Acute and subacute silent cerebral infarction in patients before elective coronary intervention

Czech version

Authors: D. Viszlayová ^1,2,3; D. Školoudík ^4,5; M. Brozman ¹; K. Langová ^5,6 ; R. Herzig ⁷; L. Pátrovič ⁸; S. Királová ⁹
Authors‘ workplace: Neurologická klinika FSVaZ UKF a FN Nitra ¹; Neurologická klinika LF UP, Olomouc ²; Neurologická klinika LF UK, Hradec Králové ³; Neurologická klinika 1. LF UK a VFN v Praze ⁴; Centrum vědy a výzkumu, FZV UP, Olomouc ⁵; Ústav lekářské biofyziky, LF UP, Olomouc ⁶; Komplexní cerebrovaskulární centrum, Neurologická klinika LF UK a FN Hradec Králové ⁷; Jessenius – diagnostické centrum a. s., Nitra ⁸; Ústav klinickej psychológie, FN Nitra ⁹
Published in: Cesk Slov Neurol N 2018; 81(5): 563-569
Category: Original Paper
doi: https://doi.org/10.14735/amcsnn2018563

Overview

Introduction:
The presence of silent cerebral infarction (SCI) might cause cognitive dysfunction, psychiatric disorders, stroke and earlier mortality. Exact incidence and prevalence of SCI is still not known, the results of previously published clinical trials vary. The aims of our study were to detect acute and subacute SCI using MRI in patients before elective coronary intervention, measure the volume of SCI and investigate the risk factors associated with SCI.

Materials and methods:
Patients indicated for elective coronary angiography, angioplasty or stenting were enrolled in this study. Brain MRI was performed before cardiac intervention. The presence of acute and subacute SCI was evaluated, SCI volume was measured and risk factors associated with SCI were investigated. Cognitive functions were tested and correlated with SCI.

Results:
Between November 2015 and July 2017, 144 patients were enrolled in the study (103 men, 41 women). At least one acute/ subacute SCI was detected on MRI in 9 out of 144 (6.3%) patients before cardiac intervention. History of stroke or transient ischemic attack (TIA) was associated with a higher risk of SCI (p = 0.05). Ipsilateral internal carotid artery stenosis > 50% was diagnosed in one patient. Patients with a history of stroke/ TIA had a larger volume of SCI (p = 0.008). We did not find stastistically significant differences in cognitive function tests between patients with SCI and without SCI (p > 0.05).

Conclusion:
Acute/ subacute SCI was detected in 6.3% of patients indicated for elective coronary intervention. History of stroke or TIA was a predictor of the presence of SCI and also its volume. No correlation was found between SCI and cognitive dysfunction.

Key words:
silent cerebral infarction – magnetic resonance imaging – stroke – coronary angiography – cognitive deficit

The authors declare they have no potential conflicts of interest concerning drugs, products, or services used in the study.

The Editorial Board declares that the manuscript met the ICMJE “uniform requirements” for biomedical papers.

Chinese summary - 摘要

选择性冠状动脉介入治疗前患者急性和亚急性无症状脑梗死

介绍：

无症状脑梗塞（SCI）的存在可能导致认知功能障碍，精神疾病，中风和早期死亡。 SCI的确切发病率和患病率尚不清楚，以前发表的临床试验结果各不相同。我们的研究目的是在选择性冠状动脉介入治疗前使用MRI检测急性和亚急性脊髓损伤，测量脊髓损伤的体积并调查与SCI相关的危险因素。

材料和方法：

选择性冠状动脉造影，血管成形术或支架置入术的患者参加了本研究。在心脏介入前进行脑MRI检查。评估急性和亚急性SCI的存在，测量SCI体积并研究与SCI相关的风险因素。测试认知功能并与SCI相关联。

结果：

2015年11月至2017年7月期间，共有144名患者参加了该研究（103名男性，41名女性）。在心脏介入治疗前144例患者中有9例（6.3％）在MRI上检测到至少一例急性/亚急性SCI。中风或短暂性脑缺血发作（TIA）的病史与SCI的高风险相关（p = 0.05）。一名患者诊断出同侧颈内动脉狭窄> 50％。有卒中/TIA病史的患者脊髓损伤量较大（p = 0.008）。我们没有发现SCI患者和没有SCI患者的认知功能测试存在显著差异（p> 0.05）。

结论：

在选择性冠状动脉介入治疗的6.3％患者中检测到急性/亚急性SCI。中风或TIA的病史是SCI存在及其体积的预测因子。 SCI与认知功能障碍之间未发现相关性。

关键词：

无症状脑梗塞 - 磁共振成像 - 中风 - 冠状动脉造影 - 认知缺陷

Sources

1. Fisher CM. Lacunes: small, deep cerebral infarcts. Neurology 1965; 15(8): 774–784. doi: 10.1212/ WNL.15.8.774.

2. Sacco RL, Kasner SE, Broderick JP et al. An updated definition of stroke for the 21st century: a statement for healthcare professional from the American Heart Association/ American Stroke Association. Stroke 2013; 44(7): 2064–2089. doi: 10.1161/ STR.0b013e318296aeca.

3. Avdibegovic E, Becirovic E, Salimbasic Z et al. Cerebral cortical atrophy and silent brain infarcts in psychiatric patients. Psychiatr Danub 2007; 19(1–2): 49–55.

4. Price TR, Manolio TA, Kronnal RA et al. Silent brain infarction on magnetic resonance imaging and neurological abnormalities in community-dwelling older adults. The cardiovascular health study. CHS Collaborative Research Group. Stroke 1997; 28(6): 1158–1164. doi: 10.1161/ 01.STR.28.6.1158.

5. Liebetrau M, Steen B, Hamann GF et al. Silent and symptomatic infarcts on cranial computerized tomography in relation to dementia and mortality: a population-based study in 85-year-old subjects. Stroke 2004; 35(8): 1816–1820. doi: 10.1161/ 01.STR.0000131928.47478.44.

6. Song IU, Kim JS, Kim YI et al. Clinical signifikance of silent cerebral infarctions in patiens with Alzheimer disease. Cogn Behav Neurol 2007; 20(2): 93–98. doi: 10.1097/ WNN.0b013e31805d859e.

7. Wright CB, Festa JR, Paik MC et al. White matter hyperintensities and subclinical infarction: associations with psychomotor speed and cognitive flexibility. Stroke 2008; 39(3): 800–805. doi: 10.1161/ STROKEAHA.107.484147.

8. Fujikawa T, Yamawaki S, Touhouda Y. Silent cerebral infarctions in patiens with late-onset mania. Stroke 1995; 26(6): 946–949. doi: 10.1161/ 01.STR.26.6.946.

9. Hamada T, Murata T, Omori M et al. Abnormal nocturnal blood pressure fall in senile-onset depression with subcortical silent cerebral infarction. Neuropsycho-biology 2003; 47(4): 187–191. doi: 10.1159/ 000071213.

10. Yamashita H, Fujikawa T, Yanai I et al. Cognitive dysfunction in recovered depressive patiens with silent cerebral infarction. Neuropsychobiology 2002; 45(1): 12–18. doi: 10.1159/ 000048667.

11. Bokura H, Kobayashi S, Yamaguchi S et al. Silent brain infarction and subcortical white matter lesions increase the risk of stroke and mortality: a prospective cohort study. J Stroke Cerebrovasc Dis 2006; 15(2): 57–63. doi: 10.1016/ j.jstrokecerebrovasdis.2005.11.001.

12. Kobayashi S, Okada K, Koide H et al. Subcortical silent brain infarction as a risk factor for clinical stroke. Stroke 1997; 28(10): 1932–1939. doi: 10.1161/ 01.STR.28.10.1932.

13. Putaala J, Haapaniemi E, Kurkinen M et al. Silent brain infarcts, leukoaraiosis, and long-term prognosis in young ischemic stroke patients. Neurology 2011; 76(20): 1742–1749. doi: 10.1212/ WNL.0b013e31821a44ad.

14. Vermeer SE, Hollander M, van Dijk EJ et al. Silent brain infarcts and white matter lesions increase strokerisk in the general population: the Rotterdam scan study. Stroke 2003; 34(5): 1126–1129. doi: 10.1161/ 01.STR.0000068408.82115.D2.

15. Longstreth WT, Dulberg C, Manolio TA et al. Incidence, manifestations, and predictors of brain infarcts defined by serial cranial magnetic resonance imaging in the elderly: the cardiovascular health study. Stroke 2002; 33: 2376–2382. doi: 10.1161/ 01.STR.0000032241.58727.49.

16. Faning JP, Wong AA, Fraser JF. The epidemiology of silent brain infraction: a systematic review of population-based cohorts. BMC Med 2014; 12: 119. doi: 10.1186/ s12916-014-0119-0.

17. Smith E, Saposnik G, Biessels GJ et al. Prevention of stroke in patients with silent cerebrovascular disease. a scientific statement for healthcare prof-fesionals from the American Heart Association/ American Stroke Association. Stroke 2017; 48(2): e44–e71. doi: 10.1161/ STR.0000000000000116.

18. American College of Radiology. ACR-ASNR-SPRpractice parameter for the performance and interpretation of magnetic resonance imaging of the brain. [online]. Available from URL: https:/ / www.acr.org/ -/ media/ ACR/ Files/ Practice-Parameters/ MR-Brain.pdf.

19. Zhu YC, Dufouil C, Tzourio C et al. Silent brain infarcts: a review of MRI diagnostic criteria. Stroke 2011; 42(4): 1140–1145. doi: 10.1161/ STROKEAHA.110.600114.

20. Marks MP, de Crespigny A, Lentz D et al. Acute and chronic stroke: navigated spin-echo diffusion-weighted MR imaging. Radiology 1996; 199(2): 403–408. doi: 10.1148/ radiology.199.2.8668785.

21. Bokura H, Kobayashi S, Yamaguchi S et al. Distinguishing silent lacunar infarction from enlarged Virchow-Robin spaces: a magnetic resonance imaging and pathological study. J Neurol 1998; 245: 116–122.

22. Inoue M, Mlynash M, Christensen S et al. Early diffusion-weighted imaging reversal after endovascular reperfusion is typically transient in patients imaged 3 to 6 hours after onset. Stroke 2014; 45(4): 1024–1028. doi: 10.1161/ STROKEAHA.113.002135.

23. Campbell B, Purushotham A, Christensen S et al. For the epithet–defuse investigators. The infarct core is well represented by the acute diffusion lesion: sustained reversal is infrequent. J Cereb Blood Flow Metab 2012; 32(1): 50–56. doi: 10.1038/ jcbfm.2011.102.

24. Allen L, Hasso AN, Handwerker J et al. Sequence-specific MR imaging findings that are useful in dating ischemic stroke. Radiographics 2012; 32(5): 1285–1297. doi: 10.1148/ rg.325115760.

25. Srinivasan A, Goyal M, Al Azri F et al. State-of-the-art imaging of acute stroke. Radiographics 2006; 26 (Suppl 1): S75–S95. doi: 10.1148/ rg.26si065501.

26. Viszlayová D, Brozman M, Langová K et al. Sonolysis in risk reduction of symptomatic and silent brain infarctions during coronary stenting (SONOREDUCE): randomized, controlled trial. Int J Cardiol 2018; 267: 62–67. doi: 10.1016/ j.ijcard.2018.05.101.

27. Vermeer SE, Longstreth WT Jr, Koudstall PJ. Silent brain infarcts: a systematic review. Lancet Neurol 2007; 6(7): 611–619. doi: 10.1016/ S1474-4422(07)70170-9.

28. Sato H, Koretsune Y, Fukunami M et al. Aspirin attenuates the incidence of silent brain lesions in patiens with nonvalvular atrial fibrillation. Circ J 2004; 68(5): 410–416.

29. EAFT Study Group. Silent brain infarction in nonrheumatic atrial fibrillation: European atrial fibrillation trial. Neurolog 1996; 46(1): 159–165.

30. Ezekowitz MD, James KE, Nazarian SM et al. Silent cerebral infarction in patiens with nonrheumatic atrial fibrillation. Circulation 1995; 92(8): 2178–2182.

31. Siachos T, Vanbakel A, Feldman DS et al. Silent strokes in patiens with heart failure. J Card Fail 2005; 11(7): 485–489. doi: 10.1016/ j.cardfail.2005.04.004.

32. Kozdag G, Ciftci E, Ural D et al. Silent cerebral infarction in chronic heart failure: ischemic and nonischemic dilated cardiomyopathy. Vasc Health Risk Manag 2008; 4(2): 463–469.

33. Yamada K, Nagakane Y, Sasajima H et al. Incidental acute infarcts identified on diffusionweighted images: a university hospital-based study. AJNR Am J Neuroradiol 2008; 29(5): 937–940. doi: 10.3174/ ajnr.A1028.

34. Saini M, Ikram K, Hilal S et al. Silent stroke not listened to rather than silent. Stroke 2012; 43(11): 3102–3104. doi: 10.1161/ STROKEAHA.112.666461.

35. ClinicalTrials.gov. Effects of TIVA with propofol versus inhalational anaesthesia on postoperative pain after hepatectomy. [online]. Available from: http:/ / clinicaltrials.gov/ ct2/ show/ .

36. Bernick C, Kuller L, Dulberg C et al. Silent MRI infarcts and the risk of future stroke: the cardiovascular health study. Cardiovascular health study collaborative reseach group. Neurology 2001; 57(7): 1222–1229.

37. Weber R, Weimar C, Wanke I et al. Risk of recurrent stroke in patiens with silent brain infarction in the PRoFESS imaging substudy. Stroke 2012; 43(2): 350–355. doi:10.1161/ STROKEAHA.111.631739.

38. Lee EJ, Kank DW, Warach S. Silent new brain lesions: innocent bystander or guilty party? J Stroke 2016; 18(1): 38–49. doi: 10.5853/ jos.2015.01410.

39. Kang DW, Latour LL, Chalela JA et al. Early ischemic lesion recurrence within a week after acute ischemic stroke. Ann Neurol 2003; 54(1): 66–74. doi: 10.1002/ ana.10592.

40. Kang DW, Latour LL, Chalela JA et al. Early and late recurrence of ischemic lesion on MRI: evidence for a prolonged stroke-pronestate? Neurology 2004; 63(12): 2261–2265.

41. Kang DW, Lattimore SU, Latour LL et al. Silent ischemic lesion recurrence on magnetic resonance paging predicts subsequent clinical vascular events. Arch Neurol 2006; 63(12): 1730–1733. doi: 10.1001/ archneur.63.12.1730.

42. Nolte CH, Albach FN, Heuschmann PU et al. Silent new DWI lesions with in the first week after stroke. Cerebrovasc Dis 2012; 33(3): 248–254. doi: 10.1159/ 000334665.

43. Král M, Šaňák D, Školoudík D et al. Kardioembolizace je nejčastější příčinou akutní ischemické cévní mozkové příhody u pacientů přijatých do Komplexního cerebrovaskulárního centra do 12 hodin od začátku příznaků –výsledky studie HISTORY. Cesk Slov Neurol N 2016, 79/ 112(1): 61–67. doi: 10.14735/ amcsnn201661.