4.6 Review

Cognitive impairment in myocardial infarction and heart failure

Journal

ACTA PHYSIOLOGICA
Volume 232, Issue 1, Pages -

Publisher

WILEY
DOI: 10.1111/apha.13642

Keywords

cell death; cognitive impairment; heart failure; microglia; myocardial infarction

Categories

Funding

  1. Chiang Mai University
  2. National Science and Technology Development Agency
  3. National Research Council of Thailand

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Myocardial infarction leads to cognitive impairment, anxiety, depression, and memory loss in heart failure patients, with the main cause being cardiac systolic dysfunction resulting in reduced cerebral perfusion. Various studies have identified neurohormonal activation, oxidative stress, inflammation, glial activation, dendritic spine loss, and brain cell death as potential contributors to cognitive decline in heart failure. Further research into the effects of different medications on brain pathology in myocardial infarction models has also been reported.
Myocardial infarction (MI) occurs when coronary blood flow is decreased due to an obstruction/occlusion of the vessels, leading to myocardial death and progression to heart failure (HF). Cognitive impairment, anxiety, depression and memory loss are the most frequent mental health problems among patients with HF. The most common cause of cognitive decline is cardiac systolic dysfunction, which leads to reduced cerebral perfusion. Several in vivo and clinical studies provide information regarding the underlying mechanisms of HF in brain pathology. Neurohormonal activation, oxidative stress, inflammation, glial activation, dendritic spine loss and brain programmed cell death are all proposed as contributors of cognitive impairment in HF. Furthermore, several investigations into the effects of various medications on brain pathology utilizing MI models have been reported. In this review, potential mechanisms involving HF-associated cognitive impairment, as well as neuroprotective interventions in HF models, are discussed and summarized. In addition, gaps in the surrounding knowledge, including the types of brain cell death and the effects of cell death inhibitors in HF, are presented and discussed. This review provides valuable information that will suggest the potential therapeutic strategies for cognitive impairment in patients with HF.

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