Localization of regional myocardial ischemia by recording of monophasic action potentials.
Identification of regional myocardial ischemia by TQ-ST segment mapping, while commonly used, is relatively imprecise and nonspecific. In 41 open-chest dogs we examined whether monophasic action potentials (MAPs) recorded from the myocardial surface by means of a new contact-electrode technique could be used to more precisely and specifically index regional myocardial ischemia. After ligation of the left anterior descending coronary artery (LAD), epicardial and endocardial MAPs from the ischemic region demonstrated shortening of plateau duration followed by a progressive loss in amplitude to 48 +/- 8% and in maximum upstroke velocity (dV/dtmax) to 9 +/- 2% of control (n = 7). Regional hyperkalemia produced by intracoronary injection of potassium chloride also resulted in regional decreases in duration, amplitude, and dV/dtmax of the MAP. Similar to previously reported effects on transmembrane action potentials, ischemia- or hyperkalemia-induced loss in MAP amplitude was due to decreases in both diastolic (negative) and systolic (positive) potential and paralleled TQ segment depression and "true" ST segment elevation in unipolar direct current-coupled electrograms recorded from an adjacent site. In eight canine hearts we compared the abilities of MAP recordings and TQ-ST segment measurements in defining a region of myocardial ischemia. Transmural ischemia with a sharp flow border was produced by LAD ligation and distal embolization with dental rubber. One hour later simultaneous MAP and TQ-ST mapping was performed in each dog at 45 to 65 epicardial sites inside and outside the ischemic region. TQ-ST voltage was significantly increased 10 to 20 mm outside the visible cyanotic border, reaching a maximum just inside the border and decreasing progressively toward the center of the ischemic region to values not significantly different from those from sites 10 mm outside the ischemic border. In contrast, MAP amplitude and dV/dtmax were normal up to 5 to 10 mm outside the cyanotic border, decreased sharply across a lateral transition zone of only 8 mm to 8.7 +/- 2.3% and 4.3 +/- 0.9% of control, respectively, at sites 4 to 6 mm inside the border, and were uniformly abnormal across the entire ischemic region. Recordings made 3 hr after LAD ligation revealed an overall decline in the magnitude of TQ-ST, making definition of the ischemic border by TQ-ST even less precise, whereas the differences between MAPs from normal and ischemic myocardium had become even more pronounced than after 1 hr. Thus, unlike TQ-ST segment measurements, MAP recordings uniquely define ischemic and nonischemic sites and more precisely localize the border of an ischemic region.(ABSTRACT TRUNCATED AT 400 WORDS)
D000200:Action Potentials; D000818:Animals; D001157:Arterial Occlusive Diseases / Q000503:physiopathology; D003327:Coronary Disease / Q000503:physiopathology*; D004285:Dogs; D004562:Electrocardiography; D006947:Hyperkalemia / Q000503:physiopathology; D009200:Myocardial Contraction; D013997:Time Factors