Search

Background Elevation of C‐reactive protein ( CRP ) as a marker of vascular inflammation at a late phase of drug‐eluting stent ( DES ) implantation may predict subsequent major adverse cardiac events ( MACE ). Methods and Results In 1234 consecutive patients undergoing DES implantation, CRP was measured both before (baseline) and 8 to 12 months after (late phase) stenting, and the relationship between elevation of CRP (>2.0 mg/L) and subsequent MACE (all cause death, nonfatal myocardial infarction, target lesion revascularization, and other additional revascularization) was assessed. As results, CRP was elevated in 38.0% of patients at baseline and in 23.6% during late phase ( P HR ) for MACE was 1.52 (95% confidence interval [95% CI ] 1.21–1.93, P =0.0004) at baseline versus 4.00 (95% CI 3.16–5.05, P CRP elevation ( HR 3.60, 95% CI : 2.78–4.68, P CKD ) ( HR 1.41, 95% CI : 1.10–1.84, P =0.01), and number of diseased segments ( HR 1.19, 95% CI : 1.08–1.30, P =0.0002) were positive predictors of MACE , whereas statin use ( HR 0.66, 95% CI 0.50–0.87, P =0.003) was a negative predictor. Propensity score–matched analysis also confirmed the effect of late‐phase CRP on MACE ( HR 3.39, 95% CI 2.52–4.56, P CRP elevation, CKD (odds ratio [ OR ] 1.71, 95% CI 1.24–2.36, P =0.001) and baseline CRP elevation ( OR 3.48, 95% CI 2.55–4.74, P DES ( OR 0.59, 95% CI 0.41–0.84, P =0.003) and statin therapy ( OR 0.68, 95% CI 0.47–0.97, P =0.03) were negative predictors. Conclusions Monitoring the late‐phase CRP may be helpful to identify a high‐risk subset for MACE among patients undergoing DES implantation.

Both the presence of peripheral arterial disease and chronic kidney disease has been reported to be independent risk factors associating with poor prognosis. However, the impact of combination of peripheral arterial disease and chronic kidney disease remains unknown.The long-term outcome in 715 consecutive patients who had undergone coronary angiogram for the evaluation of chest pain was analyzed. Patients on haemodialysis were excluded from this analysis. Cohort patients were divided into four groups according to the Ankle Brachial Index (ABI0.9) and glomerular filtration rate (GFR60 mL/min per m(2)): group A (n= 498; ABI0.9, GFR60); B (n = 65, ABI0.9, GFR60); C (n = 99; ABI0.9, GFR60); and D (n = 53; ABI0.9, GFR60). The mean follow-up period was 620 +/- 270 days and evaluated the major cardiac adverse events included survival, stroke, acute coronary syndrome and heart failure.The mean follow-up period was 620 +/- 270 days. Total long-term event was present in 89 patients (groups A-D were 9.4%, 18.5%, 15.2% and 28.3%, respectively). Long-term event rate was 28.3% for patients with the presence of peripheral arterial disease and chronic kidney disease, compared to 9.4% for those without peripheral arterial disease and chronic kidney disease (P0.0001). Kaplan-Meier event-free survival curves also showed that the combination of peripheral arterial disease and chronic kidney disease predicted long-term event rate.The combination of chronic kidney disease and ABI of less than 0.9 undergoing coronary angiogram is strongly associated with long-term event rate.