BACKGROUND: The new definition of myocardial infarction (MI) emphasizes the pre-eminent role of troponin for diagnosis. Troponin rise indicates myocardial injury, but is not synonymous with infarction or ischaemia. AIMS: To review the precipitating event for troponin elevation in patients with angiographically normal coronary arteries, in a district general hospital. METHODS: Consecutive patients with elevated troponin I (TnI) who underwent angiography for suspected coronary disease were included in the present study if they had normal or mild disease (<50% diameter loss without complex features or thrombus). Precipitating event for TnI elevation was assigned on the totality of clinical evidence. RESULTS: Twenty-one patients qualified, with an average age of 50 years (range 33-73). Sixty-two per cent of participants were female. Troponin release was attributed to tachycardia in six patients, only two of whom had haemodynamic compromise. Physical exertion was the precipitating factor in two patients; pericarditis in two patients; and severe congestive heart failure in one patient. Ten of 21 patients had no identifiable cause for a rise in TnI concentration. Five of 21 patients had left-ventricular wall motion abnormalities. There were no deaths or MI at 41 +/- 24 weeks follow up. CONCLUSION: Troponin is a sensitive marker of myocardial injury and may rise following apparently minor insults. A rise in TnI concentration may have a cause other than acute coronary syndrome and may occur without significant angiographic coronary artery disease.
BACKGROUND: The new definition of myocardial infarction (MI) emphasizes the pre-eminent role of troponin for diagnosis. Troponin rise indicates myocardial injury, but is not synonymous with infarction or ischaemia. AIMS: To review the precipitating event for troponin elevation in patients with angiographically normal coronary arteries, in a district general hospital. METHODS: Consecutive patients with elevated troponin I (TnI) who underwent angiography for suspected coronary disease were included in the present study if they had normal or mild disease (<50% diameter loss without complex features or thrombus). Precipitating event for TnI elevation was assigned on the totality of clinical evidence. RESULTS: Twenty-one patients qualified, with an average age of 50 years (range 33-73). Sixty-two per cent of participants were female. Troponin release was attributed to tachycardia in six patients, only two of whom had haemodynamic compromise. Physical exertion was the precipitating factor in two patients; pericarditis in two patients; and severe congestive heart failure in one patient. Ten of 21 patients had no identifiable cause for a rise in TnI concentration. Five of 21 patients had left-ventricular wall motion abnormalities. There were no deaths or MI at 41 +/- 24 weeks follow up. CONCLUSION: Troponin is a sensitive marker of myocardial injury and may rise following apparently minor insults. A rise in TnI concentration may have a cause other than acute coronary syndrome and may occur without significant angiographic coronary artery disease.
Authors: Edouard Gerbaud; Emmanuel Harcaut; Pierre Coste; Matthew Erickson; Mathieu Lederlin; Jean Noel Labèque; Jean Marie Perron; Hubert Cochet; Pierre Dos Santos; Catherine Durrieu-Jaïs; François Laurent; Michel Montaudon Journal: Int J Cardiovasc Imaging Date: 2011-05-03 Impact factor: 2.357
Authors: Alexander Illmann; Thomas Riemer; Raimund Erbel; Evangelos Giannitsis; Christian Hamm; Michael Haude; Gerd Heusch; Lars S Maier; Thomas Münzel; Claus Schmitt; Burghard Schumacher; Jochen Senges; Thomas Voigtländer; Harald Mudra Journal: Clin Res Cardiol Date: 2014-01 Impact factor: 5.460
Authors: Jonas Hallén; Odd Erik Johansen; Kåre I Birkeland; Lars Gullestad; Svend Aakhus; Knut Endresen; Solve Tjora; Allan S Jaffe; Dan Atar Journal: Cardiovasc Diabetol Date: 2010-09-15 Impact factor: 9.951