Heart–brain Interactions in Heart Failure

Abstract

Heart failure (HF) is a complex disease with a growing incidence worldwide. HF is accompanied by a wide range of conditions which affect disease progression, functional performance and contribute to growing healthcare costs. The interactions between a failing myocardium and altered cerebral functions contribute to the symptoms experienced by patients with HF, affecting many comorbidities and causing a poor prognosis. This article provides a condensed version of the 2018 position paper from the Study Group on Heart and Brain Interaction of the Heart Failure Association. It addresses the reciprocal impact on HF of several pathological brain conditions, including acute and chronic low perfusion of the brain, and impairment of higher cortical and brain stem functions. Treatment-related interactions - medical, interventional and device-related - are also discussed.

Beneficial effect of sodium thiosulfate extends beyond myocardial tissue in isoproterenol model of infarction: Implication for nootropic effects

“…*P < .05 vs sham, # P < .05 vs ISO A rationale for therapy for adverse neurological outcomes in cardiovascular disease patients continues to evolve to improve postsurgical patient life. [25] As a part of the effort, we used a preclinical rat model to induce myocardial infarction (MI) and subsequentassociated neurological changes. We investigated the impact of STS administration on myocardial damage in rats induced by the admin- The ISO-induced cardiac injury relates to catecholamine cardiotoxicity, which is associated with similar metabolic and structural aberrations comparable to AMI events in humans.…”

Dementia and the heart failure patient

“…Comorbidities can worsen the HF, complicate its diagnosis, and make treatment more difficult and more expensive. Of these HF-related comorbidities brain disorders are some of the most prevalent and the most difficult to manage 1 . The elderly HF patient poses a complex problem for modern health care systems to look after, and foremost amongst the complexities is the issue of cognitive decline and/or dementia which makes patient self-care more difficult and which adds dramatically to the cost of health care provision for the HF itself.…”

Angiotensin-converting enzyme inhibitor treatment early after myocardial infarction attenuates acute cardiac and neuroinflammation without effect on chronic neuroinflammation

“…The presence of neuroinflammation in chronic heart failure may derive from various contributing factors, including reduction of cerebral blood flow [27], heightened immune response [28], or whole-body oxidative stress [29]. The inverse relationship of chronic neuroinflammation to ejection fraction suggests that contractile dysfunction contributes to late microglial activation, but the precise mechanism warrants further investigation.…”