In this chapter we will discuss more about the role of homocysteine in atherosclerosis and also association between serum homocysteine with extracranial carotid atherosclerosis. Carotid atherosclerosis comprises an increase in carotid intima-media (CIMT) thickening, plaque formation and carotid stenosis. Atherogenic property of homocysteine was discovered in 1969. Atherosclerosis is initiated by endothelial dysfunction. One of the causes of endothelial abnormality is homocysteine. The development of aggregates of homocysteinylated lipoproteins with microorganisms obstructs the vasa vasorum in vulnerable plaques. In one study, serum homocysteine in the highest quartile was independently associated with extracranial carotid artery stenosis ≥50%. In another study, raised serum homocysteine was also independently associated with severe extracranial carotid stenosis in both genders. In other studies, serum homocysteine was significantly associated with carotid artery stenosis in internal carotid arteries and external carotid arteries as well as the degree of stenosis. The hypertensive patients who had raised serum homocysteine were reported to have higher risk of developing asymptomatic extracranial carotid artery stenosis.
Subarachnoid haemorrhage (SAH) occurs as a result of rupture of intracranial aneurysms. SAH causes significant morbidity and mortality. In addition, SAH leads to significant financial burden. In this chapter, we will look into the association between raised serum homocysteine and intracranial aneurysms. In a study on the Han Chinese patients with intracranial aneurysm who were admitted to the hospital, the mean serum total homocysteine level in the patient group with intracranial aneurysm was significantly higher than those in the control group. In the same study, the patients with raised serum homocysteine had 2.196 higher risk of developing intracranial aneurysms. Ren et al. proposed that homocysteine should be seen as an indicator of the risk of intracranial aneurysm and not a direct cause of intracranial aneurysm. In another study, homocysteine increases the development of intracranial aneurysms in rats. Endothelial damage is an early change in the walls of intracranial aneurysms. Polymorphisms of the genes coding for the various components of the vessel walls may be associated with the formation of intracranial aneurysms. In a previous animal study, the size of intracranial aneurysms is significantly smaller in the mice with inducible nitric oxide synthase (iNOS) compared with the mice without iNOS.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.