Association between Serum C-Reactive Protein Elevation and Left Ventricular Thrombus Formation after First Anterior Myocardial Infarction

Toshihisa Anzai, Tsutomu Yoshikawa, Hidehiro Kaneko, Yuichiro Maekawa, Shiro Iwanaga, Yasushi Asakura, Satoshi Ogawa

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Study objectives: Most left ventricular (LV) thrombi that occur after acute myocardial infarction (AMI) are formed within 2 weeks, when inflammatory cells have infiltrated into the necrotic myocardium. Inflammatory changes on the endocardial surface may induce platelet deposition and fibrin net formation through interaction with proinflammatory cytokines. We sought to determine the significance of the inflammatory response reflected by serum C-reactive protein (CRP) elevation in LV thrombus formation after AMI. Design: We examined 160 patients with first anterior AMI. Peak serum creatine kinase (CK) and CRP levels were determined by serial measurements. Echocardiography was performed 10 to 14 days after the onset. We assessed the association between the elevation of serum CRP levels and LV thrombus formation after AMI. Results: LV thrombus was observed in 13 patients (8%). There was no difference in age, sex, coronary risk factors, preinfarction angina, use of revascularization therapy and anticoagulant therapy, platelet count, and fibrinogen level on hospital admission between the two groups. The mean (± SD) peak serum CRP level was markedly increased in patients with LV thrombus compared to those without (18.0 ± 12.6 vs 9.4 ± 8.1 mg/dL; p = 0.001), despite their having similar peak CK levels. Multivariate analysis showed that a peak CRP level of ≥ 20 mg/dL was an independent predictor of thrombus formation (relative risk, 4.82; p = 0.037) among variables including older age (≥ 60 years old), peak CK level (≥ 3,000 IU/L), and peak WBC count (≥ 12,000 cells/μL). Conclusion: A greater elevation of serum CRP level was associated with a higher incidence of LV thrombus after AMI, suggesting an important role of the inflammatory response in mural thrombus formation.

Original languageEnglish
Pages (from-to)384-389
Number of pages6
JournalChest
Volume125
Issue number2
DOIs
Publication statusPublished - 2004 Feb

Fingerprint

C-Reactive Protein
Blood Proteins
Thrombosis
Myocardial Infarction
Creatine Kinase
Unstable Angina
Fibrin
Platelet Count
Anticoagulants
Fibrinogen
Echocardiography
Myocardium
Blood Platelets
Multivariate Analysis
Cytokines
Incidence
Therapeutics
Serum

Keywords

  • C-reactive protein
  • Inflammation
  • Mural thrombosis
  • Myocardial infarction
  • Remodeling

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Association between Serum C-Reactive Protein Elevation and Left Ventricular Thrombus Formation after First Anterior Myocardial Infarction. / Anzai, Toshihisa; Yoshikawa, Tsutomu; Kaneko, Hidehiro; Maekawa, Yuichiro; Iwanaga, Shiro; Asakura, Yasushi; Ogawa, Satoshi.

In: Chest, Vol. 125, No. 2, 02.2004, p. 384-389.

Research output: Contribution to journalArticle

Anzai, T, Yoshikawa, T, Kaneko, H, Maekawa, Y, Iwanaga, S, Asakura, Y & Ogawa, S 2004, 'Association between Serum C-Reactive Protein Elevation and Left Ventricular Thrombus Formation after First Anterior Myocardial Infarction', Chest, vol. 125, no. 2, pp. 384-389. https://doi.org/10.1378/chest.125.2.384
Anzai, Toshihisa ; Yoshikawa, Tsutomu ; Kaneko, Hidehiro ; Maekawa, Yuichiro ; Iwanaga, Shiro ; Asakura, Yasushi ; Ogawa, Satoshi. / Association between Serum C-Reactive Protein Elevation and Left Ventricular Thrombus Formation after First Anterior Myocardial Infarction. In: Chest. 2004 ; Vol. 125, No. 2. pp. 384-389.
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AU - Anzai, Toshihisa

AU - Yoshikawa, Tsutomu

AU - Kaneko, Hidehiro

AU - Maekawa, Yuichiro

AU - Iwanaga, Shiro

AU - Asakura, Yasushi

AU - Ogawa, Satoshi

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N2 - Study objectives: Most left ventricular (LV) thrombi that occur after acute myocardial infarction (AMI) are formed within 2 weeks, when inflammatory cells have infiltrated into the necrotic myocardium. Inflammatory changes on the endocardial surface may induce platelet deposition and fibrin net formation through interaction with proinflammatory cytokines. We sought to determine the significance of the inflammatory response reflected by serum C-reactive protein (CRP) elevation in LV thrombus formation after AMI. Design: We examined 160 patients with first anterior AMI. Peak serum creatine kinase (CK) and CRP levels were determined by serial measurements. Echocardiography was performed 10 to 14 days after the onset. We assessed the association between the elevation of serum CRP levels and LV thrombus formation after AMI. Results: LV thrombus was observed in 13 patients (8%). There was no difference in age, sex, coronary risk factors, preinfarction angina, use of revascularization therapy and anticoagulant therapy, platelet count, and fibrinogen level on hospital admission between the two groups. The mean (± SD) peak serum CRP level was markedly increased in patients with LV thrombus compared to those without (18.0 ± 12.6 vs 9.4 ± 8.1 mg/dL; p = 0.001), despite their having similar peak CK levels. Multivariate analysis showed that a peak CRP level of ≥ 20 mg/dL was an independent predictor of thrombus formation (relative risk, 4.82; p = 0.037) among variables including older age (≥ 60 years old), peak CK level (≥ 3,000 IU/L), and peak WBC count (≥ 12,000 cells/μL). Conclusion: A greater elevation of serum CRP level was associated with a higher incidence of LV thrombus after AMI, suggesting an important role of the inflammatory response in mural thrombus formation.

AB - Study objectives: Most left ventricular (LV) thrombi that occur after acute myocardial infarction (AMI) are formed within 2 weeks, when inflammatory cells have infiltrated into the necrotic myocardium. Inflammatory changes on the endocardial surface may induce platelet deposition and fibrin net formation through interaction with proinflammatory cytokines. We sought to determine the significance of the inflammatory response reflected by serum C-reactive protein (CRP) elevation in LV thrombus formation after AMI. Design: We examined 160 patients with first anterior AMI. Peak serum creatine kinase (CK) and CRP levels were determined by serial measurements. Echocardiography was performed 10 to 14 days after the onset. We assessed the association between the elevation of serum CRP levels and LV thrombus formation after AMI. Results: LV thrombus was observed in 13 patients (8%). There was no difference in age, sex, coronary risk factors, preinfarction angina, use of revascularization therapy and anticoagulant therapy, platelet count, and fibrinogen level on hospital admission between the two groups. The mean (± SD) peak serum CRP level was markedly increased in patients with LV thrombus compared to those without (18.0 ± 12.6 vs 9.4 ± 8.1 mg/dL; p = 0.001), despite their having similar peak CK levels. Multivariate analysis showed that a peak CRP level of ≥ 20 mg/dL was an independent predictor of thrombus formation (relative risk, 4.82; p = 0.037) among variables including older age (≥ 60 years old), peak CK level (≥ 3,000 IU/L), and peak WBC count (≥ 12,000 cells/μL). Conclusion: A greater elevation of serum CRP level was associated with a higher incidence of LV thrombus after AMI, suggesting an important role of the inflammatory response in mural thrombus formation.

KW - C-reactive protein

KW - Inflammation

KW - Mural thrombosis

KW - Myocardial infarction

KW - Remodeling

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