SVT and Ischemia

Abstract & Commentary

By Michael H. Crawford, MD. This article originally appeared in the October 2010 issue of Clinical Cardiology Alert. It was peer reviewed by Ethan Weiss, MD.

Source: Bukkapatnam RN, et al. Relationship of myocardial ischemia and injury to coronary artery disease in patients with supraventricular tachycardia. Am J Cardiol. 2010;106:374-377.

Supraventricular tachycardia (SVT) is known to be associated with troponin leaks and ST-wave depression on ECG, both potential markers of ischemia. However, the exact significance of these findings is unclear. Thus, these investigators from UC Davis did a retrospective review of 104 subjects admitted for SVT over five years. Patients with specific atrial arrhythmias, such as atrial fibrillation, flutter, and sinus tachycardia were excluded. During SVT, at a mean rate of 174 beats/min, one-third of patients had chest pain, 57% had ST depression, and 48% had an increased Troponin I. Among 35 patients who had stress testing or coronary angiography, 11 had CAD, and were compared to the rest of the sample. ST depression was present in 100% of these 11 patients, but also in 60% of the patients without known CAD. After adjustment for covariates, ST depression was not a predictor of CAD. Troponin I was elevated in 55% of the CAD patients and 46% of the rest (p = NS). Chest pain occurred during tachycardia in 45% with CAD and 34% without (p = NS). The presence of these three clinical variables during SVT (chest pain, ST depression, troponin elevation) was more prevalent in those with CAD (2.4 v. 0.9 risk factors, p = 0.03). The authors concluded that ECG ST depression and Troponin I elevation are not accurate markers for acute coronary syndromes in SVT patients.


This observational study highlights a clinical dilemma of SVT: Which patients have ischemic heart disease? It is well known that ischemic-appearing ST depression can occur with SVT and persist for up to 24 hours after conversion to sinus rhythm. Yet most of the patients who exhibit these ECG findings do not have underlying CAD. This study contributes to our knowledge by adding information on troponin, which shows the same phenomena: frequent elevations, but not diagnostic of the presence of CAD. In fact, over two-thirds of their patients had some evidence suggesting ischemic heart disease, yet less than one-third were shown to have CAD. Hence the authors' conclusion that these signs of ischemia do not accurately predict acute coronary syndromes. However, they probably represent so-called demand ischemia, where the oxygen demands of the tachycardia exceed the coronary artery supply.

Their results are consistent with other smaller studies, but studies of younger patients have shown a lower prevalence of troponin leakage, suggesting that older age may impair coronary vasoreactivity during tachycardia or represent a higher incidence of CAD at older ages. Their population was heterogeneous, with a mean age of 58, more that 50% women, and some with a history of CAD. Since everyone was admitted in their study, the population was probably biased toward more CAD. The real clinical issue in SVT patients is who to evaluate for CAD and how? Since classic clinical signs of ischemia are inaccurate, other clinical features, such as traditional risk factors, should be used. In most cases, non-invasive testing would make sense initially. Since about one-third of those evaluated had CAD; those with evidence of ischemia and other risk factors for CAD should probably be admitted. Those with no risk factors for CAD can probably be evaluated as outpatients.