Differing myocardial response to a single session of hemodialysis in end-stage renal disease with and without type 2 diabetes mellitus and coronary artery disease

Abstract

Background: Though hemodialysis (HD) acutely improves cardiac function, the impact of background diseases like coronary artery disease (CAD) and Type 2 diabetes (DM) in the setting of end-stage renal disease (ESRD) is not known. Tissue velocity echocardiography (TVE) offers a fast choice to follow changes in myocardial function after HD in ESRD with concomitant DM and /or CAD.

Methods: 46 subjects (17 with ESRD, Group 1; 15 with DM, Group 2; 14 with DM+CAD, Group 3) underwent standard and TVE prior to and shortly after HD. Besides standard Doppler variables, regional myocardial systolic and diastolic velocities, as well as systolic strain rate were post processed.

Results: Compared with pre-HD, post-HD body weight (kg) significantly decreased in all the three groups (51 +/- 9 vs. 48 +/- 8, 62 +/- 10 vs.59 +/- 10, and 61 +/- 9 vs. 58 +/- 9 respectively; all p < 0.01). Left ventricular end diastolic dimensions (mm) also decreased post- HD (46 +/- 5 vs. 42 +/- 7, 53 +/- 7 vs. 50 +/- 7, 51 +/- 7 vs. 47 +/- 8 respectively; all p < 0.01). Regional longitudinal peak systolic velocity in septum (cm/s) significantly increased post-HD in Group 1(5.7 +/- 1.6 vs. 7.2 +/- 2.3; p < 0.001) while remained unchanged in the other two groups. Similar trends were noted in other left ventricular walls. When the myocardial velocities (cm/s) were computed globally, the improvement was seen only in Group 1 (6.3 +/- 1.5 vs. 7.9 +/- 2.0; p < 0.001). Global early regional diastolic velocity (cm/s) improved in Group 1, remained unchanged in Group 2, while significantly decreased in Group 3(-5.9 +/- 1.3 vs. -4.1 +/- 1.8; p < 0.01). Global systolic strain rate (1/sec) increased in the first 2 Groups but remained unchanged (-0.87 +/- 0.4 vs. -0.94 +/- 0.3; p = ns) in Group 3.

Conclusion: A single HD session improves LV function only in ESRD without coexistent DM and/or CAD. The present data suggest that not only dialysis-dependent changes in loading conditions but also co-existent background diseases determine the myocardial response to HD.

Figure 1

Upper left: A typical color-Doppler velocity profile obtained by positioning the sample volume in the septum base. S1 = isovolumic contraction velocity in the first positive peak, PSV = peak systolic velocity. IVCT and IVRT respectively are isovolumic contraction and relaxation times, E'and A'are respectively early and late diastolic velocities. The velocity profile is accompanied by an ECG signal. Upper right. A systolic displacement image, obtained by integration of the respective velocity profile during systole that provides amplitude of total displacement (usually ≥ 12 mm in healthy individuals). Lower panel. Strain rate imaging in which the white arrow indicates peak systolic strain rate obtained by spatial differential of velocities at two points divided by the distance between them. In our laboratory the insonation distance of approximately 15 mm provides a favorable signal-to-noise ratio [27].

Figure 2

Global longitudinal myocardial systolic (PSV), early (E') and late diastolic (A') velocities, pre- and post-hemodialysis. † p < 0.01; ‡ p < 0.001. Results were obtained by taking average of 4 left ventricular basal segments pre- (closed symbols) and post- (open symbols) hemodialysis. Data are mean ± SD

Figure 3

Global longitudinal strain rate measured pre- and post-hemodialysis. * p < 0.001 for within-group paired comparisons between pre-and post-HD. Data represent average values of strain rate measurements obtained from the 12 left ventricular segments.