Differences between Atrial Fibrillation Detected before and after Stroke and TIA: A Systematic Review and Meta-Analysis

Background: Preliminary evidence suggests that patients with atrial fibrillation (AF) detected after stroke (AFDAS) may have a lower prevalence of cardiovascular comorbidities and lower risk of stroke recurrence than AF known before stroke (KAF). Objective: We performed a systematic search and meta-analysis to compare the characteristics of AFDAS and KAF. Methods: We searched PubMed, Scopus, and EMBASE for articles reporting differences between AFDAS and KAF until June 30, 2021. We performed random- or fixed-effects meta-analyses to evaluate differences between AFDAS and KAF in demographic factors, vascular risk factors, prevalent vascular comorbidities, structural heart disease, stroke severity, insular cortex involvement, stroke recurrence, and death. Results: In 21 studies including 22,566 patients with ischemic stroke or transient ischemic attack, the prevalence of coronary artery disease, congestive heart failure, prior myocardial infarction, and a history of cerebrovascular events was significantly lower in AFDAS than KAF. Left atrial size was smaller, and left ventricular ejection fraction was higher in AFDAS than KAF. The risk of recurrent stroke was 26% lower in AFDAS than in KAF. There were no differences in age, sex, stroke severity, or death rates between AFDAS and KAF. There were not enough studies to report differences in insular cortex involvement between AF types. Conclusions: We found significant differences in the prevalence of vascular comorbidities, structural heart disease, and stroke recurrence rates between AFDAS and KAF, suggesting that they constitute different clinical entities within the AF spectrum. PROSPERO registration number is CRD42020202622

Cost-effectiveness of cerebrospinal biomarkers for the diagnosis of Alzheimer\u27s disease

Background: Accurate and timely diagnosis of Alzheimer\u27s disease (AD) is important for prompt initiation of treatment in patients with AD and to avoid inappropriate treatment of patients with false-positive diagnoses. Methods: Using a Markov model, we estimated the lifetime costs and quality-adjusted life-years (QALYs) of cerebrospinal fluid biomarker analysis in a cohort of patients referred to a neurologist or memory clinic with suspected AD who remained without a definitive diagnosis of AD or another condition after neuroimaging. Parametric values were estimated from previous health economic models and the medical literature. Extensive deterministic and probabilistic sensitivity analyses were performed to evaluate the robustness of the results. Results: At a 12.7% pretest probability of AD, biomarker analysis after normal neuroimaging findings has an incremental cost-effectiveness ratio (ICER) of $11,032 per QALY gained. Results were sensitive to the pretest prevalence of AD, and the ICER increased to over$ 50,000 per QALY when the prevalence of AD fell below 9%. Results were also sensitive to patient age (biomarkers are less cost-effective in older cohorts), treatment uptake and adherence, biomarker test characteristics, and the degree to which patients with suspected AD who do not have AD benefit from AD treatment when they are falsely diagnosed. Conclusions: The cost-effectiveness of biomarker analysis depends critically on the prevalence of AD in the tested population. In general practice, where the prevalence of AD after clinical assessment and normal neuroimaging findings may be low, biomarker analysis is unlikely to be cost-effective at a willingness-to-pay threshold of $ 50,000 per QALY gained. However, when at least 1 in 11 patients has AD after normal neuroimaging findings, biomarker analysis is likely cost-effective. Specifically, for patients referred to memory clinics with memory impairment who do not present neuroimaging evidence of medial temporal lobe atrophy, pretest prevalence of AD may exceed 15%. Biomarker analysis is a potentially cost-saving diagnostic method and should be considered for adoption in high-prevalence centers

Cost-effectiveness of cerebrospinal biomarkers for the diagnosis of Alzheimer’s disease

Background: Accurate and timely diagnosis of Alzheimer’s disease (AD) is important for prompt initiation of treatment in patients with AD and to avoid inappropriate treatment of patients with false-positive diagnoses. Methods: Using a Markov model, we estimated the lifetime costs and quality-adjusted life-years (QALYs) of cerebrospinal fluid biomarker analysis in a cohort of patients referred to a neurologist or memory clinic with suspected AD who remained without a definitive diagnosis of AD or another condition after neuroimaging. Parametric values were estimated from previous health economic models and the medical literature. Extensive deterministic and probabilistic sensitivity analyses were performed to evaluate the robustness of the results. Results: At a 12.7% pretest probability of AD, biomarker analysis after normal neuroimaging findings has an incremental cost-effectiveness ratio (ICER) of $11,032 per QALY gained. Results were sensitive to the pretest prevalence of AD, and the ICER increased to over$50,000 per QALY when the prevalence of AD fell below 9%. Results were also sensitive to patient age (biomarkers are less cost-effective in older cohorts), treatment uptake and adherence, biomarker test characteristics, and the degree to which patients with suspected AD who do not have AD benefit from AD treatment when they are falsely diagnosed. Conclusions: The cost-effectiveness of biomarker analysis depends critically on the prevalence of AD in the tested population. In general practice, where the prevalence of AD after clinical assessment and normal neuroimaging findings may be low, biomarker analysis is unlikely to be cost-effective at a willingness-to-pay threshold of $50,000 per QALY gained. However, when at least 1 in 11 patients has AD after normal neuroimaging findings, biomarker analysis is likely cost-effective. Specifically, for patients referred to memory clinics with memory impairment who do not present neuroimaging evidence of medial temporal lobe atrophy, pretest prevalence of AD may exceed 15%. Biomarker analysis is a potentially cost-saving diagnostic method and should be considered for adoption in high-prevalence centers

Atrial cardiopathy and cognitive impairment

Cognitive impairment involves complex interactions between multiple pathways and mechanisms, one of which being cardiac disorders. Atrial cardiopathy (AC) is a structural and functional disorder of the left atrium that may be a substrate for other cardiac disorders such as atrial fibrillation (AF) and heart failure (HF). The association between AF and HF and cognitive decline is clear; however, the relationship between AC and cognition requires further investigation. Studies have shown that several markers of AC, such as increased brain natriuretic peptide and left atrial enlargement, are associated with an increased risk for cognitive impairment. The pathophysiology of cognitive decline in patients with AC is not yet well understood. Advancing our understanding of the relationship between AC and cognition may point to important treatable targets and inform future therapeutic advancements. This review presents our current understanding of the diagnosis of AC, as well as clinical characteristics and potential pathways involved in the association between AC and cognitive impairment

Adverse Outcome of Early Recurrent Ischemic Stroke Secondary to Atrial Fibrillation after Repeated Systemic Thrombolysis

Background. Recurrent ischemic stroke is associated with adverse neurological outcome in patients with atrial fibrillation. There is very scarce information regarding the neurological outcome of atrial fibrillation patients undergoing repeated systemic thrombolysis after early recurrent ischemic stroke. Clinical Case and Discussion. We describe a case of a 76-year-old woman with known paroxysmal atrial fibrillation who was admitted because of an acute right middle cerebral artery ischemic stroke and who underwent repeated systemic thrombolysis within 110 hours. The patient underwent systemic thrombolysis after the first ischemic stroke with almost complete neurological recovery. On the fourth day after treatment, an acute left middle cerebral artery ischemic stroke was diagnosed and she was treated with full-dose intravenous recombinant tissue plasminogen activator. A hemorrhagic transformation of the left middle cerebral artery infarction was noted on follow-up cranial computed tomographic scans. The patient did not recover from the second cerebrovascular event and died 25 days after admission. Conclusion. To the best of our knowledge, this is the second case reporting the adverse neurological outcome of a patient with diagnosis of atrial fibrillation undergoing repeated systemic thrombolysis after early recurrent ischemic stroke. Our report represents a contribution to the scarce available evidence suggesting that repeated systemic thrombolysis for recurrent ischemic stroke should be avoided

Stroke–Heart Syndrome: Recent Advances and Challenges

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 pop-ulations, 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

Cerebral Embolic Protection in TAVI: Friend or Foe

Cerebrovascular accidents including stroke or transient ischaemic attack are one of the most feared complications after transcatheter aortic valve implantation. Transcatheter aortic valve implantation procedures have been consistently associated with silent ischaemic cerebral embolism as assessed by diffusion-weighted MRI. To reduce the risk of cerebrovascular accidents and silent emboli, cerebral embolic protection devices were developed with the aim of preventing procedural debris reaching the cerebral vasculature. The authors summarise the available data regarding cerebral embolic protection devices and its clinical significance