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Are troponins confusing?

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Supraventricular tachycardia and elevated troponin in the absence of coronary artery disease
Colin D Chue
Published on: 23 November 2015

Published on: 23 November 2015
Supraventricular tachycardia and elevated troponin in the absence of coronary artery disease
- Colin D Chue, PRHO Cardiology
- Other Contributors:
  Helen C. Routledge, Rajai A. Ahmad
Dear Editor
Reagarding the article by Collinson and Stubbs.[1]
Background
In their editorial of cardiac troponin, Collinson and Stubbs described its usefulness in diagnosis and predicting prognosis in patients with acute coronary syndromes.[1] They also summarised the conditions in which troponin may be elevated. This included rhythm disturbances such as prolonged tachyarrhythmia in the prese...
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Dear Editor
Reagarding the article by Collinson and Stubbs.[1]
Background
In their editorial of cardiac troponin, Collinson and Stubbs described its usefulness in diagnosis and predicting prognosis in patients with acute coronary syndromes.[1] They also summarised the conditions in which troponin may be elevated. This included rhythm disturbances such as prolonged tachyarrhythmia in the presence of ischaemic heart disease. We describe two cases of supraventricular tachycardia associated with a rise in troponin I in the absence of significant coronary artery disease. We suggest that an elevated troponin should only guide management in the context of the clinical findings.
Case 1
A 46-year-old Caucasian man who was previously fit and well presented to the emergency department with a two-hour history of palpitations and chest tightness. On examination he had a tachycardia of approximately 200 beats per minute but was not haemodynamically compromised with a blood pressure of 143/103. An ECG confirmed supraventricular, likely atrioventricular re-entrant, tachycardia. This was successfully terminated with the valsalva manoeuvre and his symptoms resolved. A repeat ECG showed a sinus rhythm of 96 beats per minute with no other abnormality. However, the patient had a troponin I of 1.2 (normal range Case 2
A 78-year-old Caucasian lady was admitted to the emergency department with chest tightness lasting three hours. There was no associated nausea, vomiting, sweating or palpitations. She had a past history of type II diabetes, hypertension and atrial fibrillation. On examination she had some chest discomfort. She had a tachycardia of 150 beats per minute and a blood pressure of 125/94 with no signs of cardiac failure. An ECG showed atrial flutter with 2:1 block and left ventricular hypertrophy with a strain pattern. CK on presentation was normal at 72 (normal range 20- 183iu/l). The pain resolved spontaneously and a repeat ECG showed sinus rhythm with no other abnormality. A second CK of 154 remained within normal range but troponin I 12 hours after onset of symptoms was raised at 1.1. Four days later the patient underwent coronary angiography, which showed concentric left ventricular hypertrophy but preserved systolic function. All coronary arteries were angiographically normal. The patient was discharged two days later with medical therapy.
Discussion
The patients described had elevated cardiac troponin in the presence of angiographically normal coronary arteries. Although this has been well described in association with a range of conditions, the association with tachyarrhythmias remains largely unrecognised.
A case series published this year described four cases of atrioventricular nodal re-entry tachycardia associated with a rise in troponin in the absence of coronary artery disease.[2] The degree of troponin elevation was unrelated to the duration and rate of tachycardia, a finding consistent amongst our cases. A second report describes 21 patients in whom the troponin was elevated despite normal coronary arteries or mild coronary artery disease (<_50 diameter="diameter" loss="loss" without="without" complex="complex" features="features" or="or" thrombus="thrombus" on="on" coronary="coronary" angiography.3="angiography.3" in="in" six="six" of="of" these="these" patients="patients" the="the" rise="rise" troponin="troponin" was="was" attributed="attributed" to="to" tachyarrhythmia="tachyarrhythmia" four="four" supraventricular="supraventricular" two="two" ventricular.="ventricular." p="p"/> Collinson and Stubbs stated that troponin may be elevated in prolonged arrhythmias in the presence of underlying ischaemic heart disease.[1] They postulated that this was due to secondary ischaemic myocardial injury caused by supply-demand mismatch. Myocardial damage sustained during tachycardia is reflected by the rise in troponin. Increased oxygen demand combined with a shortened diastole and reduced oxygen supply may be responsible.[2] Our findings suggest that supply- demand mismatch in tachyarrhythmia also occurs with normal coronary arteries. Our case reports also suggest arrhythmias do not have to be prolonged to cause secondary ischaemic myocardial injury. A tachyarrhythmia as brief as 120 minutes duration can induce a significant rise in troponin I. It has been stated that only 15 minutes of mild cardiac ischaemia is sufficient to cause release of cardiac troponin I degradation products and an elevation in troponin level.[4]
There is supportive evidence for the use of cardiac troponin levels in predicting prognosis and hence guiding management in selected patients with a high pre-test probability of acute coronary syndrome. This evidence does not extend to all patients presenting with chest pain. Troponin therefore should not be used to guide treatment or diagnose myocardial infarction in the absence of clinical features of an acute coronary syndrome. In these cases assuming that the rise is caused by plaque rupture requiring intervention or classifying the patient as acute myocardial infarction might simply delay instigation of the appropriate management. We suggest that an elevated troponin should only be used to diagnose myocardial infarction and guide management in the context of the clinical findings.
References
1. Collinson PO, Stubbs PJ. Are troponins confusing? Heart 2003; 89: 1285-7.
2. Zellweger MJ, Schaer BA, Cron TA, Pfisterer ME, Osswald S. Elevated troponin levels in the absence of coronary artery disease after supraventricular tachycardia. Swiss Medicine Weekly 2003; 133: 439-41.
3. Bakshi TK, Choo MK, Edwards CC, Scott AG, Hart HH, Armstrong GP. Causes of elevated troponin I with a normal coronary angiogram. Intern Med J 2002; 32: 520-5.
4. Higgins JP, Higgins JA. Elevation of cardiac troponin I indicates more than myocardial ischaemia. Clin Invest Med 2003; 26: 133-47.
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Conflict of Interest:
None declared.
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