Myocardial electrical activity does not affect myocardial electrical impedance measurements.

OBJECTIVE: Myocardial electrical impedance (MEI) has shown to be an effective indicator of myocardial ischemia. We have previously developed a novel monitor for measuring MEI in near-real time. The object of this study was to test whether drug-induced changes in the frequency of the periodic myocardial electrical activity, as measured by the heart rate (HR), affect MEI measurements made with our monitor. METHODS: Thirty dogs were randomly assigned to one of three study groups (placebo, isoproterenol or esmolol) and then anesthetized with sodium thiamylal, intubated, ventilated, given isoflurane, and had venous, arterial, and pulmonary artery catheters placed. Median sternotomy was performed to facilitate myocardial exposure and to allow the left anterior descending (LAD) coronary artery to be isolated. Following baseline measurements, saline (control), isoproterenol or esmolol was administered and the LAD coronary artery was occluded in a timed sequence in order to study the effects of heart rate changes and demonstrate induced myocardial ischemia on MEI. RESULTS: Isoproterenol raised the HR and esmolol lowered the HR without affecting our MEI measurements. Myocardial electrical impedance increased during LAD coronary artery occlusion in all groups, as previously shown. CONCLUSION: These results demonstrate that our MEI monitor is unaffected by the frequency of the periodic myocardial electrical activity that generates the HR.

Electrotonic remodeling following myocardial infarction in dogs susceptible and resistant to sudden cardiac death.

Passive electrical remodeling following myocardial infarction (MI) is well established. These changes can alter electrotonic loading and trigger the remodeling of repolarization currents, a potential mechanism for ventricular fibrillation (VF). However, little is known about the role of passive electrical markers as tools to identify VF susceptibility post-MI. This study investigated electrotonic remodeling in the post-MI ventricle, as measured by myocardial electrical impedance (MEI), in animals prone to and resistant to VF. MI was induced in dogs by a two-stage left anterior descending (LAD) coronary artery ligation. Before infarction, MEI electrodes were placed in remote (left circumflex, LCX) and infarcted (LAD) myocardium. MEI was measured in awake animals 1, 2, 7, and 21 days post-MI. Subsequently, VF susceptibility was tested by a 2-min LCX occlusion during exercise; 12 animals developed VF (susceptible, S) and 12 did not (resistant, R). The healing infarct had lower MEI than the normal myocardium. This difference was stable by day 2 post-MI (287 +/- 32 Omega vs. 425 +/- 62 Omega, P < 0.05). Significant differences were observed between resistant and susceptible animals 7 days post-MI; susceptible dogs had a wider electrotonic gradient between remote and infarcted myocardium (R: 89 +/- 60 Omega vs. S: 180 +/- 37 Omega). This difference increased over time in susceptible animals (252 +/- 53 Omega at 21 days) due to post-MI impedance changes on the remote myocardium. These data suggest that early electrotonic changes post-MI could be used to assess later arrhythmia susceptibility. In addition, passive-electrical changes could be a mechanism driving active-electrical remodeling post-MI, thereby facilitating the induction of arrhythmias.

Dexmedetomidine for conscious sedation in difficult awake fiberoptic intubation cases.

Currently used methods of sedation for fiberoptic intubation such as benzodiazepines, propofol, or opioids have their limitations. Dexmedetomidine (DEX) is a selective alpha-2 adrenergic agonist that has been used clinically for its sympatholytic, analgesic, and sedative properties. We report on 4 patients with particularly difficult airways who underwent successful awake fiberoptic intubation with DEX. Dexmedetomidine was used to provide a moderate level of conscious sedation without causing respiratory distress or hemodynamic instability during fiberoptic intubation.

Vacuum-assisted apical suction devices induce passive electrical changes consistent with myocardial ischemia during off-pump coronary artery bypass graft surgery.

OBJECTIVE: Off-pump coronary artery bypass graft surgery is common therapy to completely revascularize diseased hearts. In order to graft posterior arteries in this procedure, the heart must be lifted from the chest cavity and manipulated to expose the surgical field using an apical suction device. This suction device may cause unwanted myocardial ischemia. METHODS: In this observational study, we measured myocardial electrical impedance, a parameter that responds to myocardial ischemia, as well as ST-segment changes during off-pump coronary artery bypass graft surgery in 12 patients with two-vessel coronary artery disease undergoing revascularisation of the left anterior descending and the posterior descending coronary arteries. During the posterior descending artery revascularisation phase of the procedure the apical suction device was oriented over the electrodes used to measure myocardial electrical impedance, thus allowing us the opportunity to assess myocardial ischemia in this region of the heart. RESULTS: In these 12 patients, myocardial electrical impedance progressively increased under the suction device during posterior coronary artery revascularisation, suggesting that myocardial ischemia developed in this region of the myocardium. ST-segment changes were negligible while the heart was vertically displaced (and the suction device attached), but increased immediately when the heart was returned to the neutral anatomical position. CONCLUSION: Our data suggest that the apical suction device may cause ischemia while the heart is vertically displaced and electrically disconnected from the body. Under these conditions, ST-segment changes may not detect myocardial ischemia. Myocardial electrical impedance has the potential to reliably detect intraoperative myocardial ischemia under these circumstances.

Early time course of myocardial electrical impedance during acute coronary artery occlusion in pigs, dogs, and humans.

Changes in myocardial electrical impedance (MEI) and physiological end points have been correlated during acute ischemia. However, the importance of MEI's early time course is not clear. This study evaluates such significance, by comparing the temporal behavior of MEI during acute total occlusion of the left anterior descending coronary artery in anesthetized humans, dogs, and pigs. Here, interspecies differences in three MEI parameters (baseline, time to plateau onset, and plateau value normalized by baseline) were evaluated using Kruskal-Wallis ANOVA and post hoc tests (P < 0.05). Noteworthy differences in the MEI time to plateau onset were observed: In dogs, MEI ischemic plateau was reached after 46.3 min (SD 12.9) min of occlusion, a significantly longer period compared with that of pigs and humans [4.7 (SD 1.2) and 4.1 min (SD 1.9), respectively]. However, no differences could be observed between both animal species regarding the normalized MEI ischemic plateau value (15.3% (SD 4.7) in pigs, vs. 19.6% (SD 2.6) in dogs). For all studied MEI parameters, only swine values resembled those of humans. The severity of myocardial supply ischemia, resulting from coronary artery occlusion, is known to be dependent on collateral flow. Thus, because dogs possess a well-developed collateral system (unlike humans or pigs), they have shown superior resistance to occlusion of a coronary artery. Here, the early MEI time course after left anterior descending coronary artery occlusion, represented by the time required to reach ischemic plateau, was proven to reflect such interspecies differences.

A phase III, double-blind, placebo-controlled, multicenter study on the efficacy of recombinant human antithrombin in heparin-resistant patients scheduled to undergo cardiac surgery necessitating cardiopulmonary bypass.

BACKGROUND: The study evaluated the efficacy of recombinant human antithrombin (rhAT) for restoring heparin responsiveness in heparin resistant patients undergoing cardiac surgery. METHODS: This was a multicenter, randomized, double-blind, placebo-controlled study in heparin-resistant patients undergoing cardiac surgery with cardiopulmonary bypass. Heparin resistance was diagnosed when the activated clotting time was less than 480 s after 400 U/kg heparin. Fifty-four heparin-resistant patients were randomized. One cohort received 75 U/kg rhAT, and the other received normal saline. If the activated clotting time remained less than 480 s, this was considered treatment failure, and 2 units fresh frozen plasma was transfused. Patients were monitored for adverse events. RESULTS: Only 19% of patients in the rhAT group received fresh frozen plasma, compared with 81% of patients in the placebo group (P < 0.001). During their hospitalization, 48% of patients in the rhAT group received fresh frozen plasma, compared with 85% of patients in the placebo group (P = 0.009). Patients in the placebo group required higher heparin doses (P < 0.005) for anticoagulation. There was no increase in serious adverse events associated with rhAT. There was increased blood loss 12 h postoperatively (P = 0.05) with a trend toward increased 24-h bleeding in the rhAT group (P = 0.06). There was no difference between the groups in blood and platelet transfusions. CONCLUSION: Treatment with 75 U/kg rhAT is effective in restoring heparin responsiveness and promoting therapeutic anticoagulation in the majority of heparin-resistant patients. Treating heparin-resistant patients with rhAT may decrease the requirement for heparin and fresh frozen plasma.

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 ohms. 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.

Comparison of three remifentanil dose-finding regimens for coronary artery surgery.

OBJECTIVES: To identify the remifentanil dosing regimen providing safe and optimal anesthetic conditions during coronary artery bypass graft surgery and to evaluate postoperative recovery characteristics. DESIGN: Open-label, randomized, parallel group. SETTING: Three centers in the United States. PARTICIPANTS: Seventy-two patients with left ventricular stroke volumes >or=50 mL. INTERVENTIONS: Patients were randomized to remifentanil doses of 1 microg/kg/min (group 1, n = 23); 2 microg/kg/min (group 2, n = 24), or 3 microg/kg/min (group 3, n = 25). Somatic, sympathetic, and hemodynamic responses indicating inadequate anesthesia were treated with bolus doses of remifentanil, 1 to 2 microg/kg, and infusion rate increases, and, if necessary, isoflurane 0.5% to 1.0% was added as a rescue anesthetic. In the intensive care unit, the remifentanil infusion was reset to 1 microg/kg/min, with midazolam administered for supplemental sedation and morphine for analgesia. MEASUREMENTS AND MAIN RESULTS: The durations of anesthesia, surgery, and cardiopulmonary bypass were similar for the 3 study groups. In addition, dose of lorazepam premedication, time to loss of consciousness, preoperative left ventricular ejection fraction, age, weight, and sex were similar for the 3 study groups. Remifentanil alone (infusion and boluses) prevented and controlled all responses to stimulation in 44% of group 3, 37% of group 2 and 9% of group 1 patients intraoperatively. Isoflurane (0.5%-1% inspired) rescue was successful in the remaining patients in each group. Hypotension indicating discontinuation of isoflurane and reductions of remifentanil infusion rates occurred in 64% to 75% of all patients. The optimal range of remifentanil infusion was 2 to 4 microg/kg/min with isoflurane to supplement the opioid. Fifty-one patients (71%) met the criteria for extubation within 6 hours postoperatively; because of surgical practice differences, only 30 patients (59%) were actually extubated. CONCLUSIONS: After lorazepam premedication, remifentanil infusion (2-4 microg/kg/min) supplemented intermittently with low inspired concentrations of isoflurane provided an effective anesthetic regimen for coronary artery bypass graft surgery. Early extubation times were feasible after remifentanil continuous infusions (1-5 microg/kg/min) used as the primary anesthetic component intraoperatively and for analgesia (