Effect of metabolic acidosis on QT intervals in patients with chronic kidney disease.

BACKGROUND: There is a strong association between chronic kidney disease (CKD) and cardiovascular events. Increased arrhythmia risk in kidney disease is one of the main predominant factors in increased mortality and sudden cardiac death. To estimate this risk, noninvasive measurement of repolarization abnormalities including QT interval and its heart rate-corrected value (QTc) with surface ECG, are commonly used parameters in clinical practice. The aim of this study is to examine the effect of CKD-related problems - mainly acidosis - on QT intervals. METHODS: 30 patients with stage 3-5 CKD whose serum bicarbonate concentrations below 20 mmol/L were included in the study. Alkali therapy with oral sodium bicarbonate was used to maintain the serum bicarbonate concentration in the normal range. At the beginning all patients had sinus rhythm on surface ECG records. Kidney function tests including serum urea, serum creatinine, uric acid, blood gas analysis, and electrolytes were analyzed at the beginning and at the end of alkali treatment. All patients underwent 12 lead-ECGs, recorded simultaneously. One cardiologist examined the ECGs manually in terms of QT intervals, corrected for heart rate (QTc), QT dispersion (QTd) and corrected QT dispersion (QTcd). RESULTS: There were statistically significant differences in QT intervals, QTc, QTd and QTcd before and after sodium bicarbonate treatment. The correlation analyses revealed that there were significant negative correlations in pretreatment ECGs of patients between QTd and QTcd with blood pH level. Multivariate analyses between biochemical parameters and QTd-QTcd intervals have revealed that pH was related to QTd and QTc. CONCLUSIONS: This study demonstrated that QT intervals on surface ECG are decreased after treatment of acidosis in CKD. Further studies are needed to show whether increased QT intervals cause ventricular arrhythmias in CKD.

Evaluation of cardiac functions of patients with benign joint hypermobility syndrome.

We sought to investigate whether echocardiography with tissue Doppler imaging identifies myocardial dysfunction in children with benign joint hypermobility syndrome (BJHS). This cross-sectional study enrolled 75 children with BJHS and 70 healthy children. We performed detailed echocardiography in individuals with BJHS without inherited connective tissue disorders. Any congenital or acquired cardiac disease was excluded by clinical and echocardiographic examination. Both groups were similar in terms of age, sex, and body mass index. The diameter of the aortic annulus and sinus valsalva were wider in patients with BJHS. There was no significant differences in ejection fraction or mitral and tricuspid annular plane systolic excursion between the two groups. Pulsed-wave Doppler-derived E/A ratios in mitral and tricuspid valves were similar in both groups. Deceleration time of early mitral inflow was prolonged in patients with BJHS. Mitral and tricuspid annulus Ea velocity were significantly lower in children with BJHS. Ea, Aa, and Ea/Aa ratios in the interventricular septum, left ventricle posterior wall, and right ventricle free wall were lower in patients with BJHS than in the control group. The E/Ea ratio was greater in patients with BJHS than in the control group. Isovolumic relaxation time and right-ventricular (RV) and left-ventricular (LV) myocardial performance indices (MPIs) were greater in patients with BJHS. This study showed the diastolic dysfunction in patients with BJHS. In addition, we detected increased LV and RV MPI. We believe that BJHS may affect proteins of the myocardial cytoskeleton and extracellular matrix.