Troponin I concentrations following primary percutaneous coronary intervention predict large infarct size and left ventricular dysfunction in patients with ST-segment elevation acute myocardial infarction

Ohlmann, Patrick; Monassier, Jean‐Pierre; Michotey, Marie Odile; Berenger, Nathalie; Jacquemin, L.; Laval, G; Roul, G.; Schneider, Francis

doi:10.1016/s0021-9150(03)00027-3

Cited by 25 publications

(26 citation statements)

References 22 publications

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“…15,16 Ohlmann et al 15 were able to demonstrate a significant correlation between infarct size and cTnI levels as early as 3 hours after primary percutaneous coronary intervention. In our study, infarct size, as estimated by the concentration of cTnI also 3 hours after thrombolysis, was the major determinant for the presence of several degradation products.…”

Section: Discussionmentioning

confidence: 98%

“…Previous studies have shown a correlation between concentrations of cTnT and cTnI and infarct size, suggesting levels 72 hours after AMI the most specific for evaluating infarct size using commercial tests that may or may not detect the degradation products. 15,16 Ohlmann et al 15 were able to demonstrate a significant correlation between infarct size and cTnI levels as early as 3 hours after primary percutaneous coronary intervention. In our study, infarct size, as estimated by the concentration of cTnI also 3 hours after thrombolysis, was the major determinant for the presence of several degradation products.…”

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confidence: 98%

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Time Course of Degradation of Cardiac Troponin I in Patients With Acute ST-Elevation Myocardial Infarction

Madsen

Christensen

Lund

et al. 2006

Circulation Research

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Abstract-Although measurement of troponin is widely used for diagnosing acute myocardial infarction (AMI), its diagnostic potential may be increased by a more complete characterization of its molecular appearance and degradation in the blood. The aim of this study was to define the time course of cardiac troponin I (cTnI) degradation in patients with acute ST-elevation myocardial infarction (STEMI). In the ASSENT-2 substudy, 26 males hospitalized with STEMI were randomized to 2 different thrombolytic drugs within 6 hours after onset of symptoms. Blood samples were obtained just before initiation of thrombolysis and at 30 minutes intervals (7 samples per patient). Western blot analysis was performed using anti-cTnI antibodies and compared with serum concentrations of cTnI. All patients exceeded the cTnI cutoff for AMI during the sampling period; at initiation of therapy, 23 had elevated cTnI values. All patients demonstrated 2 bands on immunoblot: intact cTnI and a single degradation product as early as 90 minutes after onset of symptoms. On subsequent samples, 15 of 26 patients showed multiple degradation products with up to 7 degradation bands. The appearance of fragments was correlated with higher levels of cTnI (PϽ0.001) and time to initiation of treatment (Pϭ0.058). This study defines for the first time the initial time course of cTnI degradation in STEMI. Intact cTnI and a single degradation product were detectable on immunoblot as early as 90 minutes after onset of symptoms with further degradation after 165 minutes. Infarct size and time to initiation of treatment was the major determinant for degradation. Key Words: myocardial infarction Ⅲ troponin Ⅲ troponin degradation Ⅲ diagnostics T he criteria for diagnosing acute coronary syndrome and myocardial infarction (AMI) changed in the year 2000 with the endorsement of the American College of Cardiology/ European Society of Cardiology guidelines, which designated cardiac troponin (cTn) as the biochemical marker of choice. 1 Troponin is a regulatory protein of the thin filament of striated muscle and consists of 3 tightly interacting subunits: T (37 kDa), I (24 kDa), and C (18 kDa). In addition, there are generally thought to be free cytoplasmic components 2,3 : for cardiac troponin T (cTnT), amounting to approximately 6% to 8% of the total pool; and for cardiac troponin I (cTnI), 3% to 4%. Troponin is released into the bloodstream 4 to 6 hours after AMI, peaks after approximately 18 to 24 hours, and can stay elevated for up to 14 days. Assessment of cTnI or cTnT by automated assay is today the most sensitive and specific method for diagnosing AMI. However, cTn is not released only in response to ischemic insults but by any condition that is associated with and/or causes cardiac injury, eg, decompensated heart failure, pulmonary embolism, end-stage renal disease, and stroke. 4 -11 In addition, there is significant variability in the sensitivity, selectivity, and specificity among various diagnostic cTnI immunoassays. 12 Some of these assay differences have ...

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Section: Discussionmentioning

confidence: 98%

mentioning

confidence: 98%

Time Course of Degradation of Cardiac Troponin I in Patients With Acute ST-Elevation Myocardial Infarction

Madsen

Christensen

Lund

et al. 2006

Circulation Research

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“…The data also suggest that plasma levels are independent of reperfusion status from the first day onwards, largely reflecting the slow degradation and liberation of the structural pool [15,20]. In reperfused patients, it has been shown that while both cTnT and cTnI peak early (<12 h), the disappearance of cTnI is somewhat accelerated compared to cTnT, although both are still significantly elevated at 72 h [21,22]. …”

Section: Cardiac Troponin For Infarct Size Estimationmentioning

confidence: 99%

Troponin for the Estimation of Infarct Size: What Have We Learned?

Hallén¹

2012

Cardiology

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In acute myocardial infarction (AMI), the extent of myocardial damage is closely linked to prognosis. Early determination of infarct size is therefore key to assessing the future risk of patients and instructive for optimization of therapeutic strategies. The cardiac troponins, by allowing the physician to track the extent of injury suffered by the myocardium, provide a window into the heart. This article addresses the relationship between the cardiac troponins and the infarct size in AMI. Taken together, the data suggest that the cardiac troponins provide very useful information in this respect and especially in patients with ST elevation myocardial infarction. More studies are needed to understand how cardiac troponin-estimated infarct size may be integrated with other prognostic assessments and employed systematically in risk stratification. Early data are promising and indicate that cardiac troponins could provide useful information for early risk assessment that is complementary to the determination of cardiac function and volumes.

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“…Because of a high molecular weight, CK is not eliminated by the kidney and is cleared by the liver and reticuloendothelial system [1]. Troponin Ic (cTnI) is also a very sensitive and specific marker for myocardial ischemia and necrosis [2]. However, the pathophysiology of cTnI elimination remains unclear [3], and its levels could be influenced by renal function [4].…”

Section: Introductionmentioning

confidence: 99%

Effect of Renal Failure on Peak Troponin Ic Level in Patients with Acute Myocardial Infarction

Dessap

Lellouche²,

Audard³

et al. 2007

Cardiology

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Objectives: Peak troponin Ic (cTnI) level could be influenced by renal function. We evaluated the effect of moderate to severe renal failure on peak cTnI level during acute myocardial infarction (AMI). Methods: One hundred and twenty-five consecutive patients admitted to the coronary care unit of a university hospital in France for primary angioplasty during AMI were retrospectively studied. Results: The correlations between peak cTnI level, peak creatine phosphokinase (CK) level, peak cTnI/peak CK ratio and creatinine clearance (CrCl) were assessed. The peak cTnI/peak CK ratio was considered in order to standardize the peak cTnI level with the extent of myocardial necrosis. There was no significant correlation between CrCl and peak CK (r = 0.01, p = 0.95), peak cTnI (r = –0.08, p = 0.38) or the peak cTnI/peak CK ratio (r = –0.14, p = 0.13). There was a trend towards higher peak cTnI in patients with moderate to severe renal failure. The peak cTnI/peak CK ratio did not significantly differ among patients according to CrCl stratification, whereas the ratio of log-transformed values was significantly higher in patients with moderate to severe renal failure. Conclusion: In patients with AMI, the peak cTnI level seemed to be influenced by renal function.

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Troponin I concentrations following primary percutaneous coronary intervention predict large infarct size and left ventricular dysfunction in patients with ST-segment elevation acute myocardial infarction

Cited by 25 publications

References 22 publications

Time Course of Degradation of Cardiac Troponin I in Patients With Acute ST-Elevation Myocardial Infarction

Time Course of Degradation of Cardiac Troponin I in Patients With Acute ST-Elevation Myocardial Infarction

Troponin for the Estimation of Infarct Size: What Have We Learned?

Effect of Renal Failure on Peak Troponin Ic Level in Patients with Acute Myocardial Infarction

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