2007
DOI: 10.1016/j.ijcard.2006.10.002
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Prognostic importance of troponin T and creatine kinase after elective angioplasty

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Cited by 21 publications
(20 citation statements)
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“…An increase in troponin following PCI has been convincingly shown to indicate myocyte death [3] and as this necrosis occurs secondary to myocardial ischemia, it should accordingly be labeled as myocardial infarction. Previous studies have documented troponin release following intervention in 13 to 66% of patients [1,[4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21]. These studies used either troponin T (TnT) and/or troponin I measurements, with a wide range of cut-offs for determining a significant troponin rise: for TnT, cut-offs ranged between 0.01 and 0.2 ng/ml, including a study by Miller et al using a TnT cutoff of 0.03 ng/ml, in which 41% had an elevation post-PCI [21].…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…An increase in troponin following PCI has been convincingly shown to indicate myocyte death [3] and as this necrosis occurs secondary to myocardial ischemia, it should accordingly be labeled as myocardial infarction. Previous studies have documented troponin release following intervention in 13 to 66% of patients [1,[4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21]. These studies used either troponin T (TnT) and/or troponin I measurements, with a wide range of cut-offs for determining a significant troponin rise: for TnT, cut-offs ranged between 0.01 and 0.2 ng/ml, including a study by Miller et al using a TnT cutoff of 0.03 ng/ml, in which 41% had an elevation post-PCI [21].…”
Section: Introductionmentioning
confidence: 99%
“…Troponin elevation following PCI is an important predictor of adverse in-hospital cardiac events including death, acute myocardial infarction and target lesion revascularization [4,5,13,14], as well as longer-term adverse outcomes including readmission for angina and acute myocardial infarction [6], repeat PCI, bypass surgery and cardiac death up to one year following intervention [5,10,14,17,25,26]. There is conflicting evidence from a study by Cavallini et al, in which cardiac troponin elevation following PCI did not influence two-year mortality [18], and Miller et al finding those with late elevations in TnT post-PCI were associated with a small increase of only in-hospital mortality, but not long-term events [21].…”
Section: Introductionmentioning
confidence: 99%
“…The design of our study includes the advantage of pre-and post-procedural biomarker measurement, allowing for the potential that hsTn I measurement may identify new, significant myocardial necrosis as early as the conclusion of the procedure. Some have indeed argued that much of the risk associated with peri-procedural troponin elevation is due to myocardial necrosis prior to the procedure [26] while others argue that post-procedure troponin elevation may strongly predict future clinical outcomes [27]; there is thus uncertainty regarding the appropriate interpretation of elevated troponin after revascularization.…”
Section: Discussionmentioning
confidence: 99%
“…Post-procedural elevations of cTns levels occur in 5% to 50% of subjects undergoing percutaneous coronary intervention (PCI) (Califf et al, 1998). The association between cTns elevation after elective PCI and cardiac events is conflicted during the follow-up (Fuchs et al, 2000;Nallamothu et al, 2003;Ramírez-Moreno et al, 2004;Prasad et al, 2006;Nienhuis et al, 2007;Milani et al, 2009).…”
Section: Introductionmentioning
confidence: 99%