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]. [...]

The link between kidney damage and HT remains a challenge in medical research from a century when HT concept was defined, taking in consideration than HT is a major risk factor for cardiovascular disease morta-lity worldwide, due to the increasing prevalence, poor compliance to treatment and many complications[1-3]. The hypertensive nephrosclerosis is currently diagnosed in the latest stages of the disease because, for a long period of time, the injuries are compensated by kidney and therefore the clinical presentation is not specific[4]. The current diagnostic methods are non-specific, especially for early diagnosis of hypertensive nephrosclerosis, except the renal biopsy which is considered the gold standard but is rarely indicated in clinical routine due to its invasiveness and possible severe complications[5]. The pathogenic mechanism is complex and not very well understood but renal microcirculation impairment seems to be responsible for the onset and progression of this disease[6]. Therefore, any method that can accurately assess the early microvasculature changes of renal cortex, easy to use, simple and safe, with no invasiveness, could be an important diagnostic tool in hypertensive nephrosclerosis approach. [...]

Despite the advanced technologies, the 12 leads electrocardiogram (ECG) remains an important investigation modality for providing a fast diagnostic of acute coronary syndromes (ACS). This method offers data concerning the presence, extension and severity characterizing the ischemic process (1). The ECG interpretation is still essential during the initial evaluation of patients admitted for ischemia suggestive symptoms (2).
Moreover, being a cheap, non-invasive and accessible technique, ECG continues to represent the gold-standard alternative for the differential diagnostic, for determining the appropriate treatment approach, for selecting patients susceptible of benefiting from reperfusion as well as regarding risk stratification (1).

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).