Cardiovasc Prev Pharmacother.  2023 Oct;5(4):144-150. 10.36011/cpp.2023.5.e14.

Variation in blood viscosity based on the potential cause of stroke of undetermined etiology

• Oh J
• Jung Y
• Kim J
• Min SK
• Han SW
• Baik JS

• KMID: 2547305
• DOI: http://doi.org/10.36011/cpp.2023.5.e14

Abstract

Background
This study investigated potential differences in blood viscosity (BV) among patients with stroke of undetermined etiology, negative evaluation (SUDn), specifically those with potential atherothrombosis (SUDn-AT) and those with possible embolism (SUDn-E).
Methods
This single-center study employed a retrospective observational design. The participants were patients over 20 years old with the SUDn stroke subtype who were admitted within 5 days of symptom onset. These patients were categorized as SUDn-AT or SUDn-E. Patients in the SUDn-AT group had nonsignificant stenosis (<50%) of a major brain artery relevant to their symptoms and exhibited one or more signs of systemic atherosclerosis, including atherosclerosis of at least one major brain artery other than those clinically relevant, coronary artery disease, and/or peripheral artery disease. For the SUDn-E group, the SUDn criteria from the TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification system were strictly applied.
Results
The final analysis included 153 patients, with 104 (68%) classified as SUDn-E and the remaining 32% as SUDn-AT. Patients in the SUDn-AT group had a higher systolic BV (P=0.012) and diastolic BV (P=0.020) than those in the SUDn-E group. Multivariable logistic regression analysis revealed that age (odds ratio [OR], 1.08; 95% confidence interval [CI], 1.03–1.13; P=0.003), systolic BV (OR, 3.11; 95% CI, 1.41–6.85; P=0.005), and diastolic BV (OR, 1.08; 95% CI, 1.02–1.14; P=0.009) were associated with SUDn-AT.
Conclusions
Within the TOAST system, two SUDn entities may be distinguishable, with potentially different underlying etiologies: atherothrombosis and embolic stroke of undetermined source.

Keyword

Blood viscosity; Etiology; Stroke

Reference

1. Adams HP, Bendixen BH, Kappelle LJ, Biller J, Love BB, Gordon DL, 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; 24:35–41.

2. Han SW, Kim SH, Lee JY, Chu CK, Yang JH, Shin HY, et al. A new subtype classification of ischemic stroke based on treatment and etiologic mechanism. Eur Neurol. 2007; 57:96–102.

3. Radu RA, Terecoasa EO, Bajenaru OA, Tiu C. Etiologic classification of ischemic stroke: where do we stand? Clin Neurol Neurosurg. 2017; 159:93–106.

4. Diener HC, Easton JD, Hart RG, Kasner S, Kamel H, Ntaios G. Review and update of the concept of embolic stroke of undetermined source. Nat Rev Neurol. 2022; 18:455–65.

5. Ozcan Cetin EH, Cetin MS, Canpolat U, Kalender E, Topaloglu S, Aras D, et al. The forgotten variable of shear stress in mitral annular calcification: whole blood viscosity. Med Princ Pract. 2015; 24:444–50.

6. Song SH, Kim JH, Lee JH, Yun YM, Choi DH, Kim HY. Elevated blood viscosity is associated with cerebral small vessel disease in patients with acute ischemic stroke. BMC Neurol. 2017; 17:20.

7. Furukawa K, Abumiya T, Sakai K, Hirano M, Osanai T, Shichinohe H, et al. Increased blood viscosity in ischemic stroke patients with small artery occlusion measured by an electromagnetic spinning sphere viscometer. J Stroke Cerebrovasc Dis. 2016; 25:2762–9.

8. Grotemeyer KC, Kaiser R, Grotemeyer KH, Husstedt IW. Association of elevated plasma viscosity with small vessel occlusion in ischemic cerebral disease. Thromb Res. 2014; 133:96–100.

9. Park JH, Kim JY, Baik JS, Park JH, Nam HS, Han SW. Prior antithrombotic use is significantly associated with decreased blood viscosity within 24 hours of symptom onset in patients with acute ischemic stroke. J Neurocrit Care. 2019; 12:85–91.

10. Bhatt DL, Steg PG, Ohman EM, Hirsch AT, Ikeda Y, Mas JL, et al. International prevalence, recognition, and treatment of cardiovascular risk factors in outpatients with atherothrombosis. JAMA. 2006; 295:180–9.

11. Cecchi E, Marcucci R, Poli D, Antonucci E, Abbate R, Gensini GF, et al. Hyperviscosity as a possible risk factor for cerebral ischemic complications in atrial fibrillation patients. Am J Cardiol. 2006; 97:1745–8.

12. Gutierrez J, Turan TN, Hoh BL, Chimowitz MI. Intracranial atherosclerotic stenosis: risk factors, diagnosis, and treatment. Lancet Neurol. 2022; 21:355–68.

13. Banerjee C, Chimowitz MI. Stroke caused by atherosclerosis of the major intracranial arteries. Circ Res. 2017; 120:502–13.

14. Lammie GA, Sandercock PA, Dennis MS. Recently occluded intracranial and extracranial carotid arteries. Relevance of the unstable atherosclerotic plaque. Stroke. 1999; 30:1319–25.

15. Bang OY, Lee PH, Joo SY, Lee JS, Joo IS, Huh K. Frequency and mechanisms of stroke recurrence after cryptogenic stroke. Ann Neurol. 2003; 54:227–34.

16. Watson T, Shantsila E, Lip GY. Mechanisms of thrombogenesis in atrial fibrillation: Virchow's triad revisited. Lancet. 2009; 373:155–66.

17. Lowe GD, Drummond MM, Lorimer AR, Hutton I, Forbes CD, Prentice CR, et al. Relation between extent of coronary artery disease and blood viscosity. Br Med J. 1980; 280:673–4.