Commentary: QTc dispersion may reflect vulnerability to ventricular fibrillation

BMJ 1996; 312 doi: (Published 06 April 1996) Cite this as: BMJ 1996;312:878
  1. R Campbell, head of departmenta
  1. a Department of Academic Cardiology, Freeman Hospital, Newcastle upon Tyne NE7 7DN

    Peripheral vascular disease is a marker of coronary artery disease, and QT dispersion (the difference between the longest and the shortest measurable interval on the 12 lead electrocardiogram) is emerging as an important marker of serious arrhythmias and sudden death. To link these two markers is not at first intuitive, but the common ground lies in the spectre of coronary artery disease. Darbar et al correlate peripheral vascular disease not just with any coronary artery disease but with the type that carries the highest risk of death. With a modest patient cohort (49) cardiac death was strongly correlated with the QTc dispersion. Values of > 60 ms had a 92% sensitivity and an 81% specificity in predicting this outcome. These are impressive results, particularly from a cheap, widely available test that is already performed in most such patients.

    The history of QT dispersion is comparatively short, but it is emerging as a remarkably powerful predictor of cardiac death in such diverse areas as the long QT syndromes, heart failure, and hypertrophic cardiomyopathy. Its cellular basis is still not fully established, but QT variations in surface electrocardiography in humans have been correlated with epicardial monophasic action potential durations. Thus, for whatever reason and by whatever physics, regional variation and repolarisation can be revealed by conventional body surface electrocardiography. In the positive correlations of QT dispersion and mortality shown in previous studies it is easy to imagine a mechanism related through ventricular fibrillation. Dispersion of repolarisation, which may be reflected by QT dispersion, is crucial for the initiation and maintenance of ventricular fibrillation. Acute myocardial infarction that complicates primary ventricular fibrillation may even be predicted by QT dispersion, but would we really expect that death, even cardiovascular death, would be predicted by the phenomenon in patients with peripheral vascular disease? I did not. I imagined that peripheral vascular disease was associated with occult (or overt) coronary artery disease and that death might arise by various mechanisms: infarction, failure, or arrhythmias. If QT dispersion predicted only the latter I would have expected that any mortality related to QT dispersion would be lost in other fatal end points. My concept seems wrong, or at least it is not supported by the present study. I lay considerable store by biological plausibility, and I look to corroborating data and to more detailed analysis of how patients die before I would be fully comfortable with the results.

    If QT dispersion is really so specific and so sensitive, however, it may mean that ventricular fibrillation is more prevalent than we currently acknowledge. QT dispersion may reflect a threshold measure of vulnerability to ventricular fibrillation. Thus in a patient with peripheral vascular disease in whom the myocardium is affected in such a way as to disturb repolarisation a propensity to ventricular fibrillation is established and may be revealed by a variety of triggers, including ischaemia.

    Our prognostic assessment of patients is improving, but we have little or nothing to offer as protection. Perhaps new information contained in QT dispersion analysis will open new therapeutic directions. We read and write such comments all too often with little realistic prospect that things will change. This time, however, I am optimistic. QT dispersion has been unnoticed for decades. It is proving important and is our only non-invasive marker of regional variations of refractoriness. It may be that regardless of aetiology it can reflect a propensity to ventricular fibrillation. In this simple tool we may be glimpsing the electro-physiological Holy Grail.

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