Understanding ST depression in the stress-test ECG
Mark Potse, Alain Vinet, A.-Robert LeBlanc, Jean G. Diodati, and Réginald Nadeau
34th International Congress on Electrocardiology, 2007.

other versions

abstract in J. Electrocardiol. 40 Suppl. (2007) page S45

conference proceedings paper in Anatol. J. Cardiol. 7 Suppl 1 (2007) pp 145-147


introduction  The electrocardiogram (ECG) obtained during exercise testing often shows a typical pattern of left anterolateral ST depression. A similar pattern can occur spontaneously in patients with UA/non STelevation myocardial infarction and appears to be independent of the occlusion site(s). The current textbook explanation of ST depression involves subendocardial ischemia. However, experimental models could not reproduce such phenomena at a resting heart rate. Recent theoretical work has shown that the classical relation between subendocardial ischemia and epicardial ST depression relies on an incorrect mathematical model of the myocardium. In a realistic model of the human heart, ST depression could only be obtained with subendocardial ischemic zones that covered more than half of the left ventricle. We therefore hypothesized that ECG ST depression can be explained with ischemia affecting the entire left ventricular (LV) subendocardium.

methods  The ECG was simulated with a reaction-diffusion model of the human heart, incorporating anisotropic myocardium with transmurally rotating fiber orientation at 0.25-mm resolution and an inhomogeneous boundaryelement torso model. Details of the models have been published previously.

results  Limited subendocardial ischemic zones caused ST elevation on the ECG. An ischemic zone of 50% transmural extent covering the entire LV subendocardium caused an ST-depression pattern similar to that observed during stress test.

conclusions  Our results show that "global" subendocardial ischemia may explain ST depression. ST depression is typically related to partial occlusion, sometimes affecting only a single artery. The mechanism whereby a local perfusion deficit would cause global subendocardial ischemia is unknown but may involve underperfusion of the endocardium due to increased LV pressure, cardiac insufficiency, or an autonomic reaction. Accurate analysis of patient data is required to determine the applicability of our theoretical findings in real cases.


Computational resources for this work were provided by the Réseau québécois de calcul de haute performance (RQCHP). M. Potse was supported by a postdoctoral research award from the Groupe de recherche en sciences et technologie biomédicale (GRSTB), École Polytechnique and Université de Montréal; and by the Research Center of Sacré-Coeur Hospital, Montréal, Québec, Canada.