Changes in regional myocardial function and external work in exercising dogs with ischemia

• Published in: The American journal of physiology Vol. 264; no. 1 Pt 2; p. H110
• Main Authors: Miyazaki, S, Goto, Y, Guth, B D, Miura, T, Indolfi, C, Ross, Jr, J
• Format: Journal Article
• Language: English
• Published: United States 01.01.1993
• Subjects: Animals; Coronary Disease - etiology; Coronary Disease - physiopathology; Dogs; Heart - physiopathology; Hemodynamics; Physical Exertion; Pressure; Time Factors; Ventricular Function, Left
• ISSN: 0002-9513
• DOI: 10.1152/ajpheart.1993.264.1.H110

Changes in regional myocardial work of the nonischemic wall and left ventricular (LV) asynchrony of the nonischemic wall during exercise-induced ischemia were examined in seven conscious dogs instrumented with a micromanometer for LV pressure measurement and sonomicrometers for control and ischemic wall thickness and LV external short and long axes. Ischemia was produced during steady-state exercise by a pneumatic constrictor on the left circumflex coronary artery. Time difference between peak thickening of control (anterior) and ischemic (posterior) walls was measured as an index of LV asynchrony. LV pressure-wall thickness loop area of both the control wall (LVP-CW loop) and ischemic wall was calculated as an index of regional myocardial external work. With ischemia during exercise, peak LV pressure decreased by 11%, and time difference of peak thickening in the two walls increased, accompanied by marked deformation of the LVP-CW loop during early relaxation, which was related to protodiastolic thickening of the ischemic wall. Thus, despite a significant increase in percent systolic thickening during exercise, loop area of control wall was not enhanced. These changes of the LVP-CW loop were confirmed by calculation of stress-strain loop areas as an additional index of regional myocardial external work but having true dimensions of work. Stress-strain loop area in the control wall during ischemic exercise showed a similar value to that during control exercise, thereby confirming lack of compensatory increase. Thus, during exercise-induced ischemia, regional myocardial external work in the normal region does not increase despite an increase in systolic wall thickening.