A COMPREHENSIVE REVIEW ON THE ROLE OF CARDIOVASCULAR INFLAMMATION IN FRAILTY AND COGNITIVE DECLINE AFTER MYOCADIAL INFRACTION

Dr.Hassanien Al-Hashimi; Dr. Rand Al-Janabi; Dr. Hamzah Mohsin Jasim; Saad Wael Saad Al-Mahmood; Hussein Maytham Abdulridha; Mushriq Abdul-Jabbar Hameed; Dr. Ali Al-Hashimi

Authors

Dr.Hassanien Al-Hashimi Medical Doctor, Al Diwania, Al-Qadisiya, Iraq
Dr. Rand Al-Janabi Medical Doctor, Hilla, Babil, IRAQ
Dr. Hamzah Mohsin Jasim Medical Doctor, Karbala, IRAQ
Saad Wael Saad Al-Mahmood Medical Student, Al-Ameed University, Karbala, IRAQ
Hussein Maytham Abdulridha Medical Student, Al-Ameed University, Karbala, IRAQ
Mushriq Abdul-Jabbar Hameed Medical Student, Al-Ameed University, Karbala, IRAQ
Dr. Ali Al-Hashimi Medical Student, Al-Ameed University, Karbala, IRAQ

Abstract

Cardiovascular infection is more and more diagnosed as a vital aspect contributing to frailty and cognitive decline following myocardial infarction (MI). This evaluation explores the complicated mechanisms linking systemic inflammation with physical and neurological deterioration in put up-MI sufferers. After MI, an inflammatory cascade is activated, concerning progressed stages of pro-inflammatory cytokines, oxidative pressure, and endothelial disorder. These techniques no longer most effective impair cardiovascular healing however moreover have an extended way-carrying out outcomes at the treasured frightened machine. Chronic contamination exacerbates microvascular disorder and disrupts blood-thoughts barrier integrity, lowering cerebral perfusion and accelerating neurodegenerative strategies. Frailty, characterised by way of reduced physiological reserve and resilience, is strongly related to chronic systemic contamination. This nation is compounded with the useful resource of the interaction of sarcopenia, impaired immune responses, and vascular dysregulation. Similarly, cognitive decline in positioned up-MI patients is associated with inflammatory pathways that promote amyloid deposition, tau protein hyperphosphorylation, and neuronal loss. A bidirectional courting exists, as cognitive decline can similarly impair cardiovascular health via mechanisms collectively with dysautonomia and maladaptive behaviors. Recognizing this interaction is crucial for addressing the multifactorial burden of MI-associated headaches. Emerging restoration strategies cognizance on anti-inflammatory entrepreneurs, life-style interventions, and vascular fitness optimization to mitigate those unfavourable consequences. Integrating cardiology and neurology views can also allow earlier analysis and tailored interventions, in the long run enhancing long-term results for put up-MI sufferers.

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