Endocardial electromechanical mapping in a porcine acute infarct and reperfusion model evaluating the extent of myocardial ischemia.
OBJECTIVE
Catheter-based, left ventricular, electromechanical mapping (EMM) has evolved as a diagnostic tool to characterize ischemic and injured myocardium. In the acute setting, diagnostic criteria for ischemic or infarcted myocardium are not well defined. In the present study, the capacity of separating myocardium with evolving necrosis from viable myocardium was investigated.


RESULTS
Pigs were subjected to balloon occlusion of the left anterior descending coronary artery for 45 minutes. Using the NOGATM cardiac mapping system, EMM was performed at the baseline and after two hours of reperfusion. EMMs were evaluated regarding unipolar voltage (UPV), bipolar voltage (BPV) and local linear shortening (LLS). The pigs were sacrificed four hours after reperfusion and morphological estimation of infarct size and localization was performed. Baseline UPV activity was significantly lower in the anterior, lateral and posterior basal segments as compared to the septal and posterior midventricular segments. After reperfusion, UPV, but not BPV, was significantly decreased in the apical, midventricular septal and basal segments. LLS demonstrated significant impairment of mobility in the septal midventricular segment. The thresholds for separating electromechanical activity at baseline from after infarction differed between the myocardial regions. The ability of EMM to correctly detect infarcted myocardium showed a sensitivity and specificity in the order of 50 85%, as compared to the morphological standard.


CONCLUSIONS
In a porcine acute infarct and reperfusion model, electromechanical activity thresholds, for infarct detection, could be established, but there was significant intersegmental threshold variability at baseline and after infarction. Accordingly, applying general thresholds demonstrated a poor correlation between infarct extension evaluated by EMM and morphology.
Odenstedt
Jacob
J
Cardiovascular Institute, Sahlgrenska University Hospital, S-413 45 Gothenburg, Sweden. Jacob.Odenstedt@vgregion.se
Månsson
Chrichan
C
Jansson
Sven-Olof
SO
Grip
Lars
L
D000818:Animals; D018780:Body Surface Potential Mapping / Q000379:methods*; D003331:Coronary Vessels; D004699:Endocardium / Q000473:pathology*; D005260:Female; D023421:Models, Animal; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D017202:Myocardial Ischemia / Q000473:pathology / Q000503:physiopathology; D015425:Myocardial Reperfusion / Q000379:methods*; D009336:Necrosis; D013552:Swine