Key result
Acute myocardial ischemia increases ventricular fibrillation vulnerability by slowing conduction and disrupting refractoriness.
Why the study?
The excitability characteristics of myocardium in ischemic regions caused by coronary artery ligation were studied to understand mechanisms underlying ventricular fibrillation during myocardial infarction.
Population
Canine hearts with ischemic region produced by coronary artery ligation
Comparison
Electric stimulation using a specially devised multipolar electrode
Design
Experimental study on myocardial excitability
Authors
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May promote reentry in acute ischemia; leaves open human translation of excitability changes.
Ischemia-induced changes in myocardial excitability, including asynchronous recovery and lowered vulnerable threshold, explain the high risk of ventricular fibrillation during acute myocardial infarction.
Tetsuo Tsuchida (1965) studied Myocardial Infarction (Experimental) (n=20). Coronary artery ligation (myocardial ischemia) vs. Intact myocardium / pre-ligation control was evaluated on Changes in refractory period, diastolic threshold, and conduction velocity. Experimental myocardial ischemia in a canine model caused asynchronism in refractoriness recovery, markedly low conduction velocity, and shortened refractory periods, increasing vulnerability to ventricular fibrillation.
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