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Supraventricular tachycardia promotes release of troponin I in patients with normal coronary arteries

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Abstract

Background

Troponin I and T are sensitive markers of myocardial injury. The presence of elevated troponin often prompts further investigation with coronary angiography.

Methods

We present a series of patients presenting to our unit with raised troponin I and supraventricular tachycardia (SVT) that prompted coronary angiography.

Results

All patients had normal epicardial vessels at angiogram, no evidence of muscle bridging or pulmonary embolism.

Conclusion

The presence of tachycardia sufficient to warrant hospital admission can raise troponin, and this should be viewed in context when a decision on angiography is to be taken.

Section snippets

Discussion

Our series supports the initial finding of Bakshi [2] and Zellweger [3] demonstrating normal coronary arteries in patients with SVT as their presenting event. Our cohort is the largest to date and confirms the ability of fast paroxysmal arrhythmia to result in modest troponin rise in normal hearts.

The duration of arrhythmia did not appear associated with the degree of troponin rise, however, significant heamodynamic compromise was evident in Case 2, and this was associated with a large troponin

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    Troponin elevation can be seen after supraventricular tachyarrhythmias (including supraventricular tachycardia [SVT] and atrial fibrillation[AF]), like due to shortened diastole and increased oxygen demand with subendocardial ischemia [4,5,45-48]. Troponin elevation may occur in 12–48% of patients with SVT, though this is typically not associated with coronary artery disease (CAD) [24,45-49]. The literature evaluating elevated troponin in patients with SVT is limited to case reports and series or small cohort studies, and most recommendations advise against the routine assessment of troponin in SVT [49-57].

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