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C-reactive protein and lesion morphology in patients with acute myocardial infarction
Toshihiko Sano1, Atsushi Tanaka, Masashi Namba
1Baba Memorial Hospital, Sakai, Japan.
Insights
Elevated C-reactive protein (CRP) in acute myocardial infarction (AMI) patients is linked to ruptured plaque. This suggests CRP may indicate plaque inflammation during AMI.
Area of Science:
- Cardiology
- Biomarkers
- Medical Imaging
Background:
- Elevated C-reactive protein (CRP) is clinically significant in managing acute coronary syndromes.
- Limited in vivo studies explore the link between lesion morphology and CRP in acute myocardial infarction (AMI).
Purpose of the Study:
- To investigate the relationship between lesion morphology, assessed by intravascular ultrasound (IVUS), and CRP levels during the acute phase of AMI.
Main Methods:
- Studied 90 consecutive AMI patients undergoing preintervention IVUS within 6 hours of symptom onset.
- Divided patients into elevated (>=3 mg/L) and normal CRP groups.
- Analyzed lesion morphology using IVUS and correlated with CRP levels.
Main Results:
- Significantly more plaque rupture observed in the elevated CRP group (70%) compared to the normal CRP group (43%, P=0.01).
- Multivariate logistic regression showed ruptured plaque independently correlated with elevated serum CRP (P=0.02; OR, 3.35).
Conclusions:
- Elevated CRP levels in AMI may be associated with the presence of ruptured plaque.
- Suggests elevated CRP reflects the inflammatory activity of ruptured plaque in AMI.
Background:
Elevated serum C-reactive protein (CRP) is of clinical significance in the management of acute coronary syndromes, but there have been few in vivo studies detailing the relation between lesion morphology and elevated CRP in the setting of acute myocardial infarction (AMI). In this study, we investigated the relation between lesion morphology as seen under preintervention intravascular ultrasound (IVUS) and CRP in the acute phase of AMI.
Methods And Results:
Our patient population comprised 90 consecutive patients with AMI who underwent preintervention IVUS within 6 hours of the onset of symptoms. Patients were divided into an elevated CRP group (> or =3 mg/L) or a normal CRP group on the basis of serum CRP levels. There were no differences in patient characteristics or angiographic findings. We observed significantly more plaque rupture in the elevated CRP group than in the normal CRP group (70% versus 43%, P=0.01). A multivariate logistic regression model revealed that the presence of ruptured plaque alone correlated with elevation of serum CRP (P=0.02; odds ratio, 3.35; 95% CI, 1.22 to 9.18).
Conclusions:
Elevated CRP may be related to the presence of ruptured plaque. Our results suggest that in the setting of AMI, elevated CRP levels may reflect the inflammatory activity of a ruptured plaque.
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