Global subendocardial ischemia can explain ST depression
in chronic angina|
Can. J. Cardiol. 2007, 23 Suppl. C.:145C.
Poster presented at the Canadian Cardiovascular Congress, October 2007.
introduction The ECG obtained during stress testing often shows a typical pattern of ST depression. A similar pattern can occur spontaneously in UA/NSTEMI patients. The current textbook explanation of ST depression involves regional subendocardial ischemia as a direct result of partial occlusion of a coronary artery. The resulting ST-segment changes should then predict the affected artery. However, in contrast to ST elevation, ST-depression patterns appear to be independent of the affected arteries. Moreover, experimental models could not reproduce ST depression at a resting heart rate. Recent theoretical work has shown that the classical relation between regional subendocardial ischemia and epicardial ST depression relies on an outdated mathematical model of the myocardium.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 (Heart Rhythm 4:200-206, 2007). In this study, we investigate if such a realistic model can reproduce the pattern of ST depression that is typical for the stress test.
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 boundary-element torso model. Details of the models have been published previously (IEEE T-BME 53(12):2425-2435, 2006).
results Limited subendocardial ischemic zones caused small (<0.05 mV) 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.
discussion Clinical ST depression has clasically been attributed to partial occlusion of one or more coronary arteries. Previous work on animal models has shown that partial occlusion of a coronary artery alone does not lead to ST depression. We hypothesize therefore that these models do not correspond to ST depression as it is observed in patients. In patients, ST depression typically occurs in a configuration similar to the "stress-test ECG". During stress testing, elevated LV diastolic pressure can cause a perfusion deficit in the subendocardium, leading to a global subendocardial ischemia. Our present results show that in contrast to regional subendocardial ischemia, global subendocardial ischemia can cause ST depression in the ECG. This ST depression cannot be related to the territory of the affected artery. Clinical studies will have to establish whether the phenomena that cause the stress-test ECG pattern are also responsible for ST depression in patients at rest.
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.
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