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Sudden unexpected cardiac death.

Why are we not doing more to prevent sudden unexpected cardiac death? Why is prevention of the principal cause of death occurring during acute myocardial ischaemia and impending myocardial infarction ignored? The majority are caused by ventricular fibrillation. This is most common within the first hour after the onset of an acute coronary syndrome and occurs with decreasing frequency thereafter. While this has been known and adequately documented for many years, only two approaches to combat this very early mortality have been made and both are too late to make any large impact on mortality. One has been the use of paramedics and nurses to provide immediate resuscitation with rapid transit of patients to emergency areas. The other is the use of implantable defibrillators. The former has increased the survival rate. The latter has had no effect on early death during the first attack, since the defibrillator is inserted for repetitive ventricular arrhythmias occurring many hours after the initial crisis. The main reason for the onset of ventricular fibrillation in this early acute phase of ischaemia is a myocardial metabolic crisis due to an excess uptake of free fatty acids resulting from catecholamine stimulation of tissue lipolysis. At the same time, the availability of glucose is reduced as a result of reduction in the myocardial uptake of glucose due to insulin suppression and limited glycaemia, and also inadequate myocardial glycogenolysis. In ischaemia, beta-oxidation of lipids in the mitochondria is inhibited by accumulation of acylcarnitine and acyl-coenzyme A leading to cytosolic calcium overload and potentially to arrhythmias. Detergent CoA derivatives can also favour the onset of arrhythmias. Uncoupling of oxidative metabolism with irreversible electron transfer may occur. What is needed is an otherwise harmless solution to protect against the onset of ventricular fibrillation. It should be injected intravenously immediately the patient is first seen by paramedics in the patient’s home, office or in the street, whenever acute ischaemia is suspected. It should be designed to modulate and minimize the metabolic crisis. There are already some possibilities. One is a solution of omega-3 fatty acids which have a very