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Effects of myocardial infarction on catheter defibrillation threshold
Insights
Myocardial ischemia, or reduced blood flow to the heart muscle, increases the energy required for ventricular defibrillation. This finding is crucial for the safe design and use of automatic implantable defibrillators in patients with heart disease.
Area of Science:
- Cardiology
- Biomedical Engineering
Background:
- Automatic implantable defibrillators are used in patients with ischemic heart disease.
- Understanding the impact of myocardial ischemia on defibrillation is critical for device efficacy.
Purpose of the Study:
- To determine if myocardial ischemia alters the ventricular defibrillation threshold.
- To simulate conditions relevant to automatic internal defibrillation.
Main Methods:
- Acute myocardial ischemia was induced in dogs via coronary artery embolization.
- Ventricular defibrillation threshold was measured using a catheter electrode before and after ischemia.
- The size of the ischemic zone was correlated with changes in defibrillation threshold.
Main Results:
- Ventricular defibrillation threshold (current and energy) significantly increased after induced myocardial ischemia.
- The increase in defibrillation threshold was positively correlated with the extent of myocardial ischemia.
- These changes persisted for at least 2 hours post-ischemia.
Conclusions:
- Acute myocardial ischemia increases the defibrillation threshold for catheter electrode configurations.
- This necessitates adjustments in the design and application of automatic implantable defibrillators for ischemic heart disease patients.
Abstract:
Because the automatic implantable defibrillator may be used in patients having ischemic heart disease, it is important to know whether myocardial ischemia changes the threshold for ventricular defibrillation under experimental conditions simulating automatic internal defibrillation. We determined changes in ventricular defibrillation threshold following coronary occlusion, using an electrode catheter designed for use with an automatic implantable defibrillator. Acute myocardial ischemia was produced without thoracotomy in 10 dogs (experimental group) by embolization with a plastic bead injected via a catheter into the left coronary artery. A control group of 4 dogs had only saline injected into the artery. Defibrillation threshold was measured at 15-min intervals from 1 hour before embolization to 2 hours after embolization. In the control group, voltage, current, energy, and impedance were unchanged after injection of saline into the coronary artery, and india ink perfusion revealed no ischemic areas. In the experimental group postembolization threshold current and energy were significantly higher than preembolization values: 0.47 vs 0.40 A/kg and 1.01 vs 0.80 J/kg, respectively (p less than 0.01). The magnitude of the peak change in threshold current after embolization was positively correlated (r = 0.79) with the size of the ischemic zone, determined by weighing unstained areas after india ink perfusion. Defibrillation threshold for a catheter electrode configuration increases for at least 2 hours following onset of acute myocardial ischemia. This finding must be accounted for in the design and use of an automatic implantable defibrillator.