Modeling ischemia-induced dyssynchronous myocardial contraction.
Left ventricular (LV) contraction dyssynchrony is not easily quantified. We previously described a model for quantifying LV dyssynchrony that referenced regional amplitude and phase angles to global LV systole using esmolol-induced regional dyskinesis. We tested the hypothesis that our sine wave model and phase angle analysis of regional dyssynchrony in a canine model could also assess dyssynchrony of contraction during regional ischemia. Hence we compared intracoronary esmolol and matched regional ischemia in 10 anesthetized open-chest dogs. Regional and total LV volumes (conductance catheter), piezoelectric crystal shortening, and LV pressures were measured before, during, and after esmolol-induced apical dyskinesis and matched regional ischemia. We defined regional phase angle of contraction (alpha) as the relative distance, measured in degrees, that regional minimal volume differed from global end-systole. We also compared maximal stroke volume (SV), observed effective SV (that portion of regional SV contributing to total SV for each treatment), and calculated effective SV (total regional SV x cosine alpha). Dobutamine infusion increased homogeneity of regional alpha relative to baseline. Both esmolol and ischemia significantly delayed (P < 0.05) apical contraction as quantified by increased alpha (12.4 degrees +/- 28.1 degrees to 27.4 degrees +/- 30.4 degrees and 54.2 degrees +/- 32.6 degrees , respectively) (mean +/- sd) and decreased regional effective SV (4.7 +/- 2.5 mL to 3.6 +/- 2.2 mL and 4 +/- 2.5 mL, respectively) relative to baseline. Our study indicates that intracoronary esmolol and ischemia induced qualitatively similar mechanical effects on myocardial function and that a sine wave model to estimate regional effective SV is a sensitive method to detect and quantify regional dyssynchrony induced by ischemia. Potentially, phase angle and regional amplitude analyses may prove to be effective measures to identify and quantify the beneficial effects of resynchronization therapies on myocardial function.
Strum
David P
DP
Cardiopulmonary Research Laboratory, Department of Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15261, USA.
Pinsky
Michael R
MR
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004195:Disease Models, Animal; D004280:Dobutamine / Q000494:pharmacology; D004285:Dogs; D004562:Electrocardiography; D006339:Heart Rate / Q000187:drug effects; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D017202:Myocardial Ischemia / Q000503:physiopathology*; D011412:Propanolamines / Q000494:pharmacology; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis / Q000503:physiopathology*
D011412:Propanolamines; D004280:Dobutamine; C036604:esmolol