The correlation between homocysteine level and overall burden of cerebral small vessel disease in patients with ischemic stroke_West China Medical Journal

Authors：

ZHAO Ranran ,  LUO Xiaolan

Department of Radiology, People’s Hospital of Deyang City, Deyang, Sichuan 618000, P. R. China;

Corresponding author：

LUO Xiaolan, Email: 1354216595@qq.com

Keywords：

Homocysteine; Ischemic stroke; Cerebral small vessel disease

DOI：

10.7507/1002-0179.201901182

Video：

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Objective To investigate the relationship between the level of homocysteine (HCY) and the overall burden of cerebral small vessel disease (CSVD) in patients with ischemic stroke.Methods A total of 322 patients with first-ever ischemic stroke admitted to the People’s Hospital of Deyang City between January 2016 and December 2017 were enrolled. The patients’ demographic information, clinical information, and serum HCY concentration were collected after admission. The presence or absence of a CSVD was assessed by MRI and the overall burden score for the CSVD was determined. Multivariate logistic regression analysis was used to assess whether serum HCY level was associated with the overall burden of CSVD.Results The median level of HCY was 13.2 μmol/L (inter-quartile range: 4.3 to 22.6 μmol/L). Univariate analysis showed that the difference of HCY levels among patients with different total CSVD scores was statistically significant (F=6.874, P=0.001); Spearman correlation analyses showed that the HCY level grouped by quartiles was correlated to the number of lacunar infarctions (r_s=0.267, P=0.001), Fazekas score of white matter lesions (r_s=0.122, P=0.042), and enlarged perivascular space (EPV) score (r_s=0.319, P=0.001), but was not correlated to cerebral microhemorrhage (r_s=−0.010, P=0.869). After multivariate regression analysis to adjust the effects of other factors, compared with the patients with HCY levels in the lowest quartile group, the patients with HCY levels in the highest quartile group were more likely to develop lacunar infarction [odds ratio (OR)=1.892, 95% confidence interval (CI) (1.012, 2.987)], white matter lesions [OR=1.548, 95%CI (1.018, 1.654)], severe EPV [OR=6.347, 95%CI (3.592, 13.978)], and the increase in the CSVD score [OR=2.981, 95%CI (1.974, 5.398)].Conclusion In patients with ischemic stroke, elevated HCY levels may be associated with the overall burden of the CSVD.

Citation： ZHAO Ranran, LUO Xiaolan. The correlation between homocysteine level and overall burden of cerebral small vessel disease in patients with ischemic stroke. West China Medical Journal, 2019, 34(4): 394-399. doi: 10.7507/1002-0179.201901182 Copy

1.	Pantoni L. Cerebral small vessel disease: from pathogenesis and clinical characteristics to therapeutic challenges. Lancet Neurol, 2010, 9(7): 689-701.
2.	Wardlaw JM, Smith C, Dichgans M. Mechanisms of sporadic cerebral small vessel disease: insights from neuroimaging. Lancet Neurol, 2013, 12(5): 483-497.
3.	Gorelick PB, Scuteri A, Black SE, et al. Vascular contributions to cognitive impairment and dementia a statement for healthcare professionals from the American heart association/American stroke association. Stroke, 2011, 42(9): 2672-2713.
4.	Valdes Hernandez Mdel C, Morris Z, Dickie DA, et al. Close correlation between quantitative and qualitative assessments of white matter lesions. Neuroepidemiology, 2013, 40(1): 13-22.
5.	Jackson CA, Hutchison A, Dennis MS, et al. Differing risk factor profiles of ischemic stroke subtypes evidence for a distinct lacunar arteriopathy?. Stroke, 2010, 41(4): 624-629.
6.	Spence JD. Homocysteine-lowering therapy: a role in stroke prevention?. Lancet Neurol, 2007, 6(9): 830-838.
7.	Miwa K, Tanaka M, Okazaki S, et al. Increased total homocysteine levels predict the risk of incident dementia independent of cerebral small-vessel diseases and vascular risk factors. J Alzheimers Dis, 2016, 49(2): 503-513.
8.	Teo BW, Xu H, Wang DH, et al. GFR estimating equations in a multiethnic Asian population. Am J Kidney Dis, 2011, 58(1): 56-63.
9.	Adams HP Jr, Bendixen BH, Kappelle LJ, et al. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment. Stroke, 1993, 24(1): 35-41.
10.	Wardlaw JM, Smith EE, Biessels GJ, et al. Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration. Lancet Neurol, 2013, 12(8): 822-838.
11.	Fazekas F, Chawluk JB, Alavi A, et al. Mr signal abnormalities at 1.5 T in Alzheimer’s dementia and normal aging. AJR Am J Roentgenol, 1987, 149(2): 351-356.
12.	Potter GM, Chappell FM, Morris ZA. Cerebral perivascular spaces visible on magnetic resonance imaging: development of a qualitative rating scale and its observer reliability. Cerebrovasc Dis, 2015, 39(3/4): 224-231.
13.	Staals J, Makin SD, Doubal FN, et al. Stroke subtype, vascular risk factors, and total MRI brain small-vessel disease burden. Neurology, 2014, 83(14): 1228-1234.
14.	Guo HY, Wang P, You BQ, et al. Chinese yellow wine inhibits production of homocysteine-induced extracellular matrix metalloproteinase-2 in cultured rat vascular smooth muscle cells. Clin Nutr, 2007, 26(3): 348-354.
15.	Tian X, Zhao L, Song XJ, et al. HSP27 inhibits homocysteine-induced endothelial apoptosis by modulation of ROS production and mitochondrial caspase-dependent apoptotic pathway. Biomed Res Int, 2016, 2016: 4847874.
16.	Dayal S, Arning E, Bottiglieri T, et al. Cerebral vascular dysfunction mediated by superoxide in hyperhomocysteinemic mice. Stroke, 2004, 35(8): 1957-1962.
17.	Feng C, Bai X, Xu Y, et al. Hyperhomocysteinemia associates with small vessel disease more closely than large vessel disease. Int J Med Sci, 2013, 10(4): 408-412.
18.	Gregoire SM, Smith K, Jäger HR, et al. Cerebral microbleeds and long-term cognitive outcome: longitudinal cohort study of stroke clinic patients. Cerebrovasc Dis, 2012, 33(5): 430-435.
19.	Naka H, Nomura E, Takahashi T, et al. Plasma total homocysteine levels are associated with advanced leukoaraiosis but not with asymptomatic microbleeds on T2*-weighted MRI in patients with stroke. Eur J Neurol, 2006, 13(3): 261-265.
20.	Shoamanesh A, KwokCS, Benavente O. Cerebral microbleeds: histopathological correlation of neuroimaging. Cerebrovasc Dis, 2011, 32(6): 528-534.

1. Pantoni L. Cerebral small vessel disease: from pathogenesis and clinical characteristics to therapeutic challenges. Lancet Neurol, 2010, 9(7): 689-701.
2. Wardlaw JM, Smith C, Dichgans M. Mechanisms of sporadic cerebral small vessel disease: insights from neuroimaging. Lancet Neurol, 2013, 12(5): 483-497.
3. Gorelick PB, Scuteri A, Black SE, et al. Vascular contributions to cognitive impairment and dementia a statement for healthcare professionals from the American heart association/American stroke association. Stroke, 2011, 42(9): 2672-2713.
4. Valdes Hernandez Mdel C, Morris Z, Dickie DA, et al. Close correlation between quantitative and qualitative assessments of white matter lesions. Neuroepidemiology, 2013, 40(1): 13-22.
5. Jackson CA, Hutchison A, Dennis MS, et al. Differing risk factor profiles of ischemic stroke subtypes evidence for a distinct lacunar arteriopathy?. Stroke, 2010, 41(4): 624-629.
6. Spence JD. Homocysteine-lowering therapy: a role in stroke prevention?. Lancet Neurol, 2007, 6(9): 830-838.
7. Miwa K, Tanaka M, Okazaki S, et al. Increased total homocysteine levels predict the risk of incident dementia independent of cerebral small-vessel diseases and vascular risk factors. J Alzheimers Dis, 2016, 49(2): 503-513.
8. Teo BW, Xu H, Wang DH, et al. GFR estimating equations in a multiethnic Asian population. Am J Kidney Dis, 2011, 58(1): 56-63.
9. Adams HP Jr, Bendixen BH, Kappelle LJ, et al. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment. Stroke, 1993, 24(1): 35-41.
10. Wardlaw JM, Smith EE, Biessels GJ, et al. Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration. Lancet Neurol, 2013, 12(8): 822-838.
11. Fazekas F, Chawluk JB, Alavi A, et al. Mr signal abnormalities at 1.5 T in Alzheimer’s dementia and normal aging. AJR Am J Roentgenol, 1987, 149(2): 351-356.
12. Potter GM, Chappell FM, Morris ZA. Cerebral perivascular spaces visible on magnetic resonance imaging: development of a qualitative rating scale and its observer reliability. Cerebrovasc Dis, 2015, 39(3/4): 224-231.
13. Staals J, Makin SD, Doubal FN, et al. Stroke subtype, vascular risk factors, and total MRI brain small-vessel disease burden. Neurology, 2014, 83(14): 1228-1234.
14. Guo HY, Wang P, You BQ, et al. Chinese yellow wine inhibits production of homocysteine-induced extracellular matrix metalloproteinase-2 in cultured rat vascular smooth muscle cells. Clin Nutr, 2007, 26(3): 348-354.
15. Tian X, Zhao L, Song XJ, et al. HSP27 inhibits homocysteine-induced endothelial apoptosis by modulation of ROS production and mitochondrial caspase-dependent apoptotic pathway. Biomed Res Int, 2016, 2016: 4847874.
16. Dayal S, Arning E, Bottiglieri T, et al. Cerebral vascular dysfunction mediated by superoxide in hyperhomocysteinemic mice. Stroke, 2004, 35(8): 1957-1962.
17. Feng C, Bai X, Xu Y, et al. Hyperhomocysteinemia associates with small vessel disease more closely than large vessel disease. Int J Med Sci, 2013, 10(4): 408-412.
18. Gregoire SM, Smith K, Jäger HR, et al. Cerebral microbleeds and long-term cognitive outcome: longitudinal cohort study of stroke clinic patients. Cerebrovasc Dis, 2012, 33(5): 430-435.
19. Naka H, Nomura E, Takahashi T, et al. Plasma total homocysteine levels are associated with advanced leukoaraiosis but not with asymptomatic microbleeds on T2*-weighted MRI in patients with stroke. Eur J Neurol, 2006, 13(3): 261-265.
20. Shoamanesh A, KwokCS, Benavente O. Cerebral microbleeds: histopathological correlation of neuroimaging. Cerebrovasc Dis, 2011, 32(6): 528-534.

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