Federico Lombardi, Andrea Colombo, Sebastiano Belletti, Alessandro Verzoni, Ezio Calosso, Angelo Beltrami, Cesare Fiorentini
Dipartimento di Medicina, Chirurgia e Odontoiatria, Cardiologia, Ospedale S. Paolo, Universityof Milan, Italy
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In patients with Long QT syndrome or in
survivors of acute myocardial infarction, an association between prolongation of
ventricular repolarisation and cardiac electrical instability has been consistently
reported1,2. More recently, attention has been paid for the finding that also dispersion
of ventricular repolarisation may reflect the presence of an electrophysiological
substrate favouring the occurrence of malignant ventricular arrhythmias3,4. It is well
known that QT interval may present different duration between individual leads of a
standard 12-lead electrocardiogram. This interlead difference may therefore provide a
measure of spatial inhomogeneity of the repolarisation process and may be used to
identify patients at higher arrhythmic risk in a variety of cardiovascular diseases.
In patients with coronary artery disease, QT dispersion was found to be increased after
myocardial infarction and in particular in patients with subsequent arrhythmic events.
Recent evidence suggests that transient myocardial ischaemia may also be associated
with an increased QT dispersion3,4.
There are however several points that have to be taken into account when interpreting
results based on QT dispersion measured on surface electrocardiogram. First of all in
a standard surface electrocardiogram not all leads are directly recorded. Moreover,
some frontal leads have a bipolar configuration, whereas the precordial ones are
unipolar.
The ventricular repolarisation process is inhomogeneous phenomenon also in a normal
heart if we consider different areas of the left ventricle or, within the same ventricular
wall, different layers of myocardium. Thus, some amount of inhomogeneity must be
present also in normal conditions and makes the assessment of extent of
“physiological” dispersion of repolarisation, a critical factor5. It is also important to
recall that QT interval is a rather simple indicator of the duration of ventricular
repolarisation and in many patients an abnormal morphology of T wave prevents a
precise evaluation of T wave end in all 12 leads. Several factors may affect, at different
extent, the ventricular repolarisation process: presence or absence of underlying heart
disease, autonomic nervous system, circulating catecholamines, electrolytes and drugs
are only few of them. One of the most important determinant of the duration of
ventricular repolarisation is the length of the preceding cardiac cycle. This factor has
two major consequences: first that QT interval is shorter in shorter cycles and longer
in longer cycles: an effect that is usually corrected by the use of Bazett formula6. The
second one is the fact that the duration of QT interval may vary throughout the 24 hours
as a results of either changes in cycle length duration and autonomic influences.
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