THEORETICAL ASPECTS IN THE FORMATION OF
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COGNITIVE IMPAIRMENTS IN CHRONIC HEART DISEASE
INSUFFICIENCY
Sadullaev Dilshod Izbiloevich
Bukhara State Medical Institute
https://orcid.org/0009-0001-9973-4113
https://doi.org/10.5281/zenodo.15125135
Introduction: Chronic heart failure (CHF) is a syndrome accompanied by a
decrease in cardiac output or an increase in heart filling pressure due to
structural or functional disorders of the myocardium. CHF remains an important
problem in modern medicine, being one of the main causes of hospitalization
and mortality. It affects more than 64 million people worldwide. In Europe, the
prevalence of CHF among all functional classes according to the classification of
the New York Heart Association (NYHA) is 7%, and for grades III-IV — 2.1%.
More than 600,000 patients over the age of 65 are discharged with CHF every
year, with a 25% chance of re-hospitalization within 30 days and 70% a year
after discharge. The frequency of repeated hospitalizations and mortality is
increased by factors such as low adherence to therapy, ignoring the need for
outpatient visits, and difficulty recognizing early symptoms of disease
progression, which is often associated with cognitive impairment. The
combination of CHF and cognitive dysfunction has attracted the attention of
specialists in recent years, especially in the context of the high prevalence
among the elderly. Cognitive functions include memory, gnosis, speech, praxis,
and attention. Cognitive impairments occur in 30-80% of patients with heart
failure and can range from mild cognitive impairment to dementia. These
patients often have problems with memory, decreased concentration, and
delayed information processing, which leads to a decrease in self-care and a
decrease in the ability to respond adequately to deterioration, which in turn
reduces treatment adherence. Thus, cognitive impairments worsen the quality
of life, increase the frequency of hospitalizations, increase mortality and
negatively affect the prognosis. Despite the high prevalence, the
pathophysiology of cognitive impairments in CHF has not yet been fully studied,
and little attention has been paid to their recognition and treatment. The article
reviews major studies on this topic, describes the pathophysiological
mechanisms and potential new therapeutic approaches to prevent the
progression of cognitive impairment in patients with heart failure.
Cognitive changes in heart failure: In recent years, many studies have been
conducted on the association of cognitive impairments with various areas of
THEORETICAL ASPECTS IN THE FORMATION OF
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International scientific-online conference
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brain damage in patients with CHF. Such patients often experience memory
impairment (especially verbal and visual), decreased concentration, slower
information processing, and impaired executive functions.
Patients with cognitive impairments often have several risk factors, both
systemic and related to microvascular diseases of the brain. Additionally, in
patients with heart failure, a systemic inflammatory process may contribute to
the development of cognitive impairment. In particular, molecules such as tumor
necrosis factor-α (TNF-α), interleukin-6 (IL-6) and cortisol, as well as elevated
plasma homocysteine levels, are associated with neuronal degeneration.
Increased secretion of inflammatory cytokines increases neurotoxicity through
glutamate secretion, which causes cell damage, disrupts synaptic plasticity, and
impairs memory.
In addition, there is a wealth of evidence linking atrial fibrillation (AF) with
the risk of cognitive impairment and dementia. Studies have shown that
cognitive abilities and memory deteriorate in patients with CHF and atrial
fibrillation due to a decrease in cerebral blood flow due to a loss of atrial systolic
activity and a decrease in stroke volume. Atrial fibrillation is also associated
with cognitive deficits through various mechanisms, including micro- and
macroembolic events. In patients without clinical stroke, the association
between fibrillation and cognitive impairment may indicate the presence of
latent embolisms contributing to cognitive decline. Microembolization of the
brain may occur due to a decrease in thrombomodulin levels, deterioration of
myocardial contractility and congestive heart failure
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