C.L. del Rio

Myocardial electrical impedance responds to ischemia and reperfusion in humans

Myocardial electrical impedance (MEI) is correlated to ischemia and reperfusion of the heart muscle. The entire body of work with MEI to this point has been carried out in animal subjects in vivo and excised tissue samples. In this study, we measured MEI clinically for the first time in human patients who were undergoing off-pump coronary artery bypass (OPCAB) surgery. MEI was measured with a monitor designed in this laboratory and approved by the FDA for use on human subjects. Our patient population (n=18) had a 70%-100% stenosis of the diseased coronary artery targeted for bypass. We measured MEI continuously during surgery and at 3, 6, 24, and 72 h postoperatively from two temporary pacing electrodes attached to the heart muscle. Absolute baseline impedance ranged from 173 to 729 /spl Omega/. MEI increased with occlusion of the diseased artery prior to bypass. The percent increase from baseline was inversely correlated to the percent stenosis of the diseased artery. MEI decreased below baseline immediately on reperfusion following bypass in all patients and continued decreasing over the measurement period. MEI is a reliable clinical indicator of ischemia and reperfusion in humans and may indicate the effectiveness of coronary artery surgery. The parameter may have monitoring and diagnostic value in heart disease in humans.

Use of myocardial electrical impedance to assess the efficacy of preconditioning

Myocardial electrical impedance (MEI) has been found to correlate with ischemia and ischemic preconditioning (PC). In this study, the short-term effects of adenosine preconditioning on the MEI were studied in a swine model of beating heart coronary revascularization. Juvenile farm pigs were assigned to have either no PC (CTRL) or adenosine PC (ADO), receiving subsequently two ischemia/reperfusion (IR) insults. In both groups, MEI increased immediately with induced ischemia. However, its progression to ischemic plateau after reaching a maximum rate of change took significantly longer for ADO animals (7.13/spl plusmn/1.03 min) than for the CTRL (4.56/spl plusmn/0.16 min) (P<0.05). Such period of time was defined as a time constant. MEI was able to distinguish between study groups by evaluating the time required to reach ischemic plateau and from its rate of change (first derivate).

Devices used to expose the posterior coronary artery in OPCABG surgery may cause ischemia

Off-pump coronary artery bypass graft (OPCABG) surgery is commonly used to revascularize diseased hearts. In order to graft a posterior artery in this procedure, the heart must be lifted from the chest cavity using an apical suction device to expose the surgical field. In the process, this device may cause unwanted myocardial ischemia. We measured myocardial electrical impedance (MEI), a parameter that responses to myocardial ischemia, as well as ST-segment changes during OPCABG surgery in five patients undergoing revascularization of the left anterior descending (LAD) and posterior descending coronary artery (PDA). MEI increased with the application of the suction device in these patients, suggesting myocardial ischemia. ST-segment changes were negligible while the heart was raised from the chest cavity but increased immediately when the heart was returned to the normal position. Our data suggest that the apical suction device causes ischemia that is virtually undetected with ST-segment monitoring while the heart is raised and electrically disconnected from the body. MEI has the potential to detect intra-operative ischemia monitor.

Beta-adrenergic receptor blockade attenuates the electronic uncoupling induced by coronary artery occlusion

Nine dogs (n=9) with healed anterolateral (L1Da) infarction, were chronicully instrumented for myocardial electrical impedance (MEI) measurements, and subjected to brief (2min) LCXa occlusions with (BETA) and without (CTRL) beta-adrenergic receptor blockade. Scar tissue (LADu) had significantly lower ME1 (373.5H8.8R) than normal (LCXa) myocardium (CTRL: 548.899.012, BETA: 532.2G4.1Sl). MEI increased signQicantly after 2min LCXu occlusion (CTRL and BETA). However, beta-adrenergic receplur blockade significantly attenuated the magnitude of such increase. In control conditions (CTRL) MEi increased 4..5H.8% (21.3&7.a), while wirh beta-blockade if changed only by 3.441.8% (15.66.751). In a I-D cable model of propagating action potentials (Luo-Rudy formulation), such reduction of the ischemic electronic uncoupling prevented conduction block ut the ischemic/scar interface.