Three-dimensional echocardiographic analysis of left ventricular function during hemodialysis.

BACKGROUND: The effects of hemodialysis (HD) on left ventricular (LV) function have been studied by various echocardiographic techniques (M-mode, 2D echocardiography). These studies are hampered by a low accuracy of measurements because of geometric assumptions regarding LV shape. Three-dimensional echocardiography (3DE) overcomes this limitation. METHODS: We tested the feasibility of 3DE assessment of LV function during HD. Conventional biplane Simpson rule (BSR) and single plane area length method (SPM) for LV function analysis were used as a reference. RESULTS: 12 HD patients were studied and in 10 (83%) a total of 80 3D datasets were acquired. In 3 patients, one dataset (4%) was of insufficient quality and excluded from analysis. Correlation between SPM, BSR and 3DE for calculation of end-diastolic (EDV, r = 0.89 and r = 0.92, respectively), end-systolic volume (ESV, r = 0.92 and r = 0.93, respectively) and for ejection fraction (EF, r = 0.90 and r = 0.88, respectively) was moderate. Limits-of-agreement results for EDV and ESV were poor with confidence intervals larger than 30 ml. Both 2DE methods underestimated end-diastolic and end-systolic volume, while overestimating ejection fraction. CONCLUSION: 3DE is feasible for image acquisition during HD, which opens the possibility for accurate and reproducible measurement of LV function during HD. This may improve the assessment of the acute effect of HD on LV performance, and guide therapeutic strategies aimed at preventing intradialytic hypotension.

Norepinephrine-induced vasoconstriction results in decreased blood volume in dialysis patients.

BACKGROUND: Hypotension during haemodialysis results from an inadequate cardiovascular response to ultrafiltration-induced hypovolaemia. It has been suggested that plasma volume could be increased as a result of systemic vasoconstriction. METHODS: We studied the effect of a norepinephrine (NOR) infusion (30 min), compared with no infusion, on relative blood volume (RBV) in six haemodialysis patients. During infusion we measured RBV, systolic blood pressure (SAP), heart rate (HR), stroke volume index (SI), total peripheral resistance (TPRI), ejection fraction (EF), inferior vena cava diameter (VCD) and core temperature. RESULTS: At the end of the NOR infusion, we observed a significant increase in TPRI (47+/-47% vs 4+/-17%; P<0.01) and SAP (27+/-12% vs 0+/-8%; P<0.01). Norepinephrine-induced vasoconstriction resulted in a significant decrease in RBV (-9+/-3% vs 0+/-1%; P<0.01). No significant changes were seen in SI (-4+/-21% vs 0+/-8%), HR (-5+/-19% vs -4+/-5%), EF (7+/-14% vs -2+/-10%), VCD or temperature. CONCLUSIONS: We conclude that norepinephrine-induced vasoconstriction results in a decrease in RBV. This indicates that improved haemodynamic stability during haemodialysis through vasoconstriction can be accompanied by a decrease in RBV and that part of the variability in blood volume may be due to changes in arterial tone. Such changes must be taken into account if RBV measurements are used to improve the haemodynamic tolerance of dialysis.

Myocardial contractility does not determine the haemodynamic response during dialysis.

BACKGROUND: LV systolic dysfunction in dialysis patients has been implicated in the genesis of dialysis hypotension. End-systolic elastance (E(es)), a relatively load-independent parameter of myocardial contractility, was assessed by testing the acute left ventricular (LV) response to nitroglycerine (NTG) in hypotension-prone (HP) and hypotension-resistant (HR) patients. METHODS: Routine measurement of ejection fraction (EF) was done before dialysis in 15 patients without significant valvular disease or symptoms of coronary heart disease. Continuous arterial pressure was measured by Finapres, with systolic blood pressure (SBP) as surrogate for LV end-systolic pressure. Simultaneously, LV area was measured using automated border detection. SBP and LV area data were combined online to create pressure-area loops in real time following intravenous NTG bolus. E(es) was determined offline by beat-to-beat analysis of consecutive pressure-area loops. RESULTS: SBP, at baseline 168 mmHg (128-188 mmHg), decreased to 127 mmHg (79-161 mmHg). End-systolic LV area, at baseline 6 cm2 (1-12 cm2), decreased to 4 cm2 (1-10 cm2). E(es) in the HP group (11 mmHg cm(-2); 7-22 mmHg cm(-2)) was not different from E(es) in the HR group (9 mmHg cm(-2); 4-16 mmHg cm(-2)). EF was 61% (45-73%). There was no correlation between E(es) and EF. CONCLUSIONS: In this population of dialysis patients without clinically manifest heart disease, the HP and HR groups had a similar E(es). Therefore, these two types of dialysis patients were not distinguished by a difference in myocardial contractility. The results of this study argue against a role for reduced myocardial contractility in the genesis of intradialytic hypotension.

Significance of acute versus chronic troponin T elevation in dialysis patients.

INTRODUCTION: Cardiac troponin T (cTnT) is often elevated in hemodialysis (HD) patients without acute coronary syndrome (ACS). The aim was to assess the predictive value for mortality of pre-dialysis cTnT in asymptomatic patients. If patients became symptomatic during follow-up, cTnT was followed to assess its diagnostic value for ACS. METHODS: Forty-nine asymptomatic HD patients were included: 30 patients with a history of cardiovascular disease (CV+) and 19 without (CV-). In 11 patients cTnT, myoglobin and creatine kinase (CK) were measured before and during HD. During ACS, cTnT was followed until recovery. A cTnT of > or =0.03 mug/l was considered elevated. Follow-up was 2 years. RESULTS: cTnT was elevated in 82% (40/49). More CV+ patients had an elevated cTnT (28/30) than CV- patients (12/19; p = 0.02). There was no change in cTnT, myoglobin and CK during HD. During ACS, cTnT increased above baseline, and tended to return to baseline after recovery. Mortality was 33% (16/49). Patients with elevated cTnT had a higher mortality rate (16/40) than patients with negative cTnT (0/9; p = 0.02). CONCLUSIONS: Elevated cTnT levels in asymptomatic HD patients are not caused by acute myocardial injury or by HD itself. They may be related to chronic myocardial damage and decreased clearance, and are of prognostic value. During ACS, however, a cTnT rise above the individual baseline is diagnostic of acute myocardial injury.

Increase in serum ionized calcium during diffusive dialysis does not affect left ventricular diastolic function.

An increase in serum Ca2+ during hemodialysis (HD) may lead to impaired left ventricular (LV) relaxation. Since LV diastolic function assessment in dialysis patients is hampered by preload dependence of Doppler measurements, we tested the effect of HD without ultrafiltration (UF) on these measurements. Transmitral E and A velocities, and mitral annulus e and a velocities were measured in 10 patients before and after 1 h of HD without UF. Dialysate Ca2+ was 1.75 mmol/l. Serum Ca2+ after 1 h (1.31 mmol/l; 1.28-1.46 mmol/l) was higher (p = 0.002) than before HD (1.24 mmol/l; 1.09-1.32 mmol/l). E/A (0.8; 0.4-2.8) and e/a (0.7; 0.4-1.3) after 1 h were not different than E/A (0.8; 0.6-5.1) and e/a (0.7; 0.4-1.8) before HD. The increase in serum Ca2+ does not lead to a change in Doppler parameters of LV diastolic function. Changes in these parameters after combined HD-UF are related to preload, not to serum Ca2+.

Preload dependence of new Doppler techniques limits their utility for left ventricular diastolic function assessment in hemodialysis patients.

Left ventricular (LV) hypertrophy leads to diastolic dysfunction. Standard Doppler transmitral and pulmonary vein (PV) flow velocity measurements are preload dependent. New techniques such as mitral annulus velocity by Doppler tissue imaging (DTI) and LV inflow propagation velocity measured from color M-mode have been proposed as relatively preload-independent measurements of diastolic function. These parameters were studied before and after hemodialysis (HD) with ultrafiltration to test their potential advantage for LV diastolic function assessment in HD patients. Ten patients (seven with LV hypertrophy) underwent Doppler echocardiography 1 h before, 1 h after, and 1 d after HD. Early (E) and atrial (A) peak transmitral flow velocities, peak PV systolic (s) and diastolic (d) flow velocities, peak e and a mitral annulus velocities in DTI, and early diastolic LV flow propagation velocity (V(p)) were measured. In all patients, the E/A ratio after HD (0.54; 0.37 to 1.02) was lower (P < 0.01) than before HD (0.77; 0.60 to 1.34). E decreased (P < 0.01), whereas A did not. PV s/d after HD (2.15; 1.08 to 3.90) was higher (P < 0.01) than before HD (1.80; 1.25 to 2.68). Tissue e/a after HD (0.40; 0.26 to 0.96) was lower (P < 0.01) than before HD (0.56; 0.40 to 1.05). Tissue e decreased (P < 0.02), whereas a did not. V(p) after HD (30 cm/s; 16 to 47 cm/s) was lower (P < 0.01) than before HD (45 cm/s; 32 to 60 cm/s). Twenty-four hours after the initial measurements values for E/A (0.59; 0.37 to 1.23), PV s/d (1.85; 1.07 to 3.38), e/a (0.41; 0.27 to 1.06), and V(p) (28 cm/s; 23 to 33 cm/s) were similar as those taken 1 h after HD. It is concluded that, even when using the newer Doppler techniques DTI and color M-mode, pseudonormalization, which was due to volume overload before HD, resulted in underestimation of the degree of diastolic dysfunction. Therefore, the advantage of these techniques over conventional parameters for the assessment of LV diastolic function in HD patients is limited. Assessment of LV diastolic function should not be performed shortly before HD, and its time relation to HD is essential.