Ischemic stroke complications

The systemic inflammation response to the ischemic stroke, followed by immunosuppression in focal neurologic deficits and other inflammatory damage, reduces the circulating immune cell counts and multiorgan infectious complications such as intestinal and gut dysfunction dysbiosis. Evidence showed that microbiota dysbiosis plays a role in neuroinflammation and peripheral immune response after stroke, changing the lymphocyte populations. Multiple immune cells, including lymphocytes, engage in complex and dynamic immune responses in all stages of stroke and may be a pivotal moderator in the bidirectional immunomodulation between ischemic stroke and gut microbiota 1).


Ischemic stroke (IS) is a risk factor for new coronavirus pneumonia, and patients with COVID-19 infection have a dramatically elevated risk of stroke. At the same time, patients with long-term IS are vulnerable to COVID-19 infection and have more severe disease, and carotid atherosclerosis is an early lesion in IS. A study used human-induced pluripotent stem cell (hiPSC)-derived monolayer brain cell dataset and human carotid atherosclerosis genome-wide dataset to analyze COVID-19 infection and carotid atherosclerosis patients to determine the synergistic effect of new coronavirus infection on carotid atherosclerosis patients, to clarify the common genes of both, and to identify common pathways and potential drugs for carotid atherosclerosis in patients with COVID-19 infection. Using several advanced bioinformatics tools, we present the causes of COVID-19 infection leading to increased mortality in carotid atherosclerosis patients and the susceptibility of carotid atherosclerosis patients to COVID-19. Potential therapeutic agents for COVID-19 -infected patients with carotid atherosclerosis are also proposed.

With COVID-19 being a relatively new disease, associations have been proposed for its connections with several ailments and conditions, including IS and carotid atherosclerosis. More patient-based data-sets and studies are needed to fully explore and understand the relationship 2).



see Recurrent ischemic stroke.

Patients presenting with large-territory ischemic strokes may develop intractable cerebral edema that puts them at risk of death unless intervention is performed.


Stress ulcers


In ischemic stroke or patients with TIA less than five cerebral microbleeds (CMBs) should not affect antithrombotic decisions, although with more than five CMBs the risks of future ICH and ischaemic stroke are finely balanced, and antithrombotics might cause net harm. In lobar ICH populations, a high burden of strictly lobar CMBs is associated with cerebral amyloid angiopathy (CAA) and high ICH risk; antithrombotics should be avoided unless there is a compelling indication 3).


1)
Pu B, Zhu H, Wei L, Gu L, Zhang S, Jian Z, Xiong X. The Involvement of Immune Cells Between Ischemic Stroke and Gut Microbiota. Transl Stroke Res. 2023 May 4. doi: 10.1007/s12975-023-01151-7. Epub ahead of print. PMID: 37140808.
2)
Yanchao L, Sibin Z, Gareev I, Huan X, Junfei Z, Chunyang L, Beylerli O, Sufianov A, Chao Y, Yuyan G, Xun X, Ahmad A, Peng L, Guang Y. Bioinformatics analysis of potential therapeutic targets for COVID-19 infection in patients with carotid atherosclerosis. J Infect Public Health. 2022 Mar 22;15(4):437-447. doi: 10.1016/j.jiph.2022.03.004. Epub ahead of print. PMID: 35344771.
3)
Wilson D, Werring DJ. Antithrombotic therapy in patients with cerebral microbleeds. Curr Opin Neurol. 2016 Nov 24. [Epub ahead of print] PubMed PMID: 27898582.
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