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Significance of paced ventricular electrogram fractionation in non-coronary sudden cardiac death


To test a new electrophysiological method of investigating patients at risk of non-coronary sudden cardiac death(SCD).
To obtain a 'library' of recordings from different diseases which can be related to the risk of SCD.
To expand the number of pacing protocols used at present to gain more information about the refractory state of the myocardium.
To use the data to construct diagnostic protocols which may quantify the risk of SCD in different diseases and be tested prospectively.

Sudden cardiac death (SCD) due to malignant arrhythmias in young people is a pressing medical problem and may be caused by a number of heart muscle diseases including hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM) and arrhythmogenic right ventricular dysplasia. At present there is no method of investigating these patients to either assess their risk of SCD so that preventative treatment may be instituted, or understanding the mechanisms of their fatal arrhythmia.
This proposal is to gain experience with a new technique, developed by the applicant, which may detect part of the arrhythmic substrate in patients with diseases which cause SCD. The technique involves measuring the delays in conduction of fractionated potentials in response to premature paced extrastimuli through ventricular myocardium. Its basis is that demonstration of slowed conduction of individual fractionated potentials, which correspond to activation of different fibres close to the recording electrode, will reveal dispersion of conduction which forms one component of a re-entrant substrate. This technique has been performed in 180 patients and there is a striking association between the absolute and relative delays in fractionated potentials and the likelihood of SCD in HCM, 'normal heart' ventricular fibrillation (VF) and DCM.
Although the work performed so far has studied conduction in diseased myocardium, one major factor in arrhythmogenesis is the refractoriness of the myocardium between the stimulating and recording electrodes. This will be studied by using pacing sequences which alter the diastolic interval, and hence refractory period of the myocardium, prior to the extrastimulus. These measurements will give information about tissue refractoriness and thus a more complete description of the myocardium in terms of arrhythmogenesis.


The Chancellor, Masters and Scholars of the University of Cambridge
Cranmer Terrace
SW17 ORE London
United Kingdom