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  • Title: Clinical value of plasma pentraxin 3 levels for predicting cardiac troponin elevation after percutaneous coronary intervention.
    Author: Wang Z, Sato A, Akiyama D, Kimura T, Tajiri K, Hoshi T, Sakai S, Koike A, Miyauchi T, Aonuma K.
    Journal: Life Sci; 2014 Jan 24; 95(1):40-4. PubMed ID: 24333560.
    Abstract:
    AIMS: Post-procedural myocardial necrosis manifested by elevated cardiac troponin T (cTnT) often complicates percutaneous coronary intervention (PCI). Plasma pentraxin 3 (PTX3) levels are increased in patients with arterial inflammation and especially unstable angina pectoris (UAP). This study tested whether plasma PTX3 levels can predict post-PCI cTnT elevation. MAIN METHODS: We evaluated 94 consecutive patients with AP and normal pre-PCI cTnT levels who underwent PCI. Pre-PCI virtual histology-intravascular ultrasound was performed to assess culprit plaque composition. Plasma PTX3 and serum hs-CRP levels were measured pre-PCI. Patients were divided into 2 groups according to presence (Group I, n=34) or absence (Group II, n=60) of post-PCI cTnT elevation >3 × the upper limit of normal at 24h after PCI. KEY FINDINGS: Plasma PTX3 (4.06 ± 2.05 ng/ml vs 2.17 ± 1.02 ng/ml, p<0.001), serum hs-CRP levels (0.25 ± 0.03 vs 0.16 ± 0.03 mg/dl, p=0.048), plaque burden (80.9 ± 5.3 vs 75.4 ± 10.6%, p=0.047), presence of positive remodeling (59 vs 25%, p=0.034), and percent necrotic core area (19.0 ± 7.4 vs 14.0 ± 5.9%, p=0.046) were significantly higher in Group I than in Group II. Receiver-operating characteristic curve analysis showed that with a best cut-off value of 2.83 ng/ml, plasma PTX3 level (AUC 0.823) predicted post-PCI cardiac TnT elevation better than did serum hs-CRP level (AUC 0.618). Multiple logistic regression analysis showed that plasma PTX3 level was the most independent predictor of post-PCI cardiac cTnT elevation (OR: 2.65; 95% CI: 1.56-10.1; p=0.003). SIGNIFICANCE: Plasma PTX3 level may be a useful marker for predicting post-PCI cardiac cTnT elevation, which is associated with inflammatory status of culprit lesions.
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