Principal Component Analysis of the T Wave in Patients with Chest Pain and Conduction Disturbances

Abstract

There is a need for markers reflecting the increased risk in patients with conduction disturbances. Conduction disturbances presumably cause inhomogeneous repolarization that may create an arrhythmogenic substrate. In patients with normal conduction, parameters derived from principal components analysis (PCA) of the T wave contain prognostic information. The nondipolar PCA components are assumed to reflect repolarization inhomogeneity. This study examined the PCA parameters in relation to conduction disturbances. PCA was performed on continuously recorded 12-lead ECGs in 800 patients with chest pain and nondiagnostic ECG on admission. The patients with conduction disturbance on admission were classified into separate groups and related to comparison groups without conduction disturbance recruited from the same series. For each patient, the dipolar and nondipolar components were quantified by medians of the ratio of the two largest eigenvalues (S2/S1 Median), the residue that summarizes the eigenvalues S4-S8 (TWRabsMedian) and the ratio of this residue to the total power of the T wave (TWRrelMedian). The parameters were assessed with respect to common clinical and ECG parameters, discharge diagnosis, and total mortality during a 35-month follow-up. TWRabsMedian increased with increasing conduction disturbance. In 135 patients with conduction disturbances, ROC curves for TWRabsMedian as indicator of mortality exhibited areas under a curve of 0.66, 0.65, and 0.56 at 6-month, 24-month, and 35-month follow-up. Conduction disturbances were associated with increased nondipolar PCA component and, thus, with increased repolarization inhomogeneity. The nondipolar PCA component contained a moderate amount of prognostic information not present in a simple ECG diagnosis of a conduction disturbance.

Quantification of not-dipolar components of atrial depolarization by principal component analysis of the P-wave

“…The PcA of the T-wave led to promising results, in terms of quantification of ventricular repolarization inhomogeneity that may create an arrhythmogenic ventricular substrate [9][10][11][12]. PcA can be used to estimate the dipolar and the not dipolar components of the P-wave, and thus its use could led to interesting results in terms of analysis of atrial path from surface EcG.…”

“…Such parameters are different from those employed for the T-wave analysis [10][11][12], even if, as for the T-wave, the chosen parameters are related to the first three Pcs associated to the dipolar component of the Pwave, and to the remaining Pcs associated to the not dipolar component of the P-wave (100%-EV).…”

“…Since PcA transforms the measured P-wave to virtual parameters that are mutually independent (orthogonal), the 3 largest Pcs would contain all the information in the P-wave stemming from the vectorial concept of a single electrical dipole. Following an approach already applied to the T-wave [10,12], the other principal components (in this case from the 4 th to the 32 nd ) represent the not dipolar components of the atrial depolarization.…”

“…Promising results have been obtained by measuring the QT interval (QT dispersion) and by performing the principal component analysis of the T-wave [9][10][11][12][13][14].…”

“…Principal component analysis (PcA) of the T-wave has been extensively used to quantify both the complexity and the not dipolar components of the T-wave [9][10][11][12]: particularly, if the EcG would be completely explained by a single electrical dipole, the three largest principal components (Pcs), and their corresponding orthogonal eigenvectors, would span the real three dimensional space (dipolar components), while the remaining Pcs (not dipolar components) would be zero [12]. For the T-wave it has been demonstrated that the not dipolar components, quantified by the PcA, are not zero, and reflect local repolarization heterogeneity [12]. Accordingly, the PcA of the P-wave could help in analyzing the heterogeneous propagation of sinus impulses in the atria, which seems to predispose to fibrillation.…”