ABSTRACT
Elevation of cardiac troponin I [cTnI] is not uncommon after coronary interventions. Many studies tried to find factors responsible for this elevation and its prognosis on short and long term follow up. Whether or not elevation of cardiac troponin post coronary interventions is responsible for early in hospital and late adverse outcome is still under debate. To identify different predictors of cardiac troponin I elevation after coronary interventions, and to assess the relation between cardiac troponin I elevation post coronary interventions and [early and late] adverse clinical outcome. The study included 50 consecutive patients who underwent coronary angioplasty with stenting in the Cardiac Catheterization Laboratory at Benha University Hospital during the period from December 2004 to December 2005. Full medical history and clinical data were obtained from the patients with special emphasis on the major documented risk factors for coronary artery disease [CAD] [age, sex, obesity, smoking, diabetes mellitus, hypertension, hypercholesterolemia, positive family history of CAD], and history of previous myocardial infarction [MI] or anginal attack. Twelve-lead standard surface electrocardiogram [ECG] was done routinely before and after intervention, echocardiography was also done to determine the global left ventricular systolic function, and coronary angiography was done for all patients and angiographic analysis was performed. Stenosis was considered when there was > 75% reduction in luminal diameter at coronary angiography. Quantitative measurements of the target lesion was performed before intervention by measurement of the lesion length, minimal luminal diameter and reference diameter. Percutaneous Coronary Intervention [PCI] was done and stenting for all patients . The procedure was considered successful when the residual stenosis in the dilated segment was less than 20%. Troponin I and CK-MB were measured 2 hours before the procedure and 8 and 24 hours after the procedure by immuno-inhibition based on the change in troponin I and CK-MB level. The patients were divided into 2 groups: Group I: No elevation of cTnI [0.4ng/l] and, Group II: cTnI [>0.4 ng/l], which was subdivided into Group IIA: with elevated cTnI + CK-MB > 25 IU/L, and Group IIB: with elevated cTnI + CK-MB 25 IU/L. New ST depression and T wave abnormalities post procedural were predictive of post procedural elevation of cardiac troponin I after PCI [p < 0.05]. Parameters of quantitative angiographic analysis of the lesions including preprocedural minimal luminal diameter [p < 0.01], diameter stenosis [p < 0.01] and post procedural minimal luminal diameter [p<0.01] and diameter stenosis [p < 0.05] were strongly associated with post procedural cardiac troponin I elevation. Shorter stent length was also associated with cardiac troponin I elevation post cath. [p < 0.01]. Positive predictive value of cardiac troponin I post procedural for early complications was 23.1% and negative predictive value was l00%. Concordant cardiac troponin I and CK-MB elevation post procedural were strong predictors for early in hospital complications [p<0.01]. Positive predictive value for concordant cTnI and CK-MB elevation for early complications was 60% and negative predictive value was 100%. No association was found between cardiac troponin 1 elevation post cath or concordant elevation of cardiac troponin I and CK-MB elevation with late adverse clinical outcome