Telomere length and cardiovascular risk in hypertensive patients with left ventricular hypertrophy: the LIFE study

Short telomeres are associated with aging and age-related diseases. Our aim was to determine whether short leukocyte telomere length is associated with risk factors and cardiovascular diseases in a high-risk hypertensive population. We measured leukocyte telomere lengths at recruitment in 1271 subjects with hypertension and left ventricular hypertrophy (LVH) participating in the Lifestyle Interventions and Independence for Elders (LIFE) study. At baseline, short mean telomere length was associated with coronary artery disease in males (odds ratio (OR) 0.61, 95% confidence interval (CI) 0.39-0.95), and transient ischemic attack in females (OR 0.62 95% CI 0.39-0.99). Proportion of short telomeres (shorter than 5?kb) was associated with Framingham risk score (r=0.07, P<0.05), cerebrovascular disease (OR 1.18, 95% CI 1.01-1.15) and type 2 diabetes in men (OR 1.07, 95% CI 1.02-1.11). During follow-up, proportion of short telomeres was associated with combined cardiovascular mortality, stroke or angina pectoris (hazard ratio 1.04, 95% CI 1.01-1.07). Telomere length was not associated with smoking, body mass index, pulse pressure or self-reported use of alcohol. Our data suggest that reduced leukocyte telomere length is associated with cardiovascular risk factors and diseases as well as type 2 diabetes, and is a predictor of cardiovascular disease in elderly patients with hypertension and LVH.     

High red blood cell distribution width is closely associated with risk of carotid artery atherosclerosis in patients with hypertension

BACKGROUND:

A high red blood cell distribution width (RDW) may be associated with adverse outcomes in patients with heart failure and risk of death, and cardiovascular events in people with previous myocardial infarction. Ultrasound detection of carotid plaque helps to identify asymptomatic patients with advanced subclinical atherosclerosis, which can predict risk of cardiovascular death or myocardial infarction. However, the relationship of RDW and carotid artery atherosclerosis in hypertensive people is less certain.

OBJECTIVE:

To evaluate the association between RDW and carotid artery atherosclerosis in people with hypertension.

METHODS:

RDW was determined using a Coulter counter together with white blood cell count in 156 hypertensive inpatients 60 to 85 years of age. Carotid intimal-medial thickness (IMT) and carotid atherosclerotic plaques were identified by ultrasound imaging. Total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglyceride levels were determined using a multichannel analyzer. Systolic and diastolic blood pressures were measured manually.

RESULTS:

The number of patients with carotid artery atherosclerotic plaque, as well as the carotid IMT to inner diameter ratio, were significantly different among the different RDW groups of hypertensive inpatients (P<0.01). With linear regression analysis, increased carotid IMT and higher white blood cell count were identified to be significant and independent contributors to the RDW of hypertensive inpatients (P<0.05).

CONCLUSIONS:

A close relationship between high RDW and IMT, and the incidence of carotid plaque, was identified in 156 hypertensive inpatients.     

Is cardiovascular reactivity associated with atherosclerosis among hypertensives?

Exaggerated cardiovascular reactivity to behavioral challenges among otherwise healthy individuals has been associated with carotid atherosclerosis. We evaluated whether a similar relationship exists among hypertensives, who are at a heightened atherosclerotic risk. Untreated, hypertensive men (n=251; age range, 40 to 70 years; 197 white, 54 black) completed a standardized battery of behavioral challenges while their blood pressure responses to the battery were measured. Mean and maximum carotid intima-media thickness and the occurrence of carotid plaques were subsequently determined using B-mode ultrasonography. Although greater systolic and diastolic responses to the battery were associated with greater mean and maximum intima-media thickness in univariate analyses (P<0.01), only diastolic reactivity showed a unique association with mean and maximum carotid intima-media thickness after multivariate adjustment for age, race, socioeconomic status, smoking and alcohol use, body mass index, lipid profile, glucose and insulin concentrations, and resting blood pressure (P<0.05). Carotid plaque occurrence was associated with greater systolic reactivity (P=0.05) and was marginally associated with greater diastolic reactivity (P=0.07) in univariate analyses, but neither systolic nor diastolic reactivity was uniquely associated with the presence of carotid plaques after multivariate risk-factor adjustment. Among hypertensives, exaggerated behaviorally evoked cardiovascular reactivity appears to be uniquely associated with greater carotid intima-media thickness but not with carotid plaque occurrence.     

Aldosterone and telomere length in white blood cells

BACKGROUND: Aldosterone accelerates cardiovascular aging by mechanisms that generate reactive oxygen species. Telomere length in white blood cells (WBCs) may be a bioindicator that registers the accruing burden of systemic oxidative stress. The aim of the present study was, therefore, to examine the relationship between plasma aldosterone and telomere length in WBCs. METHODS: We studied 75 normotensive and never-treated mildly hypertensive men whose blood was drawn for the measurements of plasma aldosterone concentration and the terminal restriction fragment (TRF) length in WBCs. RESULTS: The slope of the TRF-age relationship in the entire cohort showed a decrease in telomere length of 26 +/- 5 base pairs per year (r = -0.46, p <.001). Age-adjusted TRF length was the longest in the lowest aldosterone quartile (6.74 +/- 0.12 kb) and shortest in the highest aldosterone quartile (6.36 +/- 0.11 kb), with intermediate TRF lengths in the second and third aldosterone quartiles (analysis of variance [ANOVA] trend test, p =.025). In telomeric attrition equivalence, participants in the upper aldosterone quartile were 15 years older than their peers in the lowest quartile. CONCLUSIONS: The inverse relationship between aldosterone and WBC telomere length suggests not only that aldosterone is pro-oxidant but that elevated concentrations of this hormone might be linked to a higher rate of telomere attrition and perhaps increased biological aging in humans.     

Asymmetric development of peripheral atherosclerosis in patients with erectile dysfunction: an ultrasonographic study

Recent literature focused on erectile dysfunction (ED) as a reliable predictive parameter of cardiovascular diseases. ED patients have a higher prevalence of atherosclerotic lesions (increased intima-media thickness and plaques) at carotid site, but data on femoral site are still lacking. Nevertheless, there is accumulating evidence concerning a significant involvement of femoral atherosclerosis in other clinical conditions associated to ED, such as diabetes mellitus and coronary disease. Therefore, we investigated the prevalence of carotid and femoral atherosclerotic lesions and penile peak systolic velocity (PSV) in 238 ED patients by Eco-Colour Doppler ultrasonography (US). We found - irrespective of the presence of cardiovascular risk factors - a significant increase of atherosclerotic lesions in ED group with respect to 52 controls (66.4% versus 36.5%) and a higher prevalence of atherosclerosis at the femoral site (23.1% versus 5.7%), also with respect to the carotid site (8%). Moreover, PSV was significantly lower in ED patients with atherosclerosis compared to those without atherosclerotic lesions (41.9+/-15.3 cm/s versus 55.2+/-17.7 cm/s), and it was particularly low in those with combined carotid and femoral atherosclerosis (34.8+/-13.3 cm/s) and those with isolated carotid atherosclerosis (37.9+/-13.0 cm/s). These data confirm the strong relation between atherosclerosis and ED, an asymmetric development of atherosclerotic lesions in ED patients and suggest to perform an US study of both femoral and carotid district in these subjects.     

The impact of ethnicity and sex on subclinical cardiovascular disease: the Diabetes Heart Study

AIMS/HYPOTHESIS: African-Americans with type 2 diabetes and access to adequate healthcare are at lower risk of clinical coronary artery disease than are white diabetic patients. We evaluated whether ethnic differences in subclinical cardiovascular disease, coronary and carotid artery calcified plaque and carotid artery intima-medial thickness (IMT) were present in members of The Diabetes Heart Study families. SUBJECTS AND METHODS: In a bi-racial cohort of 1,180 individuals from families enriched for members with type 2 diabetes, we calculated coronary and carotid artery calcified plaque using fast-gated helical computed tomography, and measured carotid artery IMT and clinical risk factor profiles. Generalised estimating equations were used to test for an association between measures of subclinical cardiovascular disease and ethnicity and sex. RESULTS: After adjustment for age, ethnicity and kidney function, African-Americans had significantly lower amounts of coronary artery calcified plaque (mean+/-SE) (866+/-158 vs 1,915+/-135, respectively; p=0.0466) and carotid artery calcified plaque (179+/-51 vs 355+/-27, respectively; p=0.0240) relative to whites, despite having increased carotid IMT (0.71+/-0.01 vs 0.67+/-0.004 cm, respectively; p=0.0007), and higher blood pressure, albuminuria and HbA1c. Sex-specific analyses revealed that African-American men had significantly lower coronary and carotid artery calcified atheroma than white men. In women, ethnic differences in calcified carotid artery plaque, but not coronary artery plaque, were observed. CONCLUSIONS/INTERPRETATION: In families enriched for members with type 2 diabetes, African-American men had markedly lower levels of coronary and carotid artery calcified plaque than white men, despite increased carotid artery IMT and conventional risk factors. These findings suggest that susceptibility to subclinical cardiovascular disease differs markedly according to ethnicity and sex.     

Elevated plasma fibrinogen levels in patients with essential hypertension are related to vascular complications.

AIM: We investigated whether or not fibrinogen is related to the cardiovascular risk profile and complications in hypertensive subjects. METHODS: Plasma fibrinogen and laboratory tests including factor VII, homocysteine and microalbuminuria were evaluated in 127 consecutive hypertensive subjects stratified according to cardiovascular risk. Parameters were age, gender, smoking, cholesterol, diabetes, target organ damage: left ventricular hypertrophy (LVH), carotid atherosclerotic complications and retinical vessels. RESULTS: Fibrinogen levels were significantly different between patients according to risk levels (low 290+/-73, n=20, high 342+/-94 mg/dl, n=39, very high risk 350+/-72, n=29, p=0.01), hypertension grade (II-III) and organ damage. Fibrinogen was significantly higher in patients with more severe carotid atherosclerotic lesions and vascular retinal lesions (grades II-III vs 0 and I). Also in patients, matched for age and sex, without and with carotid atherosclerotic lesions, fibrinogen was significantly higher in the latter group. No significant differences were found on the basis of IVS, creatinine and microalbuminuria. In hypertensive patients, fibrinogen directly correlated with age, by multiple linear regression. In hypertensive patients with diabetes, fibrinogen was significantly higher (466+/-176 mg/dL, n=14) than in those hypertensive without diabetes (333+/-87 mg/dL, n=113, p=0.001) and in all patients there was a a significant correlation (r=0.474, p<0.001) between blood glucose and fibrinogen. CONCLUSION: Hyperfibrinogenemia is a marker of vascular damage and could be an important factor contributing to the evolution of the complications.     

Morning blood pressure surge as a destabilizing factor of atherosclerotic plaque: role of ubiquitin-proteasome activity

Whether morning blood pressure surge influences the molecular mechanisms of plaque progression toward instability is not known. Recently, we have demonstrated enhanced activity of the ubiquitin-proteasome system in human plaques and evidenced that it is associated with inflammatory-induced plaque rupture. We evaluated the inflammatory infiltration and ubiquitin-proteasome activity in asymptomatic carotid plaques of hypertensive patients with different patterns of morning blood pressure surge. Plaques were obtained from 32 hypertensive patients without morning blood pressure surge and 28 with morning blood pressure surge enlisted to undergo carotid endarterectomy for extracranial high-grade (>70%) internal carotid artery stenosis. Plaques were analyzed for macrophages, T-lymphocytes, human leukocyte antigen-DR+cells, ubiquitin-proteasome activity, nuclear factor-kappaB, inhibitor kB-beta, tumor necrosis factor-alpha, nitrotyrosine, matrix metalloproteinase-9, and collagen content (immunohistochemistry and ELISA). Compared with plaques obtained from hypertensive patients without morning blood pressure surge, plaques from with morning blood pressure surge had more macrophages, T-lymphocytes, human leukocyte antigen-DR+cells (P<0.001), ubiquitin-proteasome activity, tumor necrosis factor-alpha, nuclear factor-kB (P<0.001), nitrotyrosine, and matrix metalloproteinase-9 (P<0.01), along with a lesser collagen content and IkB-beta levels (P<0.001). Enhanced ubiquitin-proteasome activity in atherosclerotic lesions of patients with morning blood pressure surge is associated with inflammatory-dependent unstable plaque phenotype. These data suggest a potential interplay between morning blood pressure surge and ubiquitin-proteasome activity in atherosclerosis pathophysiology.     

Relationship of circulating biomarkers of inflammation and hemostasis with preclinical atherosclerotic burden in nonsmoking hypercholesterolemic men

BACKGROUND: Relations of mediators of inflammation and hemostasis with preclinical atherosclerosis have been poorly analyzed. The aim of this study was to test potential associations of these blood markers with indicators of cardiovascular risk and atherosclerotic burden in asymptomatic, nonsmoking, hypercholesterolemic men. METHODS: A total of 87 men underwent cardiovascular risk assessment by means of 10-year Framingham risk calculation (median 9%) and atherosclerotic burden evaluation by means of ultrasonographic measurement of common carotid intima-media thickness and assessment of atherosclerotic plaques at three arterial sites (three-site plaques). RESULTS: Of the markers C-reactive protein, tumor necrosis factor-alpha, interleukin-10, factor VIIc, fibrinogen, plasminogen activator inhibitor-activator, soluble intercellular adhesion molecule-1, soluble P-selectin (sP-selectin), and von Willebrand factor, only sP-selectin was positively and independently associated with high Framingham risk score (>9%) (71.7 +/- 3.6 ng/mL, n = 33 v 59.6 +/- 2.8, n = 54; mean +/- SEM; P < .05) and with three-site plaques (75.4 +/- 5.7 ng/mL, n = 14 v 62.0 +/- 2.5, n = 73; P < .05). After adjustment for all of the above markers and for cardiovascular risk factors, odd ratios of having high Framingham risk and three-site plaques were 3.38 (1.43 to 10.21) and 5.23 (1.74 to 23.52) respectively, per 1-standard deviation increase in sP-selectin. CONCLUSIONS: These results confirm that among several hemostasis and inflammation mediators, only sP-selectin blood level was associated with preclinical atherosclerosis. It might confer to sP-selectin measurement a clinical usefulness for detecting and managing high cardiovascular risk in primary prevention.     

人颈动脉粥样硬化斑块组织及外周血白细胞相对端粒长度的检测及相关性分析

目的研究人颈动脉粥样硬化斑块组织与外周血白细胞的DNA相对端粒长度是否有相关性，外周血白细胞能否反映血管组织的相对端粒长度，从而为外周血白细胞端粒长度与动脉粥样硬化的相关性研究提供依据。方法分别取12例颈动脉内膜剥脱术患者的颈动脉内膜斑块组织及外周血，提取DNA，采用实时荧光定量PCR（qRT-PCR）的方法检测相对端粒长度，并进行相关性分析。结果人颈动脉斑块的平均相对端粒长度（Relativetelomerelength，RTL）为0.56士0.12（平均值士标准差），显著高于外周血白细胞的平均相对端粒长度（0.45±0．13）（P=0.038）。多元线性回归方法校正年龄、性别、体重指数、血脂水平、高血压、糖尿病等心血管病危险因素，表明来自同一患者颈动脉斑块组织和外周血白细胞的RTL具有显著的相关性（标化相关系数β=0.87；P=-0.0001）；外周血白细胞RTL与年龄呈负相关（标化相关系数β=0.704，P〈0.001）；颈动脉斑块样本RTL与年龄呈负相关（标化相关系数β=-0.528，P=0.002）。结论人颈动脉斑块组织与外周血白细胞的相对端粒长度具有相关性，外周血白细胞是替代血管组织研究端粒长度与心血管疾病关系的一个重要指标。     

Plasminogen activator inhibitor-1 and carotid intima-media thickening in patients with newly detected primary hypertension

OBJECTIVE: To investigate the correlation between ultrasonographically evaluated intima-media thickness (IMT) of common carotid artery (CCA) and cardiovascular risk factors for subjects with newly detected, uncomplicated and untreated primary hypertension. METHODS: The study population consisted of 200 subjects (123 men and 77 women, aged 46+/-7.5 years). Blood pressure was measured in the clinical setting and by 24 h noninvasive ambulatory monitoring. Fasting levels of blood glucose, plasma lipids and lipoproteins, fibrinogen and plasminogen activator inhibitor (PAI)-1 were measured. Ultrasound examination included measurement of far-wall intima-media complex of CCA and morphologic evaluation of occurrence of plaques in carotid and femoral bifurcations. RESULTS: The prevalence of greater than normal IMT (mean IMT > or =0.80 mm) was 22%. Significant univariate correlations to the dichotomy between normal and greater than normal mean IMT were detected for age, smoking, level of LDL cholesterol, level of PAI-1 and total ultrasonographic score. Multivariate logistic regression analysis confirmed the associations between greater than normal mean IMT and plasma concentrations of LDL cholesterol and PAI-1 as well as total ultrasonographic score. CONCLUSION: Greater than normal IMT of CCA was more strictly related to other cardiovascular risk factors than it was to blood pressure and was strongly associated with the occurrence of atherosclerotic plaques in carotid and femoral arteries. The role of PAI-1 in intima-media thickening that is emerging suggests that fibrinolytic balance is an important determinant of vessel-wall homeostasis in hypertensive patients.     

Telomeres and atherosclerosis

Abstract

In humans and other multicellular organisms that have an extended lifespan, the leading causes of death are atherosclerotic cardiovascular disease and cancer. Experimental and clinical evidence indicates that these age-related disorders are linked through dysregulation of telomere homeostasis. Telomeres are DNA protein structures located at the terminal end of chromosomes and shorten with each cycle of cell replication, thereby reflecting the biological age of an organism. Critically shortened telomeres provoke cellular senescence and apoptosis, impairing the function and viability of a cell. The endothelial cells within atherosclerotic plaques have been shown to display features of cellular senescence. Studies have consistently demonstrated an association between shortened telomere length and coronary artery disease (CAD).Several of the CAD risk factors and particularly type 2 diabetes are linked to telomere shortening and cellular senescence. Our interest in telomere biology was prompted by the high incidence of premature CAD and diabetes in a subset of our population, and the hypothesis that these conditions are premature-ageing syndromes. The assessment of telomere length may serve as a better predictor of cardiovascular risk and mortality than currently available risk markers, and anti-senescence therapy targeting the telomere complex is emerging as a new strategy in the treatment of atherosclerosis. We review the evidence linking telomere biology to atherosclerosis and discuss methods to preserve telomere length.     

Echogenic carotid plaques are associated with aortic arterial stiffness in subjects with subclinical carotid atherosclerosis

A better understanding of the interrelationships between the structure and function of the large arteries would lead to optimize cardiovascular disease prevention strategies. In this study, we investigated the relationships of aortic arterial stiffness assessed by carotid-femoral pulse-wave velocity (PWV), with carotid plaque echogenicity assessed by B-mode ultrasound. We analyzed 561 subjects (without coronary heart disease or stroke) who were volunteers for free health examinations (age, 58.3+/-10.8 years; 32.6% women). Extracranial carotid plaque echogenicity was graded from 1 (plaque appearing black or almost black) to 4 (plaque appearing white or almost white) according to the Gray-Weale classification. Plaques of grades 1 and 2 were defined as echolucent plaques, and plaques of grades 3 and 4 were defined as echogenic plaques. Fifty-one subjects (9.1%) had echolucent carotid plaques, 109 (19.4%) had echogenic plaques, and 401 (71.5%) had no plaques. Subjects with echogenic plaques had higher PWV mean (12.9+/-2.8 m/s) compared with those without plaques (11.1+/-2.3 m/s, P<0.001) and compared with those with echolucent plaques (11.3+/-2.3 m/s, P<0.01). The PWV means in subjects without plaques and those with echolucent plaques were similar and not statistically different (P=0.55). When multivariate adjustment for major known cardiovascular risk factors was performed, these results were not markedly modified. Similar patterns of results were also observed in many subgroups according to age, gender, and hypertensive status. This study provides the first evidence that echogenic but not echolucent carotid plaques are associated with aortic arterial stiffness. This association applies to individuals with normal blood pressure and those with elevated blood pressure. Assessment of the joint and interaction effects of plaque morphology and arterial stiffness on the occurrence of cardiovascular events would permit a better identification of high-risk subjects.     

Presence and severity of carotid atherosclerosis in asymptomatic hypertension patients with left ventricular hypertrophy]

BACKGROUND AND PURPOSE: Arterial hypertension is associated with structural changes in the cardiovascular system. In hypertensives, a relationship has been found between left ventricular hypertrophy and carotid wall thickness, whereas the association with atherosclerotic plaque is less defined. The aim of this study was to evaluate the occurrence and severity of carotid atherosclerosis in hypertensive patients with or without left ventricular hypertrophy (LVH). MATERIALS AND METHODS: We studied 122 hypertensive subjects (62 men and 60 women), aged 60.1 +/- 12.1. Subjects were considered to have left ventricular hypertrophy if their left ventricular mass index (LVMI) at echocardiography exceeded 110 g/m2 in women and 135 g/m2 in men. Carotid intima-media thickness (IMT), external diameter and atherosclerotic plaques were evaluated by high resolution echo-color Doppler. RESULTS: IMT in both common carotid and bifurcation was significantly greater in hypertensives with LVH (p < 0.01), whereas external diameter did not differ significantly in the two groups. Increased presence (73.4 vs 32.8%) and severity (18.7 vs 5.2% for stenosis > 40%) of atherosclerotic plaque were found in the hypertrophic group. A weak but significant association was present among left ventricular mass index, ventricular wall thicknesses and carotid intima-media thickness, and plaque. CONCLUSIONS: In asymptomatic hypertensive subjects, LVH is associated with an increased risk of plaque formation and progression. Vascular hypertrophy may represent a distinct prognostic factor in hypertension and the association of cardiac and vascular hypertrophy may identify a group at high risk of future cardiovascular events.     

Shortening of telomeres in recipients of both autologous and allogeneic hematopoietic stem cell transplantation

Telomere length of peripheral blood mononuclear cells (PBMCs) from 23 autologous HSCT patients ranging from 4 to 61 years old, and 46 allogeneic HSCT recipients from 6 to 52 years old were studied to confirm whether excessive shortening of telomeres is associated with HSCT. After autologous HSCT, telomere length of PBMCs ranged from 6.8 to 12.0 kb. The comparison between transplanted PBMCs and PBMCs after autologous HSCT showed shortening by up to 1.9 kb (mean +/- s.d.: 0.64 +/- 0.50 kb). There was a difference between autologous HSCT patients and normal volunteers in the slopes of regression lines. After allogeneic HSCT, telomere length of PBMCs ranged from 6.8 to 12.0 kb. Telomeres of recipients were up to 2.1 kb (0.60 +/- 0.468 kb) shorter than those of donors. The slope of regression lines for allogeneic HSCT patients and normal volunteers were parallel. Although all patients were transplanted with more than 2.0 x 10(8) cells/kg, telomere length did not correlate with the number of transplanted cells. There was no significant correlation between telomere length and recovery of hematological parameters. However, three patients with an average telomere length of 6.8 kb after HSCT took a longer period to reach the normal hematological state. Taken together, these data suggest that most HSCTs are performed within the biological safety range of telomeres, while the patients who have telomeres shorter than 7.0 kb after HSCT should be observed carefully for long-term hematopoiesis and the occurrence of hematopoietic disorders.     

High prevalence of subclinical atherosclerosis in psoriatic arthritis patients without clinically evident cardiovascular disease or classic atherosclerosis risk factors

OBJECTIVE: To assess the presence of subclinical atherosclerosis in patients with psoriatic arthritis (PsA) without clinically evident atherosclerosis or its complications, and to assess whether demographic or clinical factors affect the development of atherosclerotic disease in a series of patients with PsA attended to in a community hospital. METHODS: Fifty-nine patients with PsA who fulfilled the Moll and Wright criteria were recruited from Hospital Xeral-Calde (Lugo, Spain). Patients seen during the period of recruitment who had classic cardiovascular risk factors or had experienced cardiovascular or cerebrovascular events were excluded. Fifty-nine healthy matched controls were also studied. Carotid artery intima-media thickness (IMT) and carotid plaques were measured in the right common carotid artery. The study was performed using high-resolution B-mode ultrasound. RESULTS: Patients with PsA exhibited greater carotid artery IMT than did matched controls (mean +/- SD 0.699 +/- 0.165 mm versus 0.643 +/- 0.111 mm; P = 0.031; difference of means 0.056; 95% confidence interval 0.005-0.108). Adjusted for age, the carotid IMT was correlated with age at the time of PsA diagnosis (partial correlation coefficient [r] = -0.264, P = 0.04), disease duration (r = 0.264, P = 0.04), total cholesterol (r = 0.233, P = 0.01), and low-density lipoprotein cholesterol (r = 0.243, P = 0.01). CONCLUSION: The present study demonstrates that patients with PsA without cardiovascular risk factors or clinically evident cardiovascular disease have a high prevalence of macrovascular disease in the form of increased carotid artery IMT compared with ethnically matched controls.     

High sensitivity C-reactive protein predicts the development of new carotid artery plaques in older persons

Background and Aim

Previous studies have shown that increased levels of C-reactive protein (CRP) predict cardiovascular events, including stroke, myocardial infarction and death from cardiovascular causes. Previous studies have also shown that increased levels of CRP are strong predictors of the progression of pre-existing carotid artery plaques. However, whether CRP is involved in the development of new plaques, that may or may not be associated with clinical events, in subjects with clean carotid arteries has been scarcely investigated.

Methods and Results

486 “InCHIANTI” Study participants (200 men and 286 women, 72% aged 65 years and over) free from carotid artery plaques at baseline, also underwent carotid artery scan three years later. We tested the association of baseline characteristics, cardiovascular risk factors and inflammatory markers with the development of new carotid artery plaques. Older participants were significantly more likely to develop new plaques. Independent of age, the relative risks of developing new plaques associated with heavy smoking and family history of atherosclerosis were 1.7 (95%CI 1.5–1.9) and 1.9 (95%CI 1.2–3.1), respectively. Participants with high (>3 μg/mL) and moderate (≥1 and ≤3 μg/mL) CRP levels had a relative risk of 2.2 (95%CI 1.9–2.6) and 1.9 (95%CI 1.6–2.3) respectively, when compared with subjects with low (<1 μg/mL) CRP levels. Surprisingly, risk factors such as hypertension, diabetes, dyslipidemia and overweight/obesity were not significant predictors of the development of new carotid artery plaques.

Conclusions

High CRP levels independently predict the development of new plaques in older persons with carotid arteries free from atherosclerotic lesions.     

Increased prevalence of severe subclinical atherosclerotic findings in long-term treated rheumatoid arthritis patients without clinically evident atherosclerotic disease

We conducted the current study to search for subclinical atherosclerosis in patients with rheumatoid arthritis (RA) without clinically evident atherosclerosis or its complications who had been treated for a long duration, and to assess whether demographic or clinical factors affect the development of atherosclerotic disease. Forty-seven white patients fulfilling the 1987 American College of Rheumatology classification criteria for RA were recruited from Hospital Xeral-Calde, Lugo, Spain. Patients were required to have been treated for at least 5 years, including current treatment with 1 or more disease-modifying antirheumatic drugs. Patients with diabetes mellitus, renal insufficiency, hypertension, cardiovascular or cerebrovascular disease, and smokers were excluded. Forty-seven matched controls were also studied. Carotid intima-media wall thickness (IMT) and carotid plaques were measured in the right common carotid artery. The study was performed using high-resolution B-mode ultrasound.Patients had greater carotid IMT (0.779 +/- 0.164 mm) than did controls (0.699 +/- 0.129 mm); (p = 0.010). Sixteen (34%) patients showed carotid plaques compared with only 7 (15%) controls (p = 0.031). There was a positive correlation between the age at the time of study and the carotid IMT. Patients with carotid plaques had significantly greater carotid IMT (0.859 +/- 0.116 mm) than those without plaques (0.739 +/- 0.171 mm) (p = 0.014). Also, RA patients with carotid plaques had a significantly longer disease duration (mean, 21.0 yr) and more extraarticular manifestations (63%) than those without plaques (mean, 12.7 yr and 26%, respectively). Age at the time of the study and disease duration were the best predictive factors for the development of severe morphologic expression of atherosclerotic disease.The present study confirms an increased frequency of severe subclinical atherosclerotic findings in long-term actively treated RA patients from northwest Spain.     

超声检测原发性高血压患者颈动脉粥样硬化

高血压是动脉粥样硬化最常见危险因素之一 ,超声能无创地检测亚临床颈动脉粥样硬化的情况 ,但高血压与超声检测的颈动脉粥样硬化之间的关系尚无一致的认识。采用高分辨力超声仪 ,检测 37名无靶器官受损的原发性高血压患者及 33名对照者的早期颈动脉粥样硬化 ,包括测量内膜中层厚度 (IMT)和斑块。高血压组颈动脉IMT较对照组明显增厚 (0 .82± 0 .0 3mmVS 0 .6 0± 0 .0 2mm ,P <0 .0 0 1) ,其斑块发生率及严重程度亦明显增加 (P <0 .0 0 1) ,而 2组间的血管内径并无明显差别。结果提示高血压患者IMT增厚 ,且斑块发生率及严重程度增加 ,高血压是颈动脉粥样硬化的危险因素 ,同时支持超声能在高血压患者出现靶器官损害的临床表现之前发现颈动脉早期粥样硬化的改变。     

老年脑梗死患者颈动脉粥样硬化斑块稳定性与红细胞分布宽度的关系

目的探讨老年脑梗死患者颈动脉粥样硬化斑块稳定性与红细胞分布宽度(red blood cell distribution width,RDW)之间的相关性。方法选择老年急性脑梗死伴颈动脉粥样硬化斑块患者165例,按颈动脉彩色超声结果,分为稳定斑块组45例和不稳定斑块组120例。收集一般临床资料及心血管病危险因素,测定体重指数、踝臂指数、血脂、糖化血红蛋白、肌酐、白细胞、血红蛋白、RDW、红细胞体积、高敏C反应蛋白(high sensitivity C-reactive pro-tein,hs-CRP)、血浆纤维蛋白原(fibrinogen,Fib)等,并进行组间比较。结果与稳定斑块组比较,不稳定斑块组RDW、hs-CRP、Fib明显增高,差异有统计学意义(P<0.05,P<0.01)。Spearman相关分析显示,颈动脉不稳定斑块与RDW(r=0.244,P<0.01)、hs-CRP(r=0.323,P<0.01)、Fib(r=0.164,P<0.05)呈正相关。logistic回归分析显示,校正性别、年龄及其他传统危险因素后,RDW为颈动脉不稳定斑块的危险因素(OR=2.020,95%CI:1.191～3.426,P<0.01)。结论老年脑梗死患者颈动脉粥样硬化斑块稳定性与RDW相关,RDW增高患者颈动脉粥样硬化斑块破裂的风险增加。