TY - JOUR
T1 - Serum C-reactive protein elevation predicts poor clinical outcome in patients with distal type acute aortic dissection
T2 - Association with the occurrence of oxygenation impairment
AU - Sugano, Yasuo
AU - Anzai, Toshihisa
AU - Yoshikawa, Tsutomu
AU - Satoh, Toru
AU - Iwanaga, Shiro
AU - Hayashi, Takeharu
AU - Maekawa, Yuichiro
AU - Shimizu, Hideyuki
AU - Yozu, Ryohei
AU - Ogawa, Satoshi
PY - 2005/6/22
Y1 - 2005/6/22
N2 - Background: Acute aortic dissection (AAD) is sometimes complicated by respiratory failure due to severe lung oxygenation impairment. Systemic activation of inflammatory system after aortic injury may play some roles in the development of this complication. The aim of this study was to determine the significance of serum C-reactive protein (CRP) elevation in the development of oxygenation impairment and clinical outcome with distal type AAD. Methods and results: A total of 61 patients, who were admitted with distal type AAD within 24 h from the onset, were examined. Serum CRP levels, white blood cell (WBC) counts and body temperature were measured serially for at least 4 days. Oxygenation impairment, defined as the lowest PaO2/FIO2 ratio ≤200 mmHg, was noted in 31 patients (51%). In patients with oxygenation impairment, peak CRP levels (20.7±7.9 vs. 12.7±3.8 mg/dl, P<0.001), peak WBC counts (14,600±3600 vs. 11,800±4300/mm 3, P=0.008) and body temperature (38.4±0.5 vs. 38.0±0.6 °C, P=0.004) were significantly higher than those without. Peak CRP level was inversely correlated with the lowest PaO2/FIO2 (P<0.001). Patients who underwent urgent surgical treatment and/or died in the hospital had higher peak CRP levels (25.1±12.3 vs. 16.1±7.4 mg/dl, P=0.010) than those who did not. Multivariate analysis revealed that a peak CRP level ≥15 mg/dl (relative risk=12.6, P<0.001) was an independent determinant of the development of oxygenation impairment. Conclusion: The greater serum CRP elevation after distal type AAD was associated with a higher incidence of oxygenation impairment and poor clinical outcome. Systemic activation of the inflammatory system after aortic injury may play an important role in the development of oxygenation impairment.
AB - Background: Acute aortic dissection (AAD) is sometimes complicated by respiratory failure due to severe lung oxygenation impairment. Systemic activation of inflammatory system after aortic injury may play some roles in the development of this complication. The aim of this study was to determine the significance of serum C-reactive protein (CRP) elevation in the development of oxygenation impairment and clinical outcome with distal type AAD. Methods and results: A total of 61 patients, who were admitted with distal type AAD within 24 h from the onset, were examined. Serum CRP levels, white blood cell (WBC) counts and body temperature were measured serially for at least 4 days. Oxygenation impairment, defined as the lowest PaO2/FIO2 ratio ≤200 mmHg, was noted in 31 patients (51%). In patients with oxygenation impairment, peak CRP levels (20.7±7.9 vs. 12.7±3.8 mg/dl, P<0.001), peak WBC counts (14,600±3600 vs. 11,800±4300/mm 3, P=0.008) and body temperature (38.4±0.5 vs. 38.0±0.6 °C, P=0.004) were significantly higher than those without. Peak CRP level was inversely correlated with the lowest PaO2/FIO2 (P<0.001). Patients who underwent urgent surgical treatment and/or died in the hospital had higher peak CRP levels (25.1±12.3 vs. 16.1±7.4 mg/dl, P=0.010) than those who did not. Multivariate analysis revealed that a peak CRP level ≥15 mg/dl (relative risk=12.6, P<0.001) was an independent determinant of the development of oxygenation impairment. Conclusion: The greater serum CRP elevation after distal type AAD was associated with a higher incidence of oxygenation impairment and poor clinical outcome. Systemic activation of the inflammatory system after aortic injury may play an important role in the development of oxygenation impairment.
KW - Acute aortic dissection
KW - C-reactive protein
KW - Clinical outcome
KW - Inflammation
KW - Oxygenation impairment
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U2 - 10.1016/j.ijcard.2004.03.076
DO - 10.1016/j.ijcard.2004.03.076
M3 - Article
C2 - 15939097
AN - SCOPUS:20444462035
SN - 0167-5273
VL - 102
SP - 39
EP - 45
JO - International Journal of Cardiology
JF - International Journal of Cardiology
IS - 1
ER -