Cognitive impairment in myocardial infarction and heart failure

Jinawong, Kewarin; Apaijai, Nattayaporn; Chattipakorn, Nipon

doi:10.1111/apha.13642

Cited by 35 publications

(21 citation statements)

References 97 publications

(293 reference statements)

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“…A reduction in cerebral blood flow (CBF) is an inciting event responsible for neuropathology in many diseases, including AMI [ 7 ]. Decreased brain oxygen and glucose supply, as a result of inadequate CBF, causes secondary brain injury, including neuroinflammation, oxidative stress, and cell death [ 19 , 20 ].…”

Section: Discussionmentioning

confidence: 99%

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Cell death inhibitors protect against brain damage caused by cardiac ischemia/reperfusion injury

et al. 2021

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Cognitive impairment has been reported in patients with myocardial infarction despite a successful reperfusion therapy. Several modes of cell death are involved in brain damage during cardiac ischemia/reperfusion (I/R) injury. Although apoptosis, necroptosis, and ferroptosis inhibitors provided neuroprotection against cerebral I/R injury, the effects of these cell death inhibitors on the brain following cardiac I/R injury have never been investigated. We hypothesized that apoptosis, necroptosis, and ferroptosis inhibitors attenuate brain damage following cardiac I/R injury. One-hundred and twenty-six male rats were used: 6 rats were assigned to sham operation and 120 rats were subjected to 30-min regional cardiac ischemia and 120-min reperfusion. Rats in cardiac I/R group were pretreated with either vehicle (n = 12) or one of cell death inhibitors. Rats treated with apoptosis, necroptosis, or ferroptosis inhibitor were subdivided into three different doses including low (L), medium (M), and high (H) doses (n = 12/group). Z-VAD, necrostatin-1 (Nec-1), and ferrostatin-1 (Fer-1) were used as apoptosis, necroptosis, and ferroptosis inhibitor, respectively. Rats were sacrificed at the end of reperfusion, and the brain was used to analyze dendritic spine density, Alzheimer’s disease (AD)-related proteins, blood–brain barrier (BBB) tight junction proteins, mitochondrial function, inflammation, and cell death. Our data showed that cardiac I/R led to brain damage and only apoptosis occurred in the hippocampus after cardiac I/R injury. In the cardiac I/R group, treatment with M-Z-VAD and all doses of Nec-1 decreased hippocampal apoptosis and amyloid beta aggregation, thereby reducing dendritic spine loss. M- and H-Fer-1 also reduced dendritic spine loss by suppressing ACSL4, TNF-α, amyloid beta, and tau hyperphosphorylation. Moreover, Bax/Bcl-2 was decreased in all treatment regimen except L-Z-VAD. Additionally, M-Z-VAD and M-Fer-1 partially attenuated mitochondrial dysfunction. Only L-Nec-1 preserved BBB proteins. In conclusion, cell death inhibitors prevented hippocampal dendritic spine loss caused by cardiac I/R injury through different mechanisms.

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Section: Discussionmentioning

confidence: 99%

“…Apoptosis, necroptosis, and ferroptosis are associated with cognitive impairment in myocardial infarction [ 7 ]. Brain apoptosis was reported in rats with cardiac I/R injury [ 8 , 9 ]; however, the occurrence of brain necroptosis and ferroptosis has not been investigated.…”

Section: Introductionmentioning

confidence: 99%

Cell death inhibitors protect against brain damage caused by cardiac ischemia/reperfusion injury

et al. 2021

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“…Prior studies have found that the expressions of Bax in the hippocampal cortex changed female mice with HF, which may affect the apoptosis process of neurons related to cognitive function in the brain ( 84 ). Furthermore, evidence have shown that the expression of caspase family, especially caspase 3 and 6, have been increased in the hippocampal tissue of mice with HF ( 85 ). Animal studies also found that the activation of the RAS in mice with HF can affect AMPK-PGC1α signaling by stimulating angiotensin II receptors and increase the apoptosis of neural stem cells in the hippocampus of rats ( 86 ).…”

Section: Pathophysiology Cellular Mechanism and Risk Factors Of CI In Hfmentioning

confidence: 99%

Cognitive Impairment in Heart Failure: Landscape, Challenges, and Future Directions

Yang

Sun

Wang

et al. 2022

Front. Cardiovasc. Med.

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Heart failure (HF) is a major global healthcare problem accounting for substantial deterioration of prognosis. As a complex clinical syndrome, HF often coexists with multi-comorbidities of which cognitive impairment (CI) is particularly important. CI is increasing in prevalence among patients with HF and is present in around 40%, even up to 60%, of elderly patients with HF. As a potent and independent prognostic factor, CI significantly increases the hospitalization and mortality and decreases quality of life in patients with HF. There has been a growing awareness of the complex bidirectional interaction between HF and CI as it shares a number of common pathophysiological pathways including reduced cerebral blood flow, inflammation, and neurohumoral activations. Research that focus on the precise mechanism for CI in HF is still ever insufficient. As the tremendous adverse consequences of CI in HF, effective early diagnosis of CI in HF and interventions for these patients may halt disease progression and improve prognosis. The current clinical guidelines in HF have begun to emphasize the importance of CI. However, nearly half of CI in HF is underdiagnosed, and few recommendations are available to guide clinicians about how to approach CI in patients with HF. This review aims to synthesize knowledge about the link between HF and cognitive dysfunction, issues pertaining to screening, diagnosis and management of CI in patients with HF, and emerging therapies for prevention. Based on data from current studies, critical gaps in knowledge of CI in HF are identified, and future research directions to guide the field forward are proposed.

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“…Impaired vascular autoregulation resulting in white matter injury, neurohormonal dysregulation, systemic inflammation, and cerebral microvascular dysfunction may also contribute to generating a state of chronic cerebral hypoxia leading to brain microinfarcts and neurodegeneration ( Adelborg et al, 2017 ). The latter may be enhanced by oxidative stress, dendritic spine loss, glial activation, and programmed cell death ( Jinawong et al, 2021 ).…”

Section: Pathophysiology Of Atrial Cardiopathy-related Cognitive Impa...mentioning

confidence: 99%

Atrial cardiopathy and cognitive impairment

Myers

Jiménez‐Ruiz

Sposato

et al. 2022

Front. Aging Neurosci.

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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.

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Cognitive impairment in myocardial infarction and heart failure

Cited by 35 publications

References 97 publications

Cell death inhibitors protect against brain damage caused by cardiac ischemia/reperfusion injury

Cell death inhibitors protect against brain damage caused by cardiac ischemia/reperfusion injury

Cognitive Impairment in Heart Failure: Landscape, Challenges, and Future Directions

Atrial cardiopathy and cognitive impairment

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