BACKGROUND AND PURPOSE—The CHA2DS2-VASc score aims to improve risk stratification of ischemic stroke among patients with atrial fibrillation to identify those who can safely forego oral ...anticoagulation. Oral anticoagulation treatment guidelines remain uncertain for CHA2DS2-VASc score of 1. We conducted a systematic review and meta-analysis of the risk of ischemic stroke for patients with atrial fibrillation and CHA2DS2-VASc score of 0, 1, or 2 not treated with oral anticoagulation.
METHODS—We searched MEDLINE, Embase, PubMed, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews, and Web of Science from the start of the database up until April 15, 2015. We included studies that stratified the risk of ischemic stroke by CHA2DS2-VASc score for patients with nonvalvular atrial fibrillation. We estimated the summary annual rate of ischemic stroke using random effects meta-analyses and compared the estimated stroke rates with published net-benefit thresholds for initiating anticoagulants.
RESULTS—1162 abstracts were retrieved, of which 10 met all inclusion criteria for the study. There was substantial heterogeneity among studies. The summary estimate for the annual risk of ischemic stroke was 1.61% (95% confidence interval 0%–3.23%) for CHA2DS2-VASc score of 1, meeting the theoretical threshold for using novel oral anticoagulants (0.9%), but below the threshold for warfarin (1.7%). The summary incident risk of ischemic stroke was 0.68% (95% confidence interval 0.12%–1.23%) for CHA2DS2-VASc score of 0 and 2.49% (95% confidence interval 1.16%–3.83%) for CHA2DS2-VASc score of 2.
CONCLUSIONS—Our meta-analysis of ischemic stroke risk in atrial fibrillation patients suggests that those with CHA2DS2-VASc score of 1 may be considered for a novel oral anticoagulant, but because of high heterogeneity, the decision should be based on individual patient characteristics.
Graphical Abstract
Graphical Abstract
Proportions represent the incidence of atrial fibrillation diagnostic yields with a sequential increase in the intensity of cardiac rhythm monitoring based on ...Sposato et al..6 Risk: recurrent ischaemic stroke risk. §Five-fold higher than prolonged cardiac monitoring–detected atrial fibrillation. †More data are needed to characterize the stroke risk of atrial fibrillation found on 24–48 h Holter. *Five-fold lower than 12-lead electrocardiogram-diagnosed atrial fibrillation. AF, atrial fibrillation; AFDAS, atrial fibrillation detected after stroke; ECG, electrocardiogram; PCM, prolonged cardiac monitoring; STM, short-term monitoring.
Poststroke atrial fibrillation (AF) represents up to 1 of 4 overall AF cases in acute ischemic stroke. Current guidelines recommend oral anticoagulation for every ischemic stroke patient in whom AF ...is diagnosed. However, in some cases, AF detected after acute ischemic stroke may be short-lasting and perhaps a nonrecurrent autonomic and inflammatory epiphenomena of stroke. The autonomic regulation of cardiac rhythm constitutes an integrated relay system. The highest level of control is exerted by the cerebral cortex, particularly the insula. The onset of AF may be associated with an imbalance of sympathetic and parasympathetic activity, a common consequence of insular infarctions. This autonomic imbalance and an interruption in the cerebral regulation of the intrinsic cardiac autonomic system constitute the most likely mechanisms responsible for the autonomic pathway. The role of inflammation in the genesis of AF within the first few days after ischemic stroke may occur through inflammatory mediators stimulating the intrinsic autonomic system and by direct damage to atrial myocardium. To what extent poststroke AF is the cause or a consequence remains uncertain.
After ischemic stroke, there is a significant burden of cardiovascular complications, both in the acute and chronic phase. Severe adverse cardiac events occur in 10% to 20% of patients within the ...first few days after stroke and comprise a continuum of cardiac changes ranging from acute myocardial injury and coronary syndromes to heart failure or arrhythmia. Recently, the term
stroke–heart syndrome
was introduced to provide an integrated conceptual framework that summarizes neurocardiogenic mechanisms that lead to these cardiac events after stroke. New findings from experimental and clinical studies have further refined our understanding of the clinical manifestations, pathophysiology, and potential long‐term consequences of the stroke–heart syndrome. Local cerebral and systemic mediators, which mainly involve autonomic dysfunction and increased inflammation, may lead to altered cardiomyocyte metabolism, dysregulation of (tissue‐resident) leukocyte populations, and (micro‐) vascular changes. However, at the individual patient level, it remains challenging to differentiate between comorbid cardiovascular conditions and stroke‐induced heart injury. Therefore, further research activities led by joint teams of basic and clinical researchers with backgrounds in both cardiology and neurology are needed to identify the most relevant therapeutic targets that can be tested in clinical trials.
Insular cortex (IC) ischemic strokes are associated with increased risk of cardiac arrhythmias. We have previously hypothesized that the anatomical substrate for post-stroke neurogenic arrhythmias ...comprises stroke-induced left atrium (LA) coronary microvascular endothelial dysfunction (CMED), and myocardial inflammatory infiltration (MII) leading to myocardial fibrosis. We investigated whether selectively induced IC ischemic stroke in rats results in histopathological changes in the LA.
Insular ischemic stroke was induced in 6-month old male Wistar rats via unilateral stereotaxic injection of endothelin-1 into the left or right IC. The control group consisted of rats injected with saline. We histologically examined the LA 28 days after stroke for CMED, MII, and fibrosis. We performed linear regression analyses to assess correlation between the 3 histopathological outcomes. We compared these findings in the distal LA and the LA-pulmonary vein border (LA-PV border), a region of rich autonomic innervation.
Right and left IC stroke led to CMED, MII, and fibrosis in the LA. MII was significantly correlated with CMED and fibrosis. The LA-PV border had significantly greater MII and fibrosis than the distal LA. There were no differences in coronary microvascular and myocardial changes between left and right IC strokes.
Left and right insular ischemic strokes resulted in CMED, MII, and fibrosis, the pathological hallmark of arrhythmogenic LA tissue. Since these changes were greater within the LA-PV border than in the distal LA tissue, the role of preganglionic fibers at the ganglionated plexi as part of neurogenic arrhythmogenesis warrants further investigation.
•Ischemic stroke induced left atrial endothelial dysfunction, inflammation and fibrosis.•Changes were more severe in the periphery of pulmonary vein ganglionated plexi.•There was no evidence of myocardial necrosis, suggesting non-ischemic mechanisms.•There was no increase of troponin T, B-Natriuretic peptide or left atrial enlargement.•Local dysautonomic and inflammatory mechanisms are possible culprits.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
OBJECTIVEPoststroke cardiac complications are common. It is unknown whether the reason is shared risk factors and preexisting heart disease or stroke-associated myocardial and coronary injury. We ...tested the hypothesis that first-ever ischemic stroke is associated with increased risk of incident cardiovascular complications in patients without known preexisting cardiac comorbid conditions.
METHODSThis population-based cohort study included residents in Ontario between 2002 and 2012 who were ≥66 years of age without known cardiovascular disease. We compared the incident risk of major adverse cardiovascular events (MACE), defined as myocardial infarction, unstable angina, congestive heart failure, coronary artery disease, coronary artery revascularization, or cardiovascular death, at 1 year in patients with first-ever ischemic stroke vs propensity-matched individuals without stroke (4:1 matching using 31 variables). To estimate cause-specific hazard ratios (HRs), we used Cox regression models adjusted for variables with weighted standardized differences >0.10 or known to influence the risk of MACE.
RESULTSWe included 21,931 patients with first-ever ischemic stroke and 71,696 propensity-matched individuals, well balanced on all variables used for propensity matching. First-ever ischemic stroke was associated with increased unadjusted incident MACE risk (HR 4.5, 95% confidence interval CI 4.3–4.8). MACE adjusted risk was highest in the first 30 days (HR 25.0, 95% CI 20.5–30.5) and declined both at 31 to 90 days (HR 4.8, 95% CI 4.1–5.7) and at 91 to 365 days (HR 2.2, 95% CI 2.0–2.4).
CONCLUSIONSIn this large population-based study, ischemic stroke was independently associated with increased risk of incident MACE. Whether this association is explained by stroke-associated cardiac injury, preexisting subclinical cardiovascular comorbid conditions, or both remains unknown.
OBJECTIVES:To investigate the hypothesis that strokes occurring in patients with COVID-19 have distinctive features, we investigated stroke risk, clinical phenotypes, and outcomes in this population.
...METHODS:We performed a systematic search resulting in 10 studies reporting stroke frequency among COVID-19 patients, which were pooled with one unpublished series from Canada. We applied random-effects meta-analyses to estimate the proportion of stroke among COVID-19. We performed an additional systematic search for cases series of stroke in COVID-19 patients (n=125) and we pooled these data with 35 unpublished cases from Canada, USA, and Iran. We analyzed clinical characteristics and in-hospital mortality stratified into age groups (<50, 50-70, >70 years). We applied cluster analyses to identify specific clinical phenotypes and their relationship with death.
RESULTS:The proportion of COVID-19 patients with stroke (1.8%, 95%CI 0.9-3.7%) and in-hospital mortality (34.4%, 95%CI 27.2-42.4%) were exceedingly high. Mortality was 67% lower in patients <50 years-old relative to those >70 years-old (OR 0.33, 95%CI 0.12-0.94, P=0.039). Large vessel occlusion was twice as frequent (46.9%) as previously reported and was high across all age groups, even in the absence of risk factors or comorbidities. A clinical phenotype characterized by older age, a higher burden of comorbidities, and severe COVID-19 respiratory symptoms, was associated with the highest in-hospital mortality (58.6%) and a 3x higher risk of death than the rest of the cohort (OR 3.52, 95%CI 1.53-8.09, P=0.003).
CONCLUSIONS:Stroke is relatively frequent among COVID-19 patients and has devastating consequences across all ages. The interplay of older age, comorbidities, and severity of COVID-19 respiratory symptoms is associated with an extremely elevated mortality.
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