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Can J Cardiol. 2011 Jan-Feb;27(1):105-9. doi: 10.1016/j.cjca.2010.12.004.

Troponin elevation in supraventricular tachycardia: primary dependence on heart rate.

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Division of Internal Medicine, Department of Medicine, Université de Sherbrooke, Sherbrooke, Québec, Canada.



It is known that some patients with supraventricular tachycardia (SVT) could have increased troponin levels without coronary artery disease.


To compare the cardiovascular risk of patients admitted with SVT with troponin T elevation (T+ patients) versus those without (T- patients), to determine if the rise in troponin levels could be predicted, and to identify the right approach in T+ patients.


Retrospective database search of patients with SVT from 2002 to 2007 either with or without troponin T elevation at admission.


Of the 73 study patients, there were 24 (32.9%) T+ patients and 49 (67.1%) T- patients. All except 5 T+ patients underwent either a stress test/MIBI or a coronary angiogram. Two noninvasive tests were positive and only 1 patient needed an angiogram and percutaneous coronary intervention; none of the other angiograms triggered any further treatment. Of the 49 T- patients, 11 had a noninvasive stress test; none of these tests was positive or triggered any further treatment. Compared with that of T- patients, the maximum heart rate was significantly higher in T+ patients (190.8 versus 170.3 beats per minute, P = .008). A correlation was found between the maximal heart rate during SVT and the level of troponin elevation (r = 0.637, P = .001).


SVT could be associated with a troponin elevation without any severe coronary artery disease. In most patients, either conservative management or noninvasive stratification seems to be sufficient; an invasive strategy could then be reserved only for high-risk patients who tested positive. The only clinical variable correlated with the troponin rise was a higher maximal heart rate during the SVT episode.

[Indexed for MEDLINE]

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