MAPPING OF VENTRICULAR REPOLARIZATION POTENTIALS IN PATIENTS WITH ARRHYTHMOGENIC RIGHT-VENTRICULAR DYSPLASIA - PRINCIPAL COMPONENT ANALYSISOF THE ST-T WAVES
L. Deambroggi et al., MAPPING OF VENTRICULAR REPOLARIZATION POTENTIALS IN PATIENTS WITH ARRHYTHMOGENIC RIGHT-VENTRICULAR DYSPLASIA - PRINCIPAL COMPONENT ANALYSISOF THE ST-T WAVES, Circulation, 96(12), 1997, pp. 4314-4318
Background Nonuniform recovery of ventricular excitability has been de
monstrated to facilitate the reentry circuits leading to the developme
nt of ventricular tachyarrhythmias. This can also occur in arrhythmoge
nic right Ventricular dysplasia (ARVD). In fact, in patients with ARVD
, abnormalities of ventricular repolarization are often observed on 12
-lead ECGs, but their predictive value for the occurrence of malignant
arrhythmias is yet to be established. Because body-surface potential
mapping has been proved to be useful for the detection of heterogeneit
ies in ventricular recovery even though they are not revealed by conve
ntional 12-lead ECGs, we attempted to analyze repolarization potential
s on the entire chest surface to find abnormalities that can be predic
tive of ventricular arrhythmias. Methods and Results Body-surface pote
ntial maps were recorded from 62 anterior and posterior thoracic leads
in 22 patients affected by ARVD, 9 with episodes of sustained ventric
ular tachycardias (VT) and 13 without. Thirty-live healthy subjects we
re also studied as control subjects. The 62 chest ECGs were simultaneo
usly recorded, digitally converted at a rate of 2000 Hz, and stored on
a hard disk of a body-surface mapping computer system. In each subjec
t, the QRST integral map was obtained by calculating at each lead poin
t the algebraic sum of all instantaneous potentials, from the QRS onse
t to the T-wave end, multiplied by the sampling interval. In most ARVD
patients, we observed a larger-than-normal area of negative values on
the right anterior thorax. This abnormal pattern could be explained b
y a delayed repolarization of the right ventricle. Nevertheless, it wa
s not related to the occurrence of VT in our patient population. To de
tect minor heterogeneities of ventricular repolarization, the principa
l component analysis was applied to the 62 ST-T waves recorded in each
subject. We assumed that a low value of the first or of the first thr
ee components (components 1, 2, and 3) indicates a greater-than-normal
variety of the ST-T waves, a likely expression of a more complex reco
very process. The mean values of the first three components were not s
ignificantly different in ARVD patients and control subjects. Neverthe
less, considering the two subsets of patients with and without VT, the
values of component 1, components 1+2, and component 1+2+3 were signi
ficantly lower in the group of ARVD patients with VT. Values of compon
ent 1 < 69% (equal to 1 SD below the mean value for control subjects)
were found in 6 of 9 VT patients and in 1 patient without VT (sensitiv
ity, 67%; specificity, 92%). A low value of component 1 was the only v
ariable significantly associated with the occurrence of VT. Conclusion
s Principal component analysis provides a better quantitative assessme
nt of the complexity of repolarization than other ECG measurements. Wh
en applied to ARVD patients, principal component analysis of the ST-T
waves recorded from the entire chest surface revealed abnormalities no
t detected by conventional ECG that can be considered indexes of arrhy
thmia vulnerability.