The impact of intracranial carotid artery calcification on the development of thrombolysis-induced intracerebral hemorrhage

Ting Chun Lin, Tzu Hao Chao, Yao Shieh, Tsong Hai Lee, Yeu Jhy Chang, Jiann Der Lee, Tsung I. Peng, Ku Chou Chang, Chia Wei Liou, Ting Yu Chang, Kuo Lun Hung, Chien Hung Chang

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Abstract

Background: We aimed to assess whether intracranial carotid artery calcification (ICAC) evident on head computed tomography is a risk factor for symptomatic intracerebral hemorrhage (sICH) following tissue plasminogen activator (tPA) treatment for acute stroke. Methods: We classified 297 consecutive patients into 2 groups (no to mild ICAC and moderate to severe ICAC) according to ICAC severity. Outcome measures included detection of intracerebral hemorrhage and assessment using a modified Rankin scale (mRS) at 1 month and 1 year after stroke. Results: ICH (any type) was significantly more common in patients with moderate to severe ICAC than in patients with no to mild ICAC (22.5% versus 12%; relative risk [RR], 1.67; 95% confidence interval [CI], 1.1-2.5; P <.05). The moderate to severe ICAC group tended to have a higher percentage of sICH, but this association was not statistically significant (RR, 1.57; 95% CI,.75-3.3, P >.05). Multivariate adjusted regression analysis revealed that moderate to severe ICAC was an independent risk factor for ICH following tPA treatment (odds ratio, 2.52; 95% CI, 1.07-5.94; P =.04). Dependent functional outcome (mRS score 3-6) at 1-month and 1-year follow-up was significantly associated with moderate to severe ICAC (RR, 1.56; 95% CI, 1.06-2.27; and RR, 1.56; 95% CI, 1.06-2.33; P <.05). However, ICAC was not an independent factor of functional dependency at 1-month and 1-year follow-up in the final multivariate regression model. Conclusion: A significantly higher percentage of patients with moderate to severe ICAC developed ICH following tPA administration for stroke. ICAC severity is an independent risk factor for ICH events. ICAC severity can help predict short-term and long-term functional dependency in tPA-treated patients, although this can be confounded by other cardiovascular risk factors and stroke severity.

Original languageEnglish
JournalJournal of Stroke and Cerebrovascular Diseases
Volume22
Issue number8
DOIs
Publication statusPublished - Nov 1 2013
Externally publishedYes

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Cerebral Hemorrhage
Carotid Arteries
Tissue Plasminogen Activator
Stroke
Confidence Intervals
Odds Ratio
Head
Tomography
Regression Analysis
Outcome Assessment (Health Care)

Keywords

  • acute ischemic stroke
  • intracranial carotid artery calcification
  • Symptomatic intracerebral hemorrhage
  • thrombolytic therapy

ASJC Scopus subject areas

  • Surgery
  • Rehabilitation
  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine

Cite this

The impact of intracranial carotid artery calcification on the development of thrombolysis-induced intracerebral hemorrhage. / Lin, Ting Chun; Chao, Tzu Hao; Shieh, Yao; Lee, Tsong Hai; Chang, Yeu Jhy; Lee, Jiann Der; Peng, Tsung I.; Chang, Ku Chou; Liou, Chia Wei; Chang, Ting Yu; Hung, Kuo Lun; Chang, Chien Hung.

In: Journal of Stroke and Cerebrovascular Diseases, Vol. 22, No. 8, 01.11.2013.

Research output: Contribution to journalArticle

Lin, Ting Chun ; Chao, Tzu Hao ; Shieh, Yao ; Lee, Tsong Hai ; Chang, Yeu Jhy ; Lee, Jiann Der ; Peng, Tsung I. ; Chang, Ku Chou ; Liou, Chia Wei ; Chang, Ting Yu ; Hung, Kuo Lun ; Chang, Chien Hung. / The impact of intracranial carotid artery calcification on the development of thrombolysis-induced intracerebral hemorrhage. In: Journal of Stroke and Cerebrovascular Diseases. 2013 ; Vol. 22, No. 8.
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abstract = "Background: We aimed to assess whether intracranial carotid artery calcification (ICAC) evident on head computed tomography is a risk factor for symptomatic intracerebral hemorrhage (sICH) following tissue plasminogen activator (tPA) treatment for acute stroke. Methods: We classified 297 consecutive patients into 2 groups (no to mild ICAC and moderate to severe ICAC) according to ICAC severity. Outcome measures included detection of intracerebral hemorrhage and assessment using a modified Rankin scale (mRS) at 1 month and 1 year after stroke. Results: ICH (any type) was significantly more common in patients with moderate to severe ICAC than in patients with no to mild ICAC (22.5{\%} versus 12{\%}; relative risk [RR], 1.67; 95{\%} confidence interval [CI], 1.1-2.5; P <.05). The moderate to severe ICAC group tended to have a higher percentage of sICH, but this association was not statistically significant (RR, 1.57; 95{\%} CI,.75-3.3, P >.05). Multivariate adjusted regression analysis revealed that moderate to severe ICAC was an independent risk factor for ICH following tPA treatment (odds ratio, 2.52; 95{\%} CI, 1.07-5.94; P =.04). Dependent functional outcome (mRS score 3-6) at 1-month and 1-year follow-up was significantly associated with moderate to severe ICAC (RR, 1.56; 95{\%} CI, 1.06-2.27; and RR, 1.56; 95{\%} CI, 1.06-2.33; P <.05). However, ICAC was not an independent factor of functional dependency at 1-month and 1-year follow-up in the final multivariate regression model. Conclusion: A significantly higher percentage of patients with moderate to severe ICAC developed ICH following tPA administration for stroke. ICAC severity is an independent risk factor for ICH events. ICAC severity can help predict short-term and long-term functional dependency in tPA-treated patients, although this can be confounded by other cardiovascular risk factors and stroke severity.",
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T1 - The impact of intracranial carotid artery calcification on the development of thrombolysis-induced intracerebral hemorrhage

AU - Lin, Ting Chun

AU - Chao, Tzu Hao

AU - Shieh, Yao

AU - Lee, Tsong Hai

AU - Chang, Yeu Jhy

AU - Lee, Jiann Der

AU - Peng, Tsung I.

AU - Chang, Ku Chou

AU - Liou, Chia Wei

AU - Chang, Ting Yu

AU - Hung, Kuo Lun

AU - Chang, Chien Hung

PY - 2013/11/1

Y1 - 2013/11/1

N2 - Background: We aimed to assess whether intracranial carotid artery calcification (ICAC) evident on head computed tomography is a risk factor for symptomatic intracerebral hemorrhage (sICH) following tissue plasminogen activator (tPA) treatment for acute stroke. Methods: We classified 297 consecutive patients into 2 groups (no to mild ICAC and moderate to severe ICAC) according to ICAC severity. Outcome measures included detection of intracerebral hemorrhage and assessment using a modified Rankin scale (mRS) at 1 month and 1 year after stroke. Results: ICH (any type) was significantly more common in patients with moderate to severe ICAC than in patients with no to mild ICAC (22.5% versus 12%; relative risk [RR], 1.67; 95% confidence interval [CI], 1.1-2.5; P <.05). The moderate to severe ICAC group tended to have a higher percentage of sICH, but this association was not statistically significant (RR, 1.57; 95% CI,.75-3.3, P >.05). Multivariate adjusted regression analysis revealed that moderate to severe ICAC was an independent risk factor for ICH following tPA treatment (odds ratio, 2.52; 95% CI, 1.07-5.94; P =.04). Dependent functional outcome (mRS score 3-6) at 1-month and 1-year follow-up was significantly associated with moderate to severe ICAC (RR, 1.56; 95% CI, 1.06-2.27; and RR, 1.56; 95% CI, 1.06-2.33; P <.05). However, ICAC was not an independent factor of functional dependency at 1-month and 1-year follow-up in the final multivariate regression model. Conclusion: A significantly higher percentage of patients with moderate to severe ICAC developed ICH following tPA administration for stroke. ICAC severity is an independent risk factor for ICH events. ICAC severity can help predict short-term and long-term functional dependency in tPA-treated patients, although this can be confounded by other cardiovascular risk factors and stroke severity.

AB - Background: We aimed to assess whether intracranial carotid artery calcification (ICAC) evident on head computed tomography is a risk factor for symptomatic intracerebral hemorrhage (sICH) following tissue plasminogen activator (tPA) treatment for acute stroke. Methods: We classified 297 consecutive patients into 2 groups (no to mild ICAC and moderate to severe ICAC) according to ICAC severity. Outcome measures included detection of intracerebral hemorrhage and assessment using a modified Rankin scale (mRS) at 1 month and 1 year after stroke. Results: ICH (any type) was significantly more common in patients with moderate to severe ICAC than in patients with no to mild ICAC (22.5% versus 12%; relative risk [RR], 1.67; 95% confidence interval [CI], 1.1-2.5; P <.05). The moderate to severe ICAC group tended to have a higher percentage of sICH, but this association was not statistically significant (RR, 1.57; 95% CI,.75-3.3, P >.05). Multivariate adjusted regression analysis revealed that moderate to severe ICAC was an independent risk factor for ICH following tPA treatment (odds ratio, 2.52; 95% CI, 1.07-5.94; P =.04). Dependent functional outcome (mRS score 3-6) at 1-month and 1-year follow-up was significantly associated with moderate to severe ICAC (RR, 1.56; 95% CI, 1.06-2.27; and RR, 1.56; 95% CI, 1.06-2.33; P <.05). However, ICAC was not an independent factor of functional dependency at 1-month and 1-year follow-up in the final multivariate regression model. Conclusion: A significantly higher percentage of patients with moderate to severe ICAC developed ICH following tPA administration for stroke. ICAC severity is an independent risk factor for ICH events. ICAC severity can help predict short-term and long-term functional dependency in tPA-treated patients, although this can be confounded by other cardiovascular risk factors and stroke severity.

KW - acute ischemic stroke

KW - intracranial carotid artery calcification

KW - Symptomatic intracerebral hemorrhage

KW - thrombolytic therapy

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