Background and objectives. Mitral regurgitation (MR) is usually dynamic and increasing with exertion. Stress may provoke symptoms, cause the progression of pulmonary hypertension (PH) and unmask subclinical changes of the left and right ventricle function. The aim of this study was to evaluate changes of right ventricle (RV) functional parameters during stress and to find out determinants of RV function in patients with MR. Materials and methods. We performed a prospective study that included patients with asymptomatic primary moderate to severe MR and preserved left ventricular (LV) ejection fraction (EF) at rest (≥60%). Conventional 2D echocardiography at rest and during stress (bicycle ergometry) and offline speckle tracking analysis were performed. Results. 80 patients were included as MR (50) and control (30) groups. Conventional functional and myocardial deformation parameters of RV were similar in both groups at all stages of exercise (p > 0.05). The grade of MR (p = 0.004) and higher LV global longitudinal strain (p = 0.037) contributed significantly to the changes of tricuspid annular plane systolic excursion (TAPSE) from rest to peak stress. Changes of MR ERA from the rest to peak stress were related to RV free wall longitudinal strain (FWLS) and four chambers longitudinal stain (4CLS) at rest (p = 0.011; r = −0.459 and p = 0.001; r = −0.572, respectively). Significant correlations between LV EF, stroke volume, cardiac output and RV fractional area change, S′, TAPSE, FWLS, 4CLS were obtained. However, systolic pulmonary artery pressure and RV functional, deformation parameters were not related (p > 0.05). Conclusions. Functional parameters of LV during exercise and severity of MR were significant determinants of RV function while PH has no correlation with it in patients with primary asymptomatic moderate to severe MR.

Long QT syndrome (LQTS) is majorly an autosomal dominantly inherited electrical dysfunction, but there are exceptions (Jervell and Lange-Nielsen syndrome is inherited in an autosomal recessive pattern). This disorder prolongs ventricular repolarization and increases the risk of ventricular arrhythmias, syncope, and even sudden cardiac death. The risk of fatal events is reduced during pregnancy, but dramatically increases during the 9 months after delivery, especially in patients with LQT2. In women with LQTS, treatment with β-blockers at appropriate doses is recommended throughout pregnancy and the high-risk postnatal period. In this review, we summarize the management of LQTS during pregnancy and beyond.