Atrial fibrillation and stroke: a practical guide

Best, Jonathan G.; Bell, Robert M.; Haque, Mohammad Mahfuzul; Chandratheva, Arvind; Werring, David J.

doi:10.1136/practneurol-2018-002089

Cited by 24 publications

(23 citation statements)

References 129 publications

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Section: Acute and Chronic Cardiac Dysfunction Pre-aismentioning

confidence: 99%

“…Atrial fibrillation and flutter cause blood stagnation in the left atrium, thus predisposing to thrombosis and cerebral embolism [45]. Valvular atrial fibrillation increases the risk of AIS 17-fold, while non-valvular atrial fibrillation increases the risk 5-fold [45]. No distinction has been made in terms of rate of risk for AIS among paroxysmal, permanent, or persistent atrial fibrillation, thus making a more aggressive monitoring strategy difficult, especially in patients with an initial diagnosis of an arrhythmia other than atrial fibrillation [45].…”

Section: Acute and Chronic Cardiac Dysfunction Pre-aismentioning

confidence: 99%

“…Valvular atrial fibrillation increases the risk of AIS 17-fold, while non-valvular atrial fibrillation increases the risk 5-fold [45]. No distinction has been made in terms of rate of risk for AIS among paroxysmal, permanent, or persistent atrial fibrillation, thus making a more aggressive monitoring strategy difficult, especially in patients with an initial diagnosis of an arrhythmia other than atrial fibrillation [45]. Systolic blood pressure higher than 140 mmHg is responsible for 1.5 million AIS-related deaths [46].…”

Section: Acute and Chronic Cardiac Dysfunction Pre-aismentioning

confidence: 99%

“…Moreover, a ratio between arterial systolic blood pressure at the ankle and brachial artery (known as the ankle-brachial index) higher than 0.9 indicates peripheral artery disease [32]. In patients with atrial fibrillation, the CHADS 2 and CHA 2 DS 2 -VASc scores have been validated to identify the risk of AIS [45].…”

Section: Cardiovascular Monitoring and Treatment Optionsmentioning

confidence: 99%

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Brain–heart interaction after acute ischemic stroke

et al. 2020

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Early detection of cardiovascular dysfunctions directly caused by acute ischemic stroke (AIS) has become paramount. Researchers now generally agree on the existence of a bidirectional interaction between the brain and the heart. In support of this theory, AIS patients are extremely vulnerable to severe cardiac complications. Sympathetic hyperactivity, hypothalamic-pituitary-adrenal axis, the immune and inflammatory responses, and gut dysbiosis have been identified as the main pathological mechanisms involved in brain-heart axis dysregulation after AIS. Moreover, evidence has confirmed that the main causes of mortality after AIS include heart attack, congestive heart failure, hemodynamic instability, left ventricular systolic dysfunction, diastolic dysfunction, arrhythmias, electrocardiographic anomalies, and cardiac arrest, all of which are more or less associated with poor outcomes and death. Therefore, intensive care unit admission with continuous hemodynamic monitoring has been proposed as the standard of care for AIS patients at high risk for developing cardiovascular complications. Recent trials have also investigated possible therapies to prevent secondary cardiovascular accidents after AIS. Labetalol, nicardipine, and nitroprusside have been recommended for the control of hypertension during AIS, while beta blockers have been suggested both for preventing chronic remodeling and for treating arrhythmias. Additionally, electrolytic imbalances should be considered, and abnormal rhythms must be treated. Nevertheless, therapeutic targets remain challenging, and further investigations might be essential to complete this complex multi-disciplinary puzzle. This review aims to highlight the pathophysiological mechanisms implicated in the interaction between the brain and the heart and their clinical consequences in AIS patients, as well as to provide specific recommendations for cardiovascular management after AIS.

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Section: Acute and Chronic Cardiac Dysfunction Pre-aismentioning

confidence: 99%

Section: Acute and Chronic Cardiac Dysfunction Pre-aismentioning

confidence: 99%

Section: Acute and Chronic Cardiac Dysfunction Pre-aismentioning

confidence: 99%

Section: Cardiovascular Monitoring and Treatment Optionsmentioning

confidence: 99%

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Brain–heart interaction after acute ischemic stroke

et al. 2020

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“…However, while total mortality for heart failure has remained stable in the last few years, due to treatment improvement and optimization (Vasan et al, 2019), hospitalization rates and mortality for AF are steadily rising (Freeman, 2017). Indeed, AF is associated with an increased risk of heart failure decompensation, as well as to arterial thromboembolism leading to ischemic stroke (Best, 2019;Carlisle, 2019). AF is, therefore, a major health issue, associated with significant social and economic costs in developed countries.…”

Section: Introductionmentioning

confidence: 99%

Pharmacological Inhibition of Serine Proteases to Reduce Cardiac Inflammation and Fibrosis in Atrial Fibrillation

et al. 2019

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Systemic inflammation correlates with an increased risk of atrial fibrillation (AF) and thrombogenesis. Systemic inflammation alters vessel permeability, allowing inflammatory and immune cell migration toward target organs, including the heart. Among inflammatory cells infiltrating the atria, macrophages and mast cell have recently attracted the interest of basic researchers due to the pathogenic mechanisms triggered by their activation. This chemotactic invasion is likely implicated in shortand long-term changes in cardiac cell-to-cell communication and in triggering fibrous tissue accumulation in the atrial myocardium and electrophysiological rearrangements of atrial cardiomyocytes, thus favoring the onset and progression of AF. Serine proteases are a large and heterogeneous class of proteases involved in several processes that are important for cardiac function and are involved in cardiac diseases, such as (i) coagulation, (ii) fibrinolysis, (iii) extracellular matrix degradation, (iv) activation of receptors (i.e., protease-activated receptors [PPARs]), and (v) modulation of the activity of endogenous signals. The recognition of serine proteases substrates and their involvement in inflammatory/profibrotic mechanisms allowed the identification of novel cardio-protective mechanisms for commonly used drugs that inhibit serine proteases. The aim of this review is to summarize knowledge on the role of inflammation and fibrosis as determinants of AF. Moreover, we will recapitulate current findings on the role of serine proteases in the pathogenesis of AF and the possible beneficial effects of drugs inhibiting serine proteases in reducing the risk of AF through decrease of cardiac inflammation and fibrosis. These drugs include thrombin and factor Xa inhibitors (used as oral anticoagulants), dipeptidyl-peptidase 4 (DPP4) inhibitors, used for type-2 diabetes, as well as novel experimental inhibitors of mast cell chymases.

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Stroke Related Brain–Heart Crosstalk: Pathophysiology, Clinical Implications, and Underlying Mechanisms

Fan,

Cao,

et al. 2024

Advanced Science

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The emergence of acute ischemic stroke (AIS) induced cardiovascular dysfunctions as a bidirectional interaction has gained paramount importance in understanding the intricate relationship between the brain and heart. Post AIS, the ensuing cardiovascular dysfunctions encompass a spectrum of complications, including heart attack, congestive heart failure, systolic or diastolic dysfunction, arrhythmias, electrocardiographic anomalies, hemodynamic instability, cardiac arrest, among others, all of which are correlated with adverse outcomes and mortality. Mounting evidence underscores the intimate crosstalk between the heart and the brain, facilitated by intricate physiological and neurohumoral complex networks. The primary pathophysiological mechanisms contributing to these severe cardiac complications involve the hypothalamic‐pituitary‐adrenal (HPA) axis, sympathetic and parasympathetic hyperactivity, immune and inflammatory responses, and gut dysbiosis, collectively shaping the stroke‐related brain–heart axis. Ongoing research endeavors are concentrated on devising strategies to prevent AIS‐induced cardiovascular dysfunctions. Notably, labetalol, nicardipine, and nitroprusside are recommended for hypertension control, while β‐blockers are employed to avert chronic remodeling and address arrhythmias. However, despite these therapeutic interventions, therapeutic targets remain elusive, necessitating further investigations into this complex challenge. This review aims to delineate the state‐of‐the‐art pathophysiological mechanisms in AIS through preclinical and clinical research, unraveling their intricate interplay within the brain–heart axis, and offering pragmatic suggestions for managing AIS‐induced cardiovascular dysfunctions.

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Atrial fibrillation and stroke: a practical guide

Cited by 24 publications

References 129 publications

Brain–heart interaction after acute ischemic stroke

Brain–heart interaction after acute ischemic stroke

Pharmacological Inhibition of Serine Proteases to Reduce Cardiac Inflammation and Fibrosis in Atrial Fibrillation

Stroke Related Brain–Heart Crosstalk: Pathophysiology, Clinical Implications, and Underlying Mechanisms

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