Jessica Gorgui

Hypertension as a Risk Factor for Ischemic Stroke in Women

Women have a high lifetime risk of stroke, and hypertension (HTN) is a major stroke risk factor. We conducted a literature review of studies evaluating blood pressure (BP) and ischemic stroke risk in women; 18 studies were identified. The stroke risk increases in a graded manner with BP levels above 115/75 mm Hg. A 10-mm Hg increase in systolic BP has been associated with a 38% increased stroke risk in women. Women with mild HTN have a higher stroke risk than in men. Increased BP variability also augments the ischemic stroke risk. Antihypertensive therapy has been associated with a significant reduction in stroke incidence. A 10-mm Hg decrease in systolic BP with antihypertensive treatment was associated with a stroke risk reduction of 31%, regardless of the type of antihypertensive agent used. A dose-response relationship has been shown between the magnitude of BP lowering and stroke risk reduction. Discontinuation of antihypertensive treatment may lead to a higher ischemic stroke risk in women than in men. Optimal BP thresholds and targets for women need to be evaluated. Hormone therapy (especially combined therapy) increases the stroke risk, mostly in older hypertensive women compared with younger and normotensive women. Hypertensive disorders of pregnancy also increase stroke risk. Age and ethnicity may modify the magnitude of the effect of HTN on ischemic stroke risk. Strategies tailored to women for the prevention and treatment of HTN are needed to prevent stroke.

Circulating Chemerin Is Associated With Carotid Plaque Instability, Whereas Resistin Is Related to Cerebrovascular Symptomatology

Objective—The rupture of unstable carotid atherosclerotic plaques is one of the main causes of cerebrovascular ischemic events. There is need for circulating markers that can predict plaque instability and risk of stroke. Proinflammatory chemerin, leptin, and resistin, along with anti-inflammatory adiponectin, are adipokines with direct influence on vascular function. We investigated the association of circulating adipokines with carotid plaque instability and cerebrovascular symptomatology. Approach and Results—Neurologically symptomatic and asymptomatic patients (n=165) scheduled for carotid endarterectomy were recruited. Fasting blood samples were collected preoperatively; adiponectin and leptin levels were determined by radioimmunoassay; and chemerin and resistin levels were measured by enzyme-linked immunosorbent assays. The instability of plaque specimens was assessed using gold-standard histological classifications. Chemerin was significantly associated with plaque instability. The fully adjusted model, accounting for age, sex, body mass index, high-sensitivity C-reactive protein, type 2 diabetes mellitus, and circulating adiponectin, leptin, and resistin, yielded an odds ratio of 0.991 (95% confidence interval 0.985–0.998) for plaque instability per unit increase in chemerin. High leptin levels were significantly associated with presence of specific features of plaque instability. In subjects with type 2 diabetes mellitus, resistin levels were significantly elevated in symptomatic when compared with asymptomatic subjects (P=0.001) and increased the risk of cerebrovascular symptomatology (adjusted odds ratio 1.264, 95% confidence interval 1.004–1.594). Conclusions—Low chemerin and high resistin levels were associated with carotid disease severity, suggesting that these adipokines may act as potential markers for plaque instability and stroke risk. Future studies are needed to assess causation between circulating adipokines and plaque instability.

Circulating adiponectin levels in relation to carotid atherosclerotic plaque presence, ischemic stroke risk, and mortality: A systematic review and meta-analyses

BACKGROUND Low circulating levels of adiponectin, an anti-inflammatory and vasculoprotective adipokine, are associated with obesity, type 2 diabetes, and atherosclerotic disease. Presence of unstable plaques in the carotid artery is a known etiological factor causing ischemic strokes. Herein, we systematically reviewed the association between circulating adiponectin and progression of carotid atherosclerotic disease, particularly evaluating the occurrence of (1) carotid atherosclerotic plaques, (2) ischemic stroke, and (3) mortality in subjects who suffered a previous ischemic stroke. METHODS Medline, Embase, Biosis, Scopus, Web of Science, and Pubmed were searched for published studies and conference abstracts. The effect size and 95% confidence intervals (CIs) of the individual studies were pooled using fixed-effect or random-effect models. The quality of the eligible studies was evaluated using the Newcastle-Ottawa quality assessment scale. Sensitivity, subgroup, and meta-regression analyses were performed to address the impact of various risk factors on the association between adiponectin and ischemic stroke risk. RESULTS Twelve studies fulfilled the inclusion criteria for 3 independent meta-analyses. The association of increasing circulating adiponectin levels (5μg/mL-increment) with presence of carotid plaque was not conclusive (n=327; OR: 1.07; 95% CI: 0.85-1.35; 2 studies), whereas high adiponectin levels showed a significant 8% increase in risk of ischemic stroke (n=13,683; 7 studies), with a more sizable association observed among men compared to women. HDL was observed to have a marginal effect on the association between adiponectin and ischemic stroke, while other evaluated parameters were not found to be effect modifiers. A non-significant association of adiponectin with mortality was yielded (n=663; OR: 2.58; 95% CI: 0.69-9.62; 3 studies). Although no publication bias was evident, there was significant between-study heterogeneity in most analyses. CONCLUSION It appears that the direction of the relationship between adiponectin and carotid atherosclerotic plaque presence is dependent on the duration, severity, and nature of the underlying disease, while increased adiponectin levels were associated with an increase in risk for ischemic stroke. Lastly, the results from the mortality meta-analysis remain inconclusive. Future properly designed studies are necessary to further elucidate the role of adiponectin on atherosclerotic plaque development, and its related outcomes.

Carotid Endarterectomy Improves Peripheral but not Central Arterial Stiffness

OBJECTIVE Carotid endarterectomy (CEA) reduces the risk of cerebrovascular events due to the presence of atherosclerotic plaque in the internal carotid artery. Arterial stiffness is an indicator of cardiovascular risk and strongly associates with the development of atherosclerosis. This study aims to assess the short-term effect of CEA on arterial stiffness and haemodynamics. DESIGN Prospective observational study. METHODS Measurements of arterial stiffness and haemodynamics, including carotid-femoral pulse wave velocity (cfPWV), carotid-radial PWV (crPWV), augmentation pressure, augmentation index, subendocardial viability ratio, central pressures and pulse pressure amplification, were performed pre- and 6 weeks post-CEA on both surgical and non-surgical sides. RESULTS Fifty-nine patients completed the study (n = 46 men, age 68.9 ± 10.1 years). crPWV was decreased after CEA on the surgical (P = 0.01) and non-surgical side (P = 0.0008), AIx75 tended to decrease only on the surgical side (P = 0.06). cfPWV did not change significantly on either side. CONCLUSION We assessed, for the first time, the short-term effect of CEA on arterial stiffness and haemodynamics. CEA improved peripheral but not central arterial stiffness. This study provides evidence for significant changes in certain arterial stiffness and haemodynamic parameters. Longer-term follow-up will assess whether these changes are sustained and whether CEA is associated with further haemodynamic benefits.

013 Differences in Arterial Stiffness Pre- and Post-Carotid Endarterectomy: Does History of Cardiovascular Disease Matter?

very rare complication of coronary artery bypass grafting (CABG). Our objective was to determine the clinical features and management options for aortocoronary SVGAs in an effort to develop an approach to identifying and managing patients with this complication. METHODS/RESULTS: We performed a systematic review of published cases in MEDLINE and SCOPUS between 1966 and December 2010. Standardized data were extracted by two independent reviewers. We identified 209 reported cases of aortocoronary SVGAs in 168 articles. Patients were predominantly male (86.6%) and had a mean age of 65.3 10.6 years. SVGAs were identified on average 13.1 6.0 years after CABG with a mean diameter of 60.7 31.8 mm. Mechanical complications were reported in 34.0% of cases at presentation. Though most patients presented with chest pain (43.5%), SVGAs were commonly identified incidentally on imaging (35.4%). The most commonly employed investigations were cardiac catheterization (66.5%) and computed tomography (60.3%). In cases in which serial follow-up were described, nearly all aneurysms continued to increase in size. Surgical management was reported in 58.4% of cases, percutaneous intervention in 15.8%, and conservative therapy in 20.1% with short-term mortality rates of 13.9%, 6.1%, and 23.8%, respectively. CONCLUSIONS: SVGAs represent a rare but increasingly recognized complication of CABG most often seen remotely from the surgery. A large subset of patients with SVGAs are asymptomatic. It is hypothesized that the aneurysms continue to grow over time albeit at variable rates. Though further study is required, both surgical and percutaneous interventions appear to have favourable outcomes. In select patients, percutaneous management offers an alternative to repeat sternotomy.