#Post-Stroke #Cardiovascular_Complications and #Neurogenic_ Cardiac_ Injur

Post-Stroke Cardiovascular Complications and Neurogenic Cardiac Injury Luciano A. Sposato, Max J. Hilz, Sara Aspberg, Santosh B. Murthy, M. Cecilia Bahit, Cheng-Yang Hsieh, Mary N. Sheppard, Jan F. Scheitz, and World Stroke Organisation Brain & Heart Task Forceon behalf of the JACC. 2020 Dec, 76 (23) 2768–2785 Abstract Over 1.5 million deaths worldwide are caused by neurocardiogenic syndromes. Furthermore, the consequences of deleterious brain-heart interactions are not limited to fatal complications. Cardiac arrhythmias, heart failure, and nonfatal coronary syndromes are also common. The brain-heart axis is implicated in post-stroke cardiovascular complications known as the stroke-heart syndrome, sudden cardiac death, and Takotsubo syndrome, among other neurocardiogenic syndromes. Multiple pathophysiological mechanisms with the potential to be targeted with novel therapies have been identified in the last decade. In the present state-of-the-art review, we describe recent advances in the understanding of anatomical and functional aspects of the brain-heart axis, cardiovascular complications after stroke, and a comprehensive pathophysiological model of stroke-induced cardiac injury. Highlights • Stroke-induced cardiac injury is caused by autonomic and inflammatory mechanisms mediated by damage to the brain-heart axis. • Some of the recently identified mechanisms could be targeted for prevention of cardiovascular complications of stroke. • Mechanistic research and clinical trials are needed to develop specific therapies for prevention of neurocardiogenic syndromes. Introduction The brain and heart interactions have been investigated for centuries and have gained special attention in the last decade. Increasing evidence supports the physiological and pathophysiological interplay of the nervous and cardiovascular systems. Over 1.5 million deaths worldwide are explained by the involvement of neurocardiogenic mechanisms, including post-stroke cardiovascular complications, sudden unexpected death in epilepsy, Takotsubo syndrome (TTS), and neurogenic sudden cardiac death (1–4). Importantly, despite the better portrayal of neurocardiogenic syndromes, little improvements have been made in the development of specific therapies targeting the brain-heart axis for preventing cardiovascular complications and death after stroke. In the present state-of-the-art review, we describe recent advances in the understanding of anatomical and functional aspects of the brain-heart axis and post-stroke cardiovascular complications (5,6), the paradigmatic expression of neurogenic cardiovascular complications. We also provide a comprehensive and updated pathophysiological model explaining post-stroke cardiovascular events (7,8).

#Chronic_Heart_Failure and #Ischemic_Stroke

Chronic Heart Failure and Ischemic Stroke Karl Georg Haeusler, MD, Ulrich Laufs, MD, and Matthias Endres, MDAUTHOR INFO & AFFILIATIONS Stroke Volume 42, Number 10 Abstract Introduction Conclusions Supplemental Material Sources of Funding References eLetters Information & Authors Metrics & Citations View Options References Tables Share Abstract Chronic heart failure (CHF) is one of the leading causes of hospitalization, morbidity, and mortality worldwide. This review summarizes current knowledge with regard to CHF as a risk factor for ischemic stroke. CHF is associated with an increased risk of thrombus formation and is accompanied by a 2- to 3-fold increased risk of stroke. Moreover, stroke in CHF patients is associated with poor outcome and higher mortality. Available evidence for additional “vascular” stroke risk factors in heart failure patients is inconsistent and is mostly derived from cohort studies or retrospective analyses. Current guidelines recommend anticoagulation for CHF patients with concomitant atrial fibrillation but not for those in sinus rhythm. Prospective studies are needed to test whether early detection and optimal treatment of CHF reduces the burden of stroke-associated neurologic and neuropsychological sequelae.

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