Brian Zenger1, Wilson W Good2, Jake A Bergquist2, Lindsay C Rupp2, Maura Perez3, Gregory J Stoddard4, Vikas Sharma5, Rob S MacLeod2. 1. Scientific Computing and Imaging Institute, University of Utah, SLC, UT, USA; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, SLC, UT, USA; Department of Biomedical Engineering, University of Utah, SLC, UT, USA; School of Medicine, University of Utah, SLC, UT, USA. Electronic address: brian.zenger@hsc.utah.edu. 2. Scientific Computing and Imaging Institute, University of Utah, SLC, UT, USA; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, SLC, UT, USA; Department of Biomedical Engineering, University of Utah, SLC, UT, USA. 3. Scientific Computing and Imaging Institute, University of Utah, SLC, UT, USA. 4. Department of Internal Medicine, University of Utah, SLC, UT, USA. 5. School of Medicine, University of Utah, SLC, UT, USA.
Abstract
OBJECTIVE: Test the hypothesis that exercise and pharmacological cardiac stressors create different electrical ischemic signatures. INTRODUCTION: Current clinical stress tests for detecting ischemia lack sensitivity and specificity. One unexplored source of the poor detection is whether pharmacological stimulation and regulated exercise produce identical cardiac stress. METHODS: We used a porcine model of acute myocardial ischemia in which animals were instrumented with transmural plunge-needle electrodes, an epicardial sock array, and torso arrays to simultaneously measure cardiac electrical signals within the heart wall, the epicardial surface, and the torso surface, respectively. Ischemic stress via simulated exercise and pharmacological stimulation were created with rapid electrical pacing and dobutamine infusion, respectively, and mimicked clinical stress tests of five 3-minute stages. Perfusion to the myocardium was regulated by a hydraulic occluder around the left anterior descending coronary artery. Ischemia was measured as deflections to the ST-segment on ECGs and electrograms. RESULTS: Across eight experiments with 30 (14 simulated exercise and 16 dobutamine) ischemic interventions, the spatial correlations between exercise and pharmacological stress diverged at stage three or four during interventions (p<0.05). We found more detectable ST-segment changes on the epicardial surface during simulated exercise than with dobutamine (p<0.05). The intramyocardial ischemia formed during simulated exercise had larger ST40 potential gradient magnitudes (p<0.05). CONCLUSION: We found significant differences on the epicardium between cardiac stress types using our experimental model, which became more pronounced at the end stages of each test. A possible mechanism for these differences was the larger ST40 potential gradient magnitudes within the myocardium during exercise. The presence of microvascular dysfunction during exercise and its absence during dobutamine stress may explain these differences.
OBJECTIVE: Test the hypothesis that exercise and pharmacological cardiac stressors create different electrical ischemic signatures. INTRODUCTION: Current clinical stress tests for detecting ischemia lack sensitivity and specificity. One unexplored source of the poor detection is whether pharmacological stimulation and regulated exercise produce identical cardiac stress. METHODS: We used a porcine model of acute myocardial ischemia in which animals were instrumented with transmural plunge-needle electrodes, an epicardial sock array, and torso arrays to simultaneously measure cardiac electrical signals within the heart wall, the epicardial surface, and the torso surface, respectively. Ischemic stress via simulated exercise and pharmacological stimulation were created with rapid electrical pacing and dobutamine infusion, respectively, and mimicked clinical stress tests of five 3-minute stages. Perfusion to the myocardium was regulated by a hydraulic occluder around the left anterior descending coronary artery. Ischemia was measured as deflections to the ST-segment on ECGs and electrograms. RESULTS: Across eight experiments with 30 (14 simulated exercise and 16 dobutamine) ischemic interventions, the spatial correlations between exercise and pharmacological stress diverged at stage three or four during interventions (p<0.05). We found more detectable ST-segment changes on the epicardial surface during simulated exercise than with dobutamine (p<0.05). The intramyocardial ischemia formed during simulated exercise had larger ST40 potential gradient magnitudes (p<0.05). CONCLUSION: We found significant differences on the epicardium between cardiac stress types using our experimental model, which became more pronounced at the end stages of each test. A possible mechanism for these differences was the larger ST40 potential gradient magnitudes within the myocardium during exercise. The presence of microvascular dysfunction during exercise and its absence during dobutamine stress may explain these differences.
Authors: Steven A J Chamuleau; Maria Siebes; Martijn Meuwissen; Karel T Koch; Jos A E Spaan; Jan J Piek Journal: Am J Physiol Heart Circ Physiol Date: 2003-06-26 Impact factor: 4.733