Abstract
The mechanisms leading to ventricular fibrillation that occur during acute myocardial
ischemia are ill understood. Whether primary ventricular fibrillation is due to a
transient imbalance of electrolytes, an alteration of membrane permeability, electrical
re-entry phenomena, or other factors, one overriding influence is the development
of regional myocardial energy crises. Acute alteration in the balance of substrate
supply may lead, during greatly reduced blood flow, to instability of myocardial electrical
conduction with the development of re-entry circuits. An immediate response to the
angor animi and initial symptoms of an acute coronary syndrome is a rapid and marked
increase in catecholamine release, which leads to adipose tissue lipolysis with an
acute increase in plasma free fatty acid concentrations, suppression of insulin activity,
and a reduction in glucose uptake by the myocardium. The utilization of free fatty
acids instead of glucose by the ischemic myocardium could precipitate regional oxygen
or energy crises. Prevention therefore should focus on minimizing the catecholamine
response and providing the myocardium with an optimum supply of energy substrates.
Since catecholamines are inotropic, the aim should be to redress the imbalance of
substrate availability by controlling adipose lipolysis with reduction of plasma free
fatty acid concentrations, increasing the availability of glucose, or both. Other
approaches include inhibition of acylcarnitine transport and manipulation of fatty
acid intermediaries. To combat primary ventricular fibrillation, preventive treatment
must be established within 6 to 10 hours of the onset of ischemia. There is already
experimental and clinical evidence that antilipolytic drugs decrease the incidence
of ventricular fibrillation, but their potential has not been explored extensively.
Keywords
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Article Info
Publication History
Accepted:
November 5,
2001
Received in revised form:
October 30,
2001
Received:
August 14,
2001
Identification
Copyright
© 2001 Excerpta Medica Inc. Published by Elsevier Inc. All rights reserved.