Preprocedural serum levels of C-reactive protein predict early complications and late restenosis after coronary angioplasty
Antonino Buffon, MDa,
Giovanna Liuzzo, MDa,
Luigi M. Biasucci, MD, FACCa,
Patrizio Pasqualetti, PhD*,
Vito Ramazzotti, MDa,
Antonio G. Rebuzzi, MDa,
Filippo Crea, MD, FACCa and
Attilio Maseri, MD, FACCa
a Istituto di Cardiologia, Università Cattolica del Sacro Cuore, Rome, Italy
* A.Fa.R., Ospedale Fetebenefratelli-Isola Tiberina, Rome, Italy
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Figure 1 Incidence of early adverse events by tertiles of CRP, SAA and fibrinogen in patients with stable (open bars) and unstable angina (solid bars). All stable angina patients with early adverse events were in the III tertile of CRP (Mantel-Haenszel test for linear association: p = 0.005) and of SAA (Mantel-Haenszel test for linear association: p = 0.004). Among unstable angina patients, the incidence of early adverse events increased from 0% in the I tertile to 30% in the III tertile of CRP levels (Mantel-Haenszel test for linear association: p = 0.013, respectively) and from 0% in the I tertile to 27% in the III tertile of SAA (Mantel-Haenszel test for linear association: p = 0.044). Fibrinogen levels did not discriminate between stable and unstable patients with or without early adverse events (Mantel-Haenszel test for linear association: p = 0.44 in stable angina and p = 0.48 in unstable angina). The incidence of early adverse events was similar in stable and unstable angina patients in the III tertile of CRP or SAA. CRP = C-reactive protein; SAA = serum amyloid A protein.
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Figure 2 Incidence of clinical restenosis by tertiles of CRP, SAA and fibrinogen in patients with stable (open bars) and unstable angina (solid bars). In stable angina patients, the incidence of restenosis increased from 33% in the I tertile to 86% in the III tertile of CRP and fibrinogen (Mantel-Haenszel test for linear association: p = 0.046) and from 32% in the I tertile to 67% in the III tertile of SAA (p = 0.13). Among the unstable angina patients the incidence of restenosis increased from 25% in the I tertile to 72% in the III tertile of CRP (Mantel-Haenszel test for linear association: p = 0.004) and from 23% in the I tertile to 67% in the III tertile of SAA (Mantel-Haenszel test for linear association: p = 0.010). In patients with unstable angina, fibrinogen levels were not associated with the incidence of restenosis (p = 0.65). The incidence of restenosis was similar in stable and unstable angina patients in the III tertile of CRP or SAA. CRP = C-reactive protein; SAA = serum amyloid A protein.
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Figure 3 Observed incidence of clinical restenosis according to CRP levels and residual diameter stenosis. Elevated levels of CRP (>0.3 mg/dl) (solid bars) compared with low levels (open bars) were associated with higher restenosis rate in patients with  30% residual stenosis (18% vs. 44%) and in patients with >30% residual stenosis (37% vs. 77%). CRP = C-reactive protein.
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Figure 4 Event-free survival from clinical restenosis (panel A) and from major adverse cardiac events (e.g., death, myocardial infarction or need for coronary revascularization) (panel B) at one year by preprocedural levels of CRP (multivariate Cox regression analysis). Among all clinical, angiographic and procedural variables considered, elevated CRP levels were the most powerful independent predictor of clinical restenosis (RR = 2.7, CI = 1.4–5.0, p = 0.002) and of major adverse cardiac events at follow-up (RR = 2.8, CI = 1.4–5.8, p = 0.005). Dotted line = I tertile of CRP levels; dashed line = II tertile of CRP levels; solid line = III tertile of CRP levels. CRP = C-reactive protein.
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