Cystatin C and risk of mortality among patients undergoing percutaneous coronary intervention.

AIMS: We tested the prognostic value of cystatin C in patients with documented coronary artery disease (CAD) who underwent percutaneous coronary artery intervention (PCI). We also tested the hypothesis that the incremental predictive value of cystatin C on all-cause mortality was superior to that of glomerular filtration rate (GFR) by the Modification of Diet in Renal Disease (MDRD) formula. METHODS AND RESULTS: Included in the study were 2,757 patients (mean age 63 years, 77% men). Blood samples for cystatin C levels were collected immediately before PCI. During a median follow-up of two years, 114 patients died. In multivariable Cox analyses, after adjustment for several confounders, GFR (p=0.004) and cystatin C concentration (p<0.0001) were independent predictors of all-cause death. Cystatin C predicted all-cause death (c-statistic: 0.794) better than GFR estimate based on creatinine (c-statistic: 0.776, p=0.008 for comparison), and significantly reclassified 15% of patients into categories that reflected their actual likelihood of death more accurately (p=0.005). Adding cystatin C and GFR in the same multivariable survival model, only cystatin C level was a significant predictor of death. CONCLUSIONS: This study presents for the first time the incremental predictive value of cystatin C over the creatinine-based MDRD formula on all-cause mortality for CAD patients undergoing PCI.

Prognostic value of isolated troponin I elevation after percutaneous coronary intervention.

BACKGROUND: Mild elevations of cardiac troponin are frequent after percutaneous coronary intervention (PCI). Their prognostic value is uncertain in the absence of changes in creatine kinase-MB (CK-MB). METHODS AND RESULTS: We evaluated the relation between isolated elevations of cardiac troponin I (cTnI) and all-cause mortality. We studied 3494 consecutive patients who underwent PCI in 16 Italian tertiary cardiology centers. CK-MB and cTnI were analyzed in a central laboratory. Duration of follow-up was 2 years. The present analysis was restricted to 2362 patients with normal CK-MB and cTnI values at baseline and no CK-MB elevation after PCI. A rise in cTnI after PCI >0.15 ng/mL, the upper reference limit, was found in 932 patients (39.4%). A rise >0.45 ng/mL (>3×upper reference limit) was found in 467 patients (19.7%). Compared with patients with normal cTnI, those with cTnI elevation >0.15 ng/mL showed a slightly increased mortality (3.8% versus 2.6%; hazard ratio, 1.53; 95% confidence interval, 0.97 to 2.42; P=0.069). A cTnI elevation >0.45 ng/mL was associated with a higher risk of mortality (4.5% versus 2.7%; hazard ratio, 1.68; 95% confidence interval, 1.01 to 2.80; P=0.044), which, however, did not remain significant after adjustment for concomitant risk factors (hazard ratio, 1.45; 95% confidence interval, 0.86 to 2.46; P=0.162). Postprocedural cTnI elevation was associated with coronary and clinical features consistent with a worse risk profile. CONCLUSIONS: In the absence of a rise in CK-MB, elevated cTnI levels after PCI are associated with a modest increased risk of death. However, this is not independent of the concomitant adverse baseline clinical characteristics of these patients.

Impact of acute renal failure following percutaneous coronary intervention on long-term mortality.

BACKGROUND: Acute renal failure (ARF) following percutaneous coronary intervention (PCI) has been shown to be associated with a worse outcome. Whether this event should be considered as a marker of disease severity or an independent contributor to mortality is still unclear. METHODS: In a multicenter, prospective cohort study we investigated the predictive variables and the impact of postprocedural ARF on 2-year all-cause mortality in 2860 consecutive patients (50% with stable angina and 50% with non-ST-elevation acute coronary syndromes) undergoing PCI. Serum creatinine determinations were made immediately before and 24 h after PCI. ARF was defined as an increase in serum creatinine of > or =0.5 mg/dl over baseline. RESULTS: One hundred and six patients (3.7%) experienced ARF. At logistic regression analysis, ARF was associated with pre-existing low values of estimated glomerular filtration rate, reduced left ventricular ejection fraction, hypertension, and prior coronary bypass surgery. Mortality data at 2 years were available for all patients: 119 patients (4.16%) had died, 3.9% of those without and 11.3% of those with ARF (univariate hazard ratio 3.16; 95% confidence interval 1.68-5.94; P = 0.0004). At Cox regression analysis, the significant predictors of mortality were age, ejection fraction, preprocedural estimated glomerular filtration rate, PCI failure, atrial fibrillation, diabetes mellitus, and fluoroscopy time. In this comprehensive mortality model, ARF maintained a borderline statistical significance (hazard ratio 1.83, 95% confidence interval 0.98-3.44; P = 0.06). CONCLUSIONS: ARF following PCI occurs almost exclusively in patients with chronic kidney disease or left ventricular dysfunction. These risk factors are also among the most powerful predictors of long-term mortality and are likely to explain most of the association between postprocedural ARF and long-term mortality. After correction for clinical determinants, however, postprocedural ARF maintains a clinically significant impact on mortality that must be taken into account for benefit vs. risk evaluation of PCI in individual patients.

Impact of the elevation of biochemical markers of myocardial damage on long-term mortality after percutaneous coronary intervention: results of the CK-MB and PCI study.

AIMS: Retrospective studies and post hoc analyses have suggested that mild elevations in the creatine kinase-MB (CK-MB) isoenzyme following percutaneous coronary intervention (PCI) may be associated with an increased risk of death in the long term. However, this finding is still controversial, and the prognostic significance of elevations of more sensitive markers of myocardial damage, such as the cardiac troponins, has not been established. In this multicentre prospective cohort study, we evaluated the influence of post-procedural elevations of CK-MB and troponin I (cTnI) on long-term mortality. METHODS AND RESULTS: The CK-MB and PCI study included 3494 consecutive patients undergoing PCI from February 2000 to October 2000 in 16 Italian tertiary centres. Blood samples were collected at baseline, and at 8-12 and 18-24 h after the procedure, and were analysed in a core biochemistry laboratory. CK-MB elevation was detected in 16% of the patients, and was associated with increased 2-year mortality [7.2 vs. 3.8%; odds ratio (OR): 1.9; 95% confidence interval (CI): 1.3-2.8; P<0.001). The degree of CK-MB elevation (peak CK-MB ratio) independently predicted the risk of death (adjusted OR per unit: 1.04; 95% CI: 1.01-1.07; P=0.009). A cTnI elevation was detected in 44.2% of the cases and was not associated with a significant increase in mortality (4.9 vs. 4.0%; OR: 1.2; 95% CI: 0.9-1.7; P=0.2). CONCLUSION: Post-procedural elevations of CK-MB, but not cTnI, influence 2-year mortality.