET-1 levels also appear to predict a higher cerebrovascular morbidity of cAD patients even after carotid endarterectomy.

Aged↗
PubMed1970

Elevation of aortic proline hydroxylase: a biochemical defect in experimental arteriosclerosis.

The relation of collagen synthesis to experimentally induced arteriosclerosis was studied by measuring proline hydroxylase activity. Gross aortic plaques were produced in rabbits by daily injection of epinephrine (intravenous) and thyroxine (intraperitoneal) for 4, 9, or 14 days. Activity of proline hydroxylase was significantly increased after 4 days of treatment and reached a peak, five- to sixfold increase, after 14 days of treatment. The increase in enzyme activity was correlated with the severity of observed arteriosclerosis. Increase in proline hydroxylase activity may be a possible biochemical defect in the aortas of rabbits with arteriosclerosis induced by injury.

Amino Acid Metabolism, Inborn Errors↗
PubMed1998

Cross sectional observation of the effects of carbon disulphide on arteriosclerosis in rayon manufacturing workers.

OBJECTIVE: A prospective cohort study was designed to clarify the relations between occupational exposure to carbon disulphide (CS2) and its effects on arteriosclerosis in workers in 11 Japanese rayon manufacturing factories. This report is a cross sectional baseline observation in the first study year. METHODS: Study subjects were 432 male rayon workers (mean (range) age 35.5 (19.1-47.8); duration of exposure 13.4 (0.3-29.0)) and 402 male referent workers (age 35.8 (18.9-49.8)). Exposure to CS2 was assessed by determining the concentration of 2-thiothiazolidine-4-carboxylic acid (TTCA) in urine. Mean (SD) TTCA was 3.42 (2.73) mg/g creatinine (Cr) (n = 422). About a quarter of the urine samples were > 5 mg/g Cr, a biological exposure index recommended by the American Conference of Governmental Industrial Hygienists. Health effects on arteriosclerosis were evaluated by measuring blood pressure, serum lipids, pulse wave velocity of the aorta, stiffness and blood flow of the carotid artery, and blood coagulation and fibrinolysis indices, and by use of brain magnetic resonance imaging, electrocardiogram (at rest and after exercise), ophthalmograph, and Rose's questionnaire. Information on potential confounding factors was collected by self administered questionnaire. RESULTS: Prevalence of microaneurysm of the retinal artery was significantly higher in workers exposed to CS2 (8.1%) than in referent workers (3.4%), and increased with age. Other examinations did not show any differences between the two groups even after allowance for confounding factors. CONCLUSIONS: Significant effects of CS2 on arteriosclerosis were not found in current rayon manufacturing workers, with the exception of induction of microaneurysm of the retinal artery.

Adult↗
PubMed2004

Inhibition of accelerated graft arteriosclerosis by gene transfer of soluble fibroblast growth factor receptor-1 in rat aortic transplants.

OBJECTIVE: Because increased fibroblast growth factor-1 (FGF-1) and FGF receptor (FGFR) expression correlate with the development of accelerated graft arteriosclerosis in transplanted human hearts, this study sought to determine whether local gene transfer of soluble FGFR-1, capable of binding both FGF-1 and FGF-2, could blunt the development of accelerated graft arteriosclerosis in the rat aortic transplant model. METHODS AND RESULTS: A construct encoding the FGFR-1 ectodomain, capable of neutralizing FGF-2 action, was expressed in rat aortic allografts, using adenoviral gene transfer at the time of transplantation. Neointima formation was inhibited in aortic allografts transduced with soluble FGFR-1, compared with allografts transduced with Null virus. CONCLUSIONS: FGFs play a causal role in the development of accelerated graft arteriosclerosis in the rat aortic transplant model. Targeted interruption of FGF function could potentially reduce neointima formation in patients with heart and kidney transplants.

Adenoviridae↗
PubMed1996

Triple drug immunosuppression significantly reduces aortic allograft arteriosclerosis in the rat.

We evaluated the effect of triple drug immunosuppression (cyclosporine A 10 mg . kg(-1) . d(-1), methylprednisolone 0.5 mg . kg(-1) . d(-1) on the development of allograft arteriosclerosis (chronic rejection). The recipients of rat aortic allografts from the DA (AG-B4,RT1a) to the WF (AG-B2,RT1u) strain were either treated with triple drug immunosuppression (n=23) or left untreated (n=23) and used as controls. The grafts were removed 7, 14, 30, 90, and 180 days after transplantation, and vascular wall changes were evaluated by quantitative histology, [3H]thymidine autoradiography, and immunohistochemistry. Nonimmunosuppressed aortic allografts developed progressive arteriosclerotic alterations 1 to 6 months after transplantation that were virtually identical to those observed during chronic rejection in human cardiac allografts. Linear regression analysis revealed that triple drug immunosuppression with clinically relevant dosages of drugs significantly reduced intimal thickening (r=.69 versus r=.88, P<.05). Concomitantly, there was a marked reduction in the number of inflammatory cells (P<.01) and their rate of proliferation (P<.025) in the allograft adventitia during the period of acute inflammation (30 days after transplantation). Immunohistochemistry revealed that the number of helper T cells (W3/25) and monocyte/macrophages (OX42) but not cytotoxic T cells (OX8) or natural killer cells (3.2.3) was significantly (P<.05) reduced. The number of adventitial cells expressing interleukin-2 receptor (CD25) (P<.05), MHC class II (OX6) (P<.05) and leukocyte function-associated antigen-1 alpha-chain (CD11a) (P<.025) was also significantly reduced at 30 days. Triple drug immunosuppression downregulated the induction of MHC class II and intercellular adhesion molecule-1 on the graft endothelium but had no significant effect on the number of subendothelial inflammatory cells. In addition, [3H]thymidine autoradiography demonstrated that triple drug immunosuppression significantly reduced the rate of cell proliferation in the media, composed of smooth-muscle cells, 30 and 90 days after transplantation. Thus, triple drug immunosuppression efficiently reduced the development of allograft arteriosclerosis by down-regulating the inflammatory response and the level of immune++ activation in the allograft adventitia during the acute rejection period, resulting in diminished intimal thickening of the graft in the long run. These results support the concept that allograft arteriosclerosis is due to or at least initiated by immune injury of the graft.

Animals↗
PubMedDate not supplied

Systemic arterial compliance in patients with arteriosclerosis obliterans of the lower limbs. Observations on the effect of intravenous propranolol.

Hemodynamic parameters and systemic arterial compliance were measured in patients with arteriosclerosis obliterans of the lower limbs before and after acute administration of propranolol. Arterial compliance was evaluated from a simple viscoelastic model, enabling the calculation of diastolic drainage and diastolic blood flow as indices of the reservoir role of the larger arteries in overall circulation. In comparing basal conditions with normal subjects of the same age, patients with arteriosclerosis obliterans exhibited a significant decrease in arterial compliance (p less than 0.01) and heart rate (p less than 0.02) with a significant increase in systolic pressure (p less than 0.001). Diastolic drainage was increased (p less than 0.01) and was positively correlated with diastolic time (r = 0.73, p less than 0.001). Diastolic blood flow remained within normal ranges (52 +/- 2 vs 49 +/- 3 ml/m2/sec). After acute propranolol intravenous administration, heart rate and stroke volume decreased (p less than 0.001), while total peripheral resistance increased (p less than 0.001). Systemic arterial compliance and diastolic blood flow significantly decreased (p less than 0.01). The study provided evidence that in patients with arteriosclerosis obliterans, the diastolic blood flow was maintained in basal conditions despite the observed reduction in arterial compliance, and that intravenous propranolol administration decreased systemic arterial compliance and diastolic blood flow.

Adult↗
PubMedDate not supplied

Prevalence of severe arteriosclerosis obliterans in patients with diabetes mellitus. Relation to smoking and form of therapy.

Noninvasive methods were used to determine the prevalence and severity of arteriosclerosis obliterans associated with diabetes in 674 subjects including 153 recruited as controls. A resting ankle systolic blood pressure that was less than 90% of the arm pressure indicated severe arteriosclerosis obliterans. Of the 71 subjects with severe disease, 64 (90%) had a history of smoking, which is significantly greater than the 60% overall smoking rate (p less than 0.001). In non-insulin-dependent diabetic smokers, the diet-treated subjects had 2.5 times the prevalence of severe arteriosclerosis obliterans as those treated with insulin (p = 0.01); the sulfonylurea-treated subjects had twice the prevalence of severe disease as those treated with insulin (p = 0.015).

Adult↗
PubMedDate not supplied

Effect of acetylsalicylic acid on pulmonary arteriosclerosis induced by a one-year Dirofilaria immitis infection.

The ability of aspirin to block arteriosclerosis that developed in response to chronic, low-level injury to pulmonary arteries was evaluated in 21 dogs during their 1-year infection with Dirofilaria immitis. Three groups, with seven dogs in each group, were studied before and after sustained injury produced by the transplantation of 28 adult Dirofilaria immitis into each dog. Group A received no treatment and served as controls; Group B received no treatment for 6 months and then received 7 mg/kg of aspirin daily) for 6 months; Group C received 7 mg/kg of aspirin daily for the entire year. The pulmonary arterial response was evaluated by hemodynamic and arteriographic studies at 6 and 12 months and by scanning electron microscopy at the end of the 12-month study. All groups developed a similar, mild pulmonary hypertension. The arteriographic changes of dilation and flow obstruction were worse in Groups A and B than in Group C at 6 months, and at 12 months both Groups B and C were less obstructed than Group A. Scanning electron microscopy revealed large, complex myointimal proliferations in Group A, whereas the two aspirin-treated groups had smaller, less complex lesions that covered a much smaller surface area. We concluded that: 1) aspirin markedly reduced the microscopic and macroscopic arteriosclerosis in Groups B and C; 2) aspirin in Group B not only arrested further development but also permitted resolution of arteriosclerosis while the arteries were still being injured.

Angiography↗
PubMed1995

Upregulation and modulation of inducible nitric oxide synthase in rat cardiac allografts with chronic rejection and transplant arteriosclerosis.

BACKGROUND: The Lewis-F344 rat cardiac transplantation model produces cardiac allografts with chronic rejection characterized by arteriosclerotic lesions composed of macrophages and smooth muscle cells. Modulation of the inflammatory response with a diet deficient in essential fatty acids protects against the development of intimal thickening. Little is known about the components of the inflammatory response mediating this process. The cytokine-inducible isoform of nitric oxide synthase (iNOS) regulates the high-output nitric oxide pathway that confers activation properties to macrophages and regulates vasomotion, monocyte adherence, and smooth muscle cell proliferation in the vasculature. The purpose of the present study was to determine whether the iNOS pathway was upregulated during the course of chronic cardiac rejection. METHODS AND RESULTS: We studied iNOS mRNA and protein expression patterns in a series of Lewis-F344 cardiac allografts with early and late chronic rejection and after modulation of the inflammatory response (in an effort to attenuate arteriosclerosis). Relative gene transcript levels were measured with a 32P-dCTP reverse-transcriptase polymerase chain reaction assay designed to amplify iNOS mRNA. The distribution of the iNOS gene product was examined by immunocytochemistry with a polyclonal antibody against iNOS. NOS transcript levels increased significantly in cardiac allografts (days 7, 14, 28, and 75) compared with paired host hearts (exposed to the same circulation) and syngrafts (P < .003). Immunostaining localized the iNOS antigen within subpopulations of mononuclear inflammatory cells in cardiac allografts--presumably, activated macrophages. The number of iNOS-positive mononuclear cells was 25-fold higher in cardiac allografts compared with paired host hearts and syngrafts (P < .009). In cardiac allografts of 75 days or older, there also was striking iNOS staining within some medial and intimal smooth muscle cells in various vessels. Modulation of the inflammatory response (with a diet deficient in essential fatty acids) produced significant decreases in the intimal thickening score and in the percentage of diseased vessels in 28-day cardiac allografts compared with allografts from rats fed a control diet. There was a correlate decrease in iNOS transcript levels and in the number of iNOS-positive mononuclear cells in the 28-day cardiac allografts from rats fed the essential fatty acid-deficient diet. CONCLUSIONS: The early and persistent upregulation of iNOS in chronic cardiac rejection and the coincident reduction in arteriosclerosis and downregulation of iNOS suggest that this inducible regulator may contribute to the inflammatory response mediating transplant arteriosclerosis.

Amino Acid Oxidoreductases↗
PubMed1994

Murine model of accelerated transplant arteriosclerosis.

To define the role of specific gene deletions and mutations in the development of transplant arteriosclerosis, we generated an accelerated model of the disease in mice. Carotid arteries were transplanted between B.10A(2R) (H-2h2) donor mice and C57BL/6J (H-2b) recipients and compared with arteries isografted between H-2b mice. Immunosuppressive drugs were not used. Within 7 days, the allografted carotid artery formed a neointima composed of mononuclear leukocytes (CD45+) that were predominantly monocytes or macrophages (ie, CD11b+ cells with single-lobed nuclei). CD4+ and CD8+ cells were present as well. By 30 days, the neointima became exuberant, and mononuclear leukocytes were largely replaced by smooth muscle cells. Cells staining for proliferating-cell nuclear antigen were abundantly present in the intima at both early and late time points, indicating the proliferation of mononuclear leukocytes and smooth muscle cells. The area of the intima increased from day 7 to day 30 (P < .0005), as did the number of nuclei (P = .0005), but the density of the nuclei decreased (P = .02), suggesting the formation of extracellular matrix. Six of the eight isografts formed no neointima, and in samples from the remaining two, a single layer of smooth muscle neointimal cells covered just a portion of the vessel circumference. This model, which reproduces many of the features of human transplant arteriosclerosis but at an accelerated pace, should prove useful for determining the roles in transplant arteriosclerosis of genes that code for components of immunologic and inflammatory responses.

Animals↗
PubMed1998

Immune sources of transforming growth factor-beta1 reduce transplant arteriosclerosis: insight derived from a knockout mouse model.

Activated CD4-positive T cells are essential in the early stages of arteriosclerotic lesion development after cardiac transplantation. Besides its parenchymal effects, transforming growth factor-beta1 (TGF-beta1) mediates immunosuppressive effects on proliferation and activation of CD4 cells. This study was designed to assess immune contributions of TGF-beta1 to arteriosclerosis by comparing the effect of TGF-beta1-deficient and -competent infiltrating inflammatory cells on the development of intimal thickening in a heterotopic mouse transplant model (CBA to C57B6). Transplant arteriosclerosis was evaluated in cardiac grafts placed into knockout recipients heterozygous for TGF-beta1 (n=7) and was compared with those placed into wild-type recipients (n=11). At 55 days, allografts in TGF-beta1-deficient recipients had increased concentric intimal thickening. Computer-assisted analysis of all elastin-positive vessels (n=173) showed significantly increased luminal occlusion (67.8+/-5.6%) in grafts from TGF-beta1-deficient recipients compared with wild-type recipients (47.4+/-4.1%, P=0.003). To determine whether TGF-beta1 deficiency altered CD4 activation patterns, we studied intragraft cytokine expression. Using 32P-reverse-transcriptase polymerase chain reaction assays, we show that TGF-beta1-deficient recipients had an increased expression of the transcription factor STAT 4, interferon gamma, and interleukin-2 (Th1-type response) and unaltered or reduced expression of the transcription factor STAT 6, interleukin-4, and interleukin-10 (Th2-type response). Hence, when present, immune sources of TGF-beta1 attenuate transplant arteriosclerosis. This effect is associated with attenuation of Th1 forces.

Animals↗
PubMed2001

Exacerbated vein graft arteriosclerosis in protein kinase Cdelta-null mice.

Smooth muscle cell (SMC) accumulation is a key event in the development of atherosclerosis, including vein bypass graft arteriosclerosis. Because members of the protein kinase C (PKC) family signal cells to undergo proliferation, differentiation, or apoptosis, we generated PKCdelta knockout mice and performed vein bypass grafts on these animals. PKCdelta(-/-) mice developed normally and were fertile. Vein segments from PKCdelta(-/-) mice isografted to carotid arteries of recipient mice of either genotype led to a more severe arteriosclerosis than was seen with PKCdelta(+/+) vein grafts. Arteriosclerotic lesions in PKCdelta(-/-) mice showed a significantly higher number of SMCs than were found in wild-type animals; this was correlated with decreased SMC death in lesions of PKCdelta(-/-) mice. SMCs derived from PKCdelta(-/-) aortae were resistant to cell death induced by any of several stimuli, but they were similar to wild-type SMCs with respect to mitogen-stimulated cell proliferation in vitro. Furthermore, pro-apoptotic treatments led to diminished caspase-3 activation, poly(ADP-ribose) polymerase cleavage, and cytochrome c release in PKCdelta(-/-) relative to wild-type SMCs, suggesting that their apoptotic resistance involves the loss of free radical generation and mitochondrial dysfunction in response to stress stimuli. Our data indicate that PKCdelta maintains SMC homeostasis and that its function in the vessel wall per se is crucial in the development of vein graft arteriosclerosis.

Animals↗
PubMed1999

Donor MHC and adhesion molecules in transplant arteriosclerosis.

Transplant-associated arteriosclerosis remains an obstacle to long-term graft survival. To determine the contribution to transplant arteriosclerosis of MHC and adhesion molecules from cells of the donor vasculature, we allografted carotid artery loops from six mutant mouse strains into immunocompetent CBA/CaJ recipients. The donor mice were deficient in either MHC I molecules or MHC II molecules, both MHC I and MHC II molecules, the adhesion molecule P-selectin, intercellular adhesion molecule (ICAM)-1, or both P-selectin and ICAM-1. Donor arteries in which ICAM-1, MHC II, or both MHC I and MHC II were absent showed reductions in neointima formation of 52%, 33%, and 38%, respectively, due primarily to a reduction in smooth muscle cell (SMC) accumulation. In P-selectin-deficient donor arteries, neointima formation did not differ from that in controls. In donor arteries lacking both P-selectin and ICAM-1, the size of the neointima was similar to that in those lacking ICAM-1 alone. In contrast, neointima formation increased by 52% in MHC I-deficient donor arteries. The number of CD4-positive T cells increased by 2.8-fold in MHC I-deficient arteries, and that of alpha-actin-positive SMCs by twofold. These observations indicate that ICAM-1 and MHC II molecules expressed in the donor vessel wall may promote transplant-associated arteriosclerosis. MHC I molecules expressed in the donor may have a protective effect.

Animals↗
PubMed1999

Effects of triflusal on arteriosclerosis progression assessed with high-resolution arterial ultrasound.

In order to evaluate the effect of triflusal (2-acetyloxy-4-trifluoromethyl benzoic acid), an orally active antiplatelet agent, on arteriosclerosis progression, a pilot, parallel, double-dummy, double-blind clinical trial vs acetylsalicylic acid (ASA) was carried out in patients with subclinical atherosclerotic lesions. The trial consisted of a 2-week run-in placebo phase, followed by a 12-month oral treatment with triflusal (600 mg/day) or ASA (300 mg/day). The primary variable was identified in the ultrasonic biopsy (UB) score; the secondary variables were the UB class changes of each arterial site, the rate of progression (ROP), the intima-media thickness (IMT), and the symptoms of arteriosclerosis. Data were evaluated by use of analysis of variance and Chi-square test. Forty-three patients (31 men, 12 women, mean age 62.8 +/- 8.4 SD) were randomized to triflusal (15 men, 6 women, mean age 64.3 +/- 6.7) or to ASA (16 men, 6 women, mean age 61.3 +/- 9.6). The analysis of variance on the UB score showed no difference between treatments: the patients' UB scores remained unchanged with no progression, thus indicating that no patient worsened during treatment. When all arterial sites under evaluation are considered, 86% of the sites in the triflusal group and 85% in the ASA group remained unchanged. No relevant change was recorded in vital signs and routine laboratory tests. Gastric disturbances were reported by two and three patients treated with triflusal and ASA, respectively. In conclusion, triflusal appears as effective as ASA in slowing arteriosclerosis progression.

Administration, Oral↗
PubMed2004

Difference in the risk factors for coronary, renal and other peripheral arteriosclerosis in heterozygous familial hypercholesterolemia.

BACKGROUND: The aim of the present study was to clarify the risk factors of several types of arteriosclerosis lesions in Japanese individuals with heterozygous familial hypercholesterolemia (FH): renal arteriosclerosis (RAS), abdominal aortic sclerosis (AOS), iliac arteriosclerosis (IAS) and coronary artery disease (CAD). METHODS AND RESULTS: Coronary angiography (CAG) and abdominal aortic angiography (AAA) were performed in 117 consecutive heterozygous FH subjects (79 men, 38 women; age 22-76). RAS (stenotic lesion or aneurysm) was observed in 39 cases (33%), predominantly in the proximal portion (74%) and both sides equally (right/left = 27/23). Most cases of RAS (64%) presented with <25% stenosis. The differences in the contributing risk factors for the progression and development of RAS, AOS, IAS and CAD in FH were then analyzed. Multiple logistic regression analyses showed independent risk factors for formation of atherosclerosis in each artery were: age alone for RAS; age and plasma low-density lipoprotein cholesterol (LDL-C) for AOS; age, LDL-C and high-density lipoprotein cholesterol (HDL-C) for IAS; and HDL-C and diabetes mellitus for CAD. CONCLUSION: In Japanese subjects with heterozygous FH, there are distinct risk factors for the development and progression of atherosclerosis in the renal, iliac, abdominal aorta, and coronary arteries.

Arteriosclerosis↗
PubMed2004

White-coat hypertension contributes to the presence of carotid arteriosclerosis.

It remains unclear whether white-coat hypertension is associated with vascular organ damage (e.g., carotid arteriosclerosis) in the same way sustained hypertension is. We therefore compared the progression of carotid arteriosclerosis among Japanese individuals showing normal blood pressures, sustained hypertension or white-coat hypertension. A total of 30 subjects (mean age, 58 years) with white-coat hypertension, 30 (mean age, 54 years) with untreated sustained hypertension who had no plaque formation in the carotid arteries, and 30 normotensive subjects (mean age, 58 years) were enrolled in this study. The white-coat and sustained hypertensive subjects were matched with respect to their clinical blood pressures, but their ambulatory blood pressures differed. Conversely, white-coat hypertensive and normotensive subjects were matched with respect to ambulatory blood pressures, but their clinical blood pressures differed. Carotid intimal-medial thickness was measured by B-mode ultrasonography, and the cross-sectional area of the common carotid artery was calculated. The three groups were similar with respect to age, sex ratio, height, laboratory data and the incidence of smoking. Body weights and body mass indexes were significantly higher among patients with sustained hypertension than among either normotensive or white-coat hypertensive patients. Intimal-medial thicknesses and carotid cross-sectional areas were similar in patients with white-coat and sustained hypertension and significantly higher than in normotensive subjects. Collectively, these findings suggest that white-coat hypertension contributed to the presence of carotid arteriosclerosis in our subjects in a manner similar to sustained hypertension. Thus, clinical evaluation of white-coat hypertension should be conducted with the potential for target organ damage in mind.

Adult↗
PubMed2006

Correlation between brachial-ankle pulse wave velocity and arterial compliance and cardiovascular risk factors in elderly patients with arteriosclerosis.

The objective of this study was to investigate an association between major cardiovascular risk factors and each of brachial-ankle pulse wave velocity (baPWV), ankle-brachial index (ABI), capacitive arterial compliance (C1), and oscillatory arterial compliance (C2) in elderly patients with arteriosclerosis. We analyzed 160 elderly patients with arteriosclerosis. Vessel wall properties were assessed by baPWV and ABI using a VP-1000 Automatic Arteriosclerosis Measurement System, and C1 and C2 were measured using a DO-2020 Cardiovascular Profiling Instrument. In multiple regression analysis, baPWV was significantly correlated with systolic blood pressure (SBP), mean artery pressure, pulse pressure, diastolic blood pressure (DBP), age, and heart rate (r = 0.670, 0.627, 0.580, 0.523, 0.490, 0.200; p < 0.05), ABI was significantly correlated with pulse pressure, SBP and age (r = -0.250, -0.206, -0.168; p < 0.05), C1 was significantly correlated with pulse pressure, SBP, mean artery pressure, age, DBP and heart rate (r = -0.481, -0.469, -0.363, -0.356, -0.239, -0.188; p < 0.05), and C2 was significantly correlated with age, SBP, pulse pressure, DBP, fasting blood glucose, mean artery pressure and heart rate (r = -0.411, -0.395, -0.383, -0.277, -0.213, -0.183, -0.173; p < 0.05). There were no close correlations between baPWV, ABI, or C1 and fasting blood glucose, total cholesterol, triglycerides, or body mass index. Moreover, there were significant correlations between baPWV and C1 (r = -0.444, p < 0.001), and between baPWV and C2 (r = -0.257, p < 0.01). In conclusion, these findings underscore the efficacy of baPWV and ABI in identifying the vascular damage of the aged.

Age Factors↗