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Numerous vascular risk factors and vascular diseases contribute to cognitive impairment and dementia. Many studies and registries show an association of atrial fibrillation (AF) with cognitive impairment, cognitive decline, and dementia. This is true for vascular dementia and Alzheimer's disease. The assumed multifactorial mechanisms include ischemic stroke, both apparent and silent, cerebral microinfarcts, cerebral hemorrhage, and reduced cerebral blood flow. A number of retrospective observational and prospective studies support that anticoagulation in patients with AF may reduce the risk of cognitive decline and dementia. This holds for both vitamin K antagonists (e.g., warfarin) and direct oral anticoagulants. However, it still remains unproven if anticoagulation reduces cognitive decline and dementia in AF patients based on randomized trials. [ABSTRACT FROM AUTHOR]

We assessed the association of herpes zoster (HZ) with stroke/transient ischaemic attack (TIA) in the general population according to age with controlling risk factors for stroke, using a nationwide representative cohort. The study was based on a prospective dynamic cohort consisting of 1 million Koreans representing all age groups, genders and geographical areas in the Korea Health Insurance Database. New events of stroke/TIA and HZ were identified using the diagnostic codes in the International Classification of Diseases, tenth revision. The risk for stroke/TIA after HZ was compared with HZ-free stroke/TIA individuals according to age group. A total of 766 179 adults were followed up for 11 years from 2003. The incidence of the first-diagnosed HZ cases was 9.40 per 1000 person-years, and that of the first-diagnosed stroke/TIA cases was 9.77 per 1000 person-years. The risk for stroke/TIA was higher in patients who had previous HZ episodes than in those who had never experienced HZ (incidence rate ratio 1.90; 95% CI 1.85–1.95). In addition, this risk persisted for several years after HZ. The risk of stroke/TIA after HZ gradually decreased with age; adjusted hazard ratio (HR) 2.04 in 18- to 30-year-olds, HR 1.74 in 30- to 40-year-olds, HR 1.43 in 40- to 50-year-olds, HR 1.23 in 50- to 60-year-olds, HR 1.24 in 60- to 70-year-olds, and HR 1.29 in those >70 years old, after controlling risk factors for stroke/TIA. Our findings provide evidence that HZ carries an increased risk of stroke or TIA and that the effect of HZ on stroke decreases with increasing age. [ABSTRACT FROM AUTHOR]

Background Brain lesions on diffusion-weighted imaging (DWI) are frequently found after carotid artery stenting (CAS), but their clinical relevance remains unclear. Objectives This study sought to investigate whether periprocedural ischemic DWI lesions after CAS or carotid endarterectomy (CEA) are associated with an increased risk of recurrent cerebrovascular events. Methods In the magnetic resonance imaging (MRI) substudy of ICSS (International Carotid Stenting Study), 231 patients with symptomatic carotid stenosis were randomized to undergo CAS (n = 124) or CEA (n = 107). MRIs were performed 1 to 7 days before and 1 to 3 days after treatment. The primary outcome event was stroke or transient ischemic attack in any territory occurring between the post-treatment MRI and the end of follow-up. Time to occurrence of the primary outcome event was compared between patients with (DWI+) and without (DWI–) new DWI lesions on the post-treatment scan in the CAS and CEA groups separately. Results Median time of follow-up was 4.1 years (interquartile range: 3.0 to 5.2). In the CAS group, recurrent stroke or transient ischemic attack occurred more often among DWI+ patients (12 of 62) than among DWI– patients (6 of 62), with a cumulative 5-year incidence of 22.8% (standard error [SE]: 7.1%) and 8.8% (SE: 3.8%), respectively (unadjusted hazard ratio: 2.85; 95% confidence interval: 1.05 to 7.72; p = 0.04). In DWI+ and DWI– patients, 8 and 2 events, respectively, occurred within 6 months after treatment. In the CEA group, there was no difference in recurrent cerebrovascular events between DWI+ and DWI– patients. Conclusions Ischemic brain lesions discovered on DWI after CAS seem to be a marker of increased risk for recurrent cerebrovascular events. Patients with periprocedural DWI lesions might benefit from more aggressive and prolonged antiplatelet therapy after CAS. (A Randomised Comparison of the Risks, Benefits and Cost Effectiveness of Primary Carotid Stenting With Carotid Endarterectomy: International Carotid Stenting Study; ISRCTN25337470 ) [ABSTRACT FROM AUTHOR]

Background Chronic kidney disease is an independent predictor of perioperative cardiovascular morbidity and mortality. We analysed the preoperative estimated glomerular filtration rate (eGFR) as a risk factor for perioperative major adverse cardiovascular and cerebrovascular events (MACCE) in non-cardiac surgery. Methods In a post hoc analysis of the ANESCARDIOCAT database, patients were classified into six stages of eGFR calculated with the abbreviated Modification of Diet in Renal Disease Study and the Chronic Kidney Disease Epidemiology Collaboration equations: >90 (1), 60–89.9 (2), 45–59.9 (3a), 30–44.9 (3b), 15–29.9 (4), and <15 (5) ml min−1 1.73 m−2. We analysed differences in MACCE, length of hospital stay, and all-cause mortality between eGFR stages. Results The eGFR was available in 2323 patients. Perioperative MACCE occurred in 4.5% of patients and cardiac-related mortality was 0.5%. Five hundred and forty-three (23.4%) patients had an eGFR of <60 ml min−1 1.73 m−2 and 127 (5.4%) had an eGFR below 45 ml min−1 1.73 m−2. Logistic regression analysis showed that MACCE increased with eGFR impairment (P<0.001), with a marked increase from stage 3b onwards (odds ratio 1.8 vs 3.9 in 3a and 3b, respectively, P=0.047). All-cause mortality was not related to eGFR (P=0.071), but increased substantially between stages 3b and 4. The length of stay correlated with eGFR (P<0.001). Conclusions Perioperative MACCE increase with declining eGFR, primarily when <45 ml min−1 1.73 m−2. We recommend the use of preoperative eGFR for cardiovascular risk assessment. [ABSTRACT FROM PUBLISHER]

Background Major adverse cardiac and cerebrovascular events (MACCE) represent the most common cause of serious perioperative morbidity and mortality. Our aim was to identify risk factors for MACCE in a broad surgical population with intermediate-to-high surgery-specific risk and to build and validate a model to predict the risk of MACCE. Methods A prospective, multicentre study of patients undergoing surgical procedures under general or regional anaesthesia in 23 hospitals. The main outcome was the occurrence of at least one perioperative MACCE, defined as any of the following complications from admittance to discharge: cardiac death, cerebrovascular death, non-fatal cardiac arrest, acute myocardial infarction, congestive heart failure, new cardiac arrhythmia, angina, or stroke. The MACCE predictive index was based on β-coefficients and validated in an external data set. Results Of 3387 patients recruited, 146 (4.3%) developed at least one MACCE. The regression model identified seven independent risk factors for MACCE: history of coronary artery disease, history of chronic congestive heart failure, chronic kidney disease, history of cerebrovascular disease, preoperative abnormal ECG, intraoperative hypotension, and blood transfusion. The area under the receiver-operating characteristic curve was 75.9% (95% confidence interval, 71.2–80.6%). Conclusions The risk score based on seven objective and easily assessed factors can accurately predict MACCE occurrence after non-cardiac surgery in a population at intermediate-to-high surgery-specific risk. [ABSTRACT FROM AUTHOR]

Objectives: We aimed to define the relationship between cerebral atherosclerosis and stroke after coronary artery bypass grafting (CABG). Background: Although cerebral atherosclerosis may play a crucial role in the advent of post-CABG stroke, only extracranial carotid artery disease has been extensively studied, and the effects of atherosclerosis on the mechanisms underlying post-CABG stroke remain unclear. Methods: Pre-operative magnetic resonance angiography was performed on 1,367 consecutive CABG patients to assess intracranial and extracranial cerebral atherosclerosis. Disease severity was evaluated by atherosclerosis score, as determined by the number of steno-occlusions of cerebral arteries and the degree thereof. Post-CABG strokes (within 14 days) were classified as atherosclerotic (strokes attributable to pre-defined atherosclerosis) or other (strokes caused by other mechanisms). Associations between post-CABG stroke and each type of atherosclerotic disease (extracranial carotid artery disease, intracranial, extracranial, or extracranial and/or intracranial cerebral atherosclerosis), differentiated according to the involved arteries, were analyzed. Results: Stroke occurred in 33 patients, and the atherosclerosis score was independently associated with stroke development (odds ratio: 1.35; 95% confidence interval: 1.16 to 1.56). Atherosclerotic stroke was defined in 15 (45%), and constituted >40% of both immediate (within 24 h) and delayed strokes. Intracranial, extracranial, and extracranial and/or intracranial cerebral atherosclerosis were significantly associated with stroke. Conclusions: Cerebral atherosclerosis was closely related to the occurrence of post-CABG stroke, being both an independent risk factor for and the cause of a significant proportion of strokes. Pre-operative evaluation of intracranial and extracranial cerebral arteries, apart from the extracranial carotid artery, may be useful to predict the likelihood of post-CABG stroke. [ABSTRACT FROM AUTHOR]

Objectives: This study tried to determine the association between left atrial (LA) fibrosis, detected using delayed-enhanced magnetic resonance imaging (DE-MRI), and the CHADS2 score (point system based on individual clinical risk factors including congestive heart failure, hypertension, age, diabetes, and prior stroke) variables, specifically stroke. Background: In patients with atrial fibrillation (AF), conventional markers for the risk of stroke base their higher predictive effect on clinical features, particularly previous stroke history, and not individual LA pathophysiological properties. We aimed to determine the association between LA fibrosis, detected using DE-MRI, and the CHADS2 score variables, specifically stroke. Methods: Patients with AF who presented to the AF clinic and received a DE-MRI of the LA were evaluated. Their risk factor profiles, including a CHADS2 score, were catalogued. The degree of LA fibrosis was determined as a percentage of the LA area. Any history of previous strokes, warfarin use, or cerebrovascular disease was recorded. Results: A total of 387 patients, having a mean age of 65 ± 12 years, 36.8% female, were included in this study. A history of previous stroke was present in 36 (9.3%) patients. Those patients with previous strokes had a significantly higher percentage of LA fibrosis (24.4 ± 12.4% vs. 16.2 ± 9.9%, p < 0.01). A larger amount of LA fibrosis was also seen in those patients with a higher CHADS2 score (≥2: 18.7 ± 11.4 vs. <2: 14.7 ± 9.2, p < 0.01). A logistic regression analysis of all variables except strokes (CHAD score) demonstrated that LA fibrosis independently predicted cerebrovascular events (p = 0.002) and significantly increased the predictive performance of the score (area under the curve = 0.77). Conclusions: Our preliminary, multicenter results suggest DE-MRI–based detection of LA fibrosis is independently associated with prior history of strokes. We propose that the amount of DE-MRI–determined LA fibrosis could represent a marker for stroke and a possible therapeutic target with potential applicability for clinical treatment for patients with AF. [Copyright &y& Elsevier]

Abstract: Objectives: The 21st century has an increasing elderly population at risk of cerebrovascular disease (CVD). Efficient care for recovering functional status is emphasized among policy makers. We investigated whether rehabilitation and its early initiation provided for CVD patients produced functional recovery in acute care hospitals. Methods: Using a Japanese administrative database during a 4-month interval from 2004 to 2008 in patients ages ≥15 years, we measured the demographics, consciousness level at admission, comorbidities, complications, procedures, ventilation administration, initiation day of rehabilitation, and hospital characteristics. Outcomes included total charges (TC) and functional status measured by the Barthel index (BI). Multivariate analysis measured the impact of rehabilitation and its early initiation on outcomes. To reduce the selection bias of rehabilitation and the ecological fallacy, we used propensity score matching and the linear mixed model. Results: Excluding 488 deceased patients, we analyzed 45,014 CVD patients. Rehabilitation at a generalized unit produced greater BI improvement than no rehabilitation or at intensive care units. A longer hospitalization, but not a 1-day delay of rehabilitation initiation, resulted in less BI improvement and more TC. A higher patient volume and academic hospitals were associated with more TC but not with BI improvement. Conclusions: Rehabilitation, but not the timing of rehabilitation, might accompany functional recovery in acute care hospitals. Because the hospital mix or medical units can explain the variation in the quality of rehabilitation, policy makers, along with monitoring unnecessary long hospitalizations, should encourage a referral policy for rehabilitation-intensive facilities and develop effective rehabilitation using technology to optimize functional outcomes. [Copyright &y& Elsevier]

Experimental studies suggest that oxidative stress and systemic inflammation are involved in the pathogenesis of ischemic stroke. Consuming a diet with a high total antioxidant capacity IT AC) has been related to reduced inflammation and increased circulating antioxidants in cross-sectional and randomized intervention studies. This study investigates the relation between dietary TAC and risk of ischemic and hemorrhagic stroke in 41,620 men and women not previously diagnosed with stroke or myocardial infarction, representing the Italian segment of the European Prospective Investigation into Cancer and Nutrition. Controlling for potential confounders, a diet rich in TAC was associated with a reduction in HR for all types of stroke, but this association was only marginally significant (P-trend = 0.0541. When only ischemic stroke cases were considered, data suggest a stronger inverse association with dietary TAC, with HR = 0.41 (95% Cl = 0.23-0.74). Regarding single antioxidants, data from subanalyses on stroke types suggest that vitamin C is significantly associated with a decreased risk of ischemic stroke [HR = 0.58 (95% Cl = 0.34-0.99)], whereas vitamin E was associated with increased HR of hemorrhagic stroke in the highest tertile of intake [HR = 2.94 (95% Cl = 1.13-7.62(1. In conclusion, our findings suggest that antioxidants may play a role in reducing the risk of cerebral infarction but not hemorrhagic stroke. However, a high intake of vitamin E could be positively associated to the risk of brain hemorrhagic events; therefore, more focused investigations about this observation are needed. [ABSTRACT FROM AUTHOR]

The prevalence of atrial fibrillation (AF) is related to age and is projected to rise exponentially as the population ages and the prevalence of cardiovascular risk factors increases. The risk of ischemic stroke is significantly increased in AF patients, and there is evidence of a graded increased risk of stroke associated with advancing age. Oral anticoagulation (OAC) is far more effective than antiplatelet agents at reducing stroke risk in patients with AF. Therefore, increasing numbers of elderly patients are candidates for, and could benefit from, the use of anticoagulants. However, elderly people with AF are less likely to receive OAC therapy. This is mainly due to concerns about a higher risk of OAC-associated hemorrhage in the elderly population. Until recently, older patients were under-represented in randomized controlled trials of OAC versus placebo or antiplatelet therapy, and therefore the evidence base for the value of OAC in the elderly population was not known. However, analyses of the available trial data indicate that the expected net clinical benefit of warfarin therapy is highest among patients with the highest untreated risk for stroke, which includes the oldest age category. An important caveat with warfarin treatment is maintenance of a therapeutic international normalized ratio, regardless of the age of the patient, where time in therapeutic range should be ≥65%. Therefore, age alone should not prevent prescription of OAC in elderly patients, given an appropriate stroke and bleeding risk stratification. [ABSTRACT FROM AUTHOR]

Objectives: The aim of this study was to understand the initial mechanism of arterial thrombus formation induced by vulnerable human atherosclerotic plaques to re-assess and improve current antithrombotic strategies. Background: Rupture of atherosclerotic plaques causes arterial thrombus formation that might lead to myocardial infarction and ischemic stroke. Atherothrombosis is considered as an inseparable tangle of platelet activation and coagulation processes, involving plaque components such as tissue factor (TF) and collagen as well as blood-borne TF and coagulation factor XIIa (FXIIa). A combination of anticoagulants and antiplatelet agents is the present treatment. Methods: Human atheromatous plaque material was exposed to blood or blood components at physiological calcium/magnesium concentration. Platelet aggregation and coagulation were measured under static and arterial flow conditions by state-of-the-art microscopic and physiological techniques. Plaque TF, plaque collagen, FXIIa, and platelet glycoprotein VI (GPVI) were specifically inhibited. Results: Plaques induced thrombus formation by 2 discrete steps. The rapid first phase of GPVI-mediated platelet adhesion and aggregation onto plaque collagen occurred within 1 min. The second phase of coagulation started after a delay of >3 min with the formation of thrombin and fibrin, and was driven entirely by plaque TF. Coagulation occurred only in flow niches provided by platelet aggregates, with no evidence for a role of blood-borne TF and FXIIa. Inhibition of GPVI but not plaque TF inhibited plaque-induced thrombus formation. Conclusions: The major thrombogenic plaque components—collagen and TF—induce platelet activation and coagulation, respectively, in 2 consecutive steps. Targeting specifically the first step is crucial and might be sufficient to inhibit atherothrombus formation. [Copyright &y& Elsevier]

Flavonols are strong antioxidants in plant foods and tea is a major dietary source. There is evidence from prospective cohort studies that tea and flavonols are inversely related to stroke incidence. We conducted a metaanalysis of prospective cohort studies to assess quantitatively the strength of the association between flavonol intake and stroke incidence. Prospective cohort studies with data from individuals free of cardiovascular diseases (CVD) or stroke at baseline were included in the metaanalysis. Persons were followed for between 6 and 28 y. Data from 6 cohorts involving 111067 persons with at least 2155 nonfatal and fatal cases were pooled. A random effects model was used. In all studies included, adjustments were made for major CVD risk factors except for 2 that did not adjust for alcohol and energy intake. A high intake of flavonols compared with a low intake was inversely associated with nonfatal and fatal stroke with a pooled relative risk of 0.80 (95% Cl: 0.65, 0.98). Visual inspection of Begg's funnel plot and Egger's test (P = 0.01) indicated potential publication bias. We conclude that flavonols may reduce stroke risk. [ABSTRACT FROM AUTHOR]

: ObjectivesThe purpose of the study was to assess the mechanism responsible for increased stroke risk in patients with atrial septal aneurysm (SA) and patent foramen ovale (PFO), and to determine the efficacy of medical therapy for preventing stroke recurrence or death.: BackgroundAtrial septal aneurysm and PFO are associated with stroke. However, the mechanism for this association is undefined, and the efficacy of medical therapy has not been investigated in a randomized fashion.: MethodsThe Patent foramen ovale In Cryptogenic Stroke Study (PICSS) evaluated transesophageal echocardiography findings in patients enrolled in the Warfarin-Aspirin Recurrent Stroke Study, a randomized double-blind trial to evaluate the efficacy of warfarin compared with aspirin.: ResultsLarge PFO and prominent eustachian valve (EV) or right atrial (RA) filamentous strands were found more frequently in patients with SA compared with those without SA (37.7% vs. 10.9%, p < 0.001 and 59.4% vs. 43.1%, p = 0.02). Patients with SA and PFO had no significant difference in time to recurrent stroke or death compared with those having neither (hazard ratio [HR] 1.08, 95% confidence interval [CI] 0.49 to 2.38, p = 0.84; two-year event rates 15.9% vs. 14.5%). Patients with SA, PFO, and RA anatomy predisposing to paradoxical embolization also had no difference compared with those without these findings (HR 1.22, 95% CI 0.43 to 3.47, p = 0.71; two-year event rates 18.2% vs. 14.2%). There was no significant difference in time to recurrent stroke or death between the patients treated with warfarin or aspirin (HR 1.00, 95% CI 0.22 to 4.47, p = 1.0; two-year event rates 16.0% vs. 15.8%).: ConclusionsAtrial septal aneurysm is associated with the presence of large PFO and prominent EV or RA filamentous strands. On medical therapy, patients with SA and PFO did not experience increased risk of adverse events, and there was no difference between treatment results for warfarin and for aspirin. [Copyright &y& Elsevier]

Examines clinical and biological evidence which support the hypothesis that consumption of dairy products may be associated with reduced blood pressure and risk of stroke. Number of United States citizens that die of stroke each year; Identification of stroke risk factors; Related studies on dairy foods and stroke; Cardiovascular effects of dairy foods and their nutrients.

Atherosclerosis is a multifocal, smoldering, immunoinflammatory disease of medium-sized and large arteries fuelled by lipids. Endothelial cells, leukocytes, and intimal smooth muscle cells are the major players in the development of this disease. The most devastating consequences of atherosclerosis, such as heart attack and stroke, are caused by superimposed thrombosis. Therefore, the vital question is not why atherosclerosis develops but rather why atherosclerosis, after years of indolent growth, suddenly becomes complicated with luminal thrombosis. If thrombosis-prone plaques could be detected and thrombosis averted, atherosclerosis would be a much more benign disease. Approximately 76% of all fatal coronary thrombi are precipitated by plaque rupture. Plaque rupture is a more frequent cause of coronary thrombosis in men (∼80%) than in women (∼60%). Ruptured plaques are characterized by a large lipid-rich core, a thin fibrous cap that contains few smooth muscle cells and many macrophages, angiogenesis, adventitial inflammation, and outward remodeling. Plaque rupture is the most common cause of coronary thrombosis. Ruptured plaques and, by inference, rupture-prone plaques have characteristic pathoanatomical features that might be useful for their detection in vivo by imaging. This article describes the pathogenesis of atherosclerosis, how it begets thrombosis, and the possibility to detect thrombosis-prone plaques and prevent heart attack. [Copyright &y& Elsevier]