Acute decompensated heart failure has an increasing incidence and poor prognosis, being a major cause of death and hospital readmission and requiring urgent optimized therapy[1]. Under the influence of some decompensation risk factor, such as infections, arrhythmias, decompensation of some comorbidities, lack of adherence to the treatment, patients with a history of heart failure may suffer a progressive symptomatology worsening
therefore, more than 70% of cases of acute heart failure represent the clinical worsening of chronic heart failure - ADHF[2]. [...]

Hypertension associates with sudden cardiac death, its relationship with ventricular arrhythmias being demonstrated by numerous studies (1). Multiple mechanisms were proposed in order to explain this association, involving both structural and electrophysiological myocardial changes. The electrical ventricular remodeling includes non-uniform prolongation of action potential and duration heterogeneity of refractory periods and conduction velocities of adjacent myocardial areas. All of these changes are referred to as increased dispersion of ventricular repolarization.
As cellular basis for this important mechanism of arrhythmogenesis, 3 myocardial cell types were described, with distinct electrophysiological properties: epicardial, endocardial and midmiocardial M cells (2). Differences between their repolarization periods have as an electrocardiographic correspondence changes in T wave features (2). Subsequently, several non-invasive electrocardiographic (ECG) parameters were proposed for quantification of the repolarization dispersion such as QT interval duration, QT dispersion (QTd), T wave microalternans, and more recently, T peak - T end interval (Tpe), T peak - T end/QT ratio (Tpe/QT) and T peak - T end interval dispersion (dTpe).