Abstract

The long interdialytic interval in thrice-weekly hemodialysis is associated with excess cardiovascular risk. However, the mechanisms behind these adverse consequences are not fully understood. This study investigated the interdialytic changes in right and left ventricular function during the 2- and 3-day intervals. Observational study with 2 random crossover sequences of recordings: 3-day followed by 2-day interval or vice versa. 41 stable patients with end-stage renal disease on standard thrice-weekly hemodialysis therapy. 3-day (long) versus 2-day (short) interdialytic interval. Interdialytic change in echocardiographic indexes of left and right ventricular function. 2-dimensional echocardiographic and tissue Doppler imaging studies were performed with a Vivid 7 cardiac ultrasound system at the start and end of the 3- and 2-day interdialytic intervals. During both intervals studied, elevations in cardiac output, stroke volume, left ventricular mass index, and peak early diastolic velocities of the left ventricle were evident. Interdialytic weight gain (3.0±1.7 vs 2.4±1.3 [SD] kg) and inferior vena cava diameter increase (0.54±0.3 vs 0.25±0.3) were higher during the 3-day versus the 2-day interval (P<0.001). Left ventricular systolic and diastolic function indexes were generally no different between interdialytic intervals. In contrast, interdialytic increases in left and right atrial volume, right ventricular systolic pressure (RVSP; 15.3±10.2 vs 4.7±5.2mmHg; P<0.001), and tricuspid regurgitation maximum velocity (0.46±0.45 vs 0.14±0.33m/s; P=0.001) were significantly greater during the 3- versus the 2-day interval. Multivariable analysis suggested that changes in interdialytic weight gain, right ventricle diastolic function, and pulmonary vascular resistance were determinants of the change in RVSP. Observational study design. Excess volume accumulation over the long interdialytic interval in hemodialysis patients results in higher left and right atrial enlargement and RVSP elevation, which clinically corresponds to pulmonary circulation overload, providing one plausible pathway for the excess mortality risk during this period.

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