Abstract. 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 preloadindependent 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 Ͻ 0.01) than before HD (0.77; 0.60 to 1.34). E decreased (P Ͻ 0.01), whereas A did not. PV s/d after HD (2.15; 1.08 to 3.90) was higher (P Ͻ 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 Ͻ 0.01) than before HD (0.56; 0.40 to 1.05). Tissue e decreased (P Ͻ 0.02), whereas a did not. V p after HD (30 cm/s; 16 to 47 cm/s) was lower (P Ͻ 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.Intradialytic hypotension is an important complication of hemodialysis (HD), and its pathogenesis is not completely understood. It frequently requires intervention, which limits the efficacy of HD. The incidence is 25% with a range of 15 to 50% (1-3) and increases with age. Hypotension results from a decreased product of stroke volume (SV), heart rate, and systemic vascular resistance. Compensatory mechanisms, such as tachycardia and arterial vasoconstriction, require adequate venous return. Ultrafiltration (UF) withdraws volume from the hemodynamically active "central" circulation, whereas most of the volume overload resides in the interstitial and, to a lesser extent, in the intracellular compartment. The venous system contains an important buffer against hypovolemia (2,4 -6). However, if plasma-refilling rate lags behind UF rate, then intravascular volume depletion may exceed the limit of the buffer capacity, ...

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An elevated pulse pressure leads to an increased pulsatile cardiac load, and results from arterial stiffening. The aim of our study was to test whether a reduction in volume overload by ultrafiltration (UF) during haemodialysis (HD) leads to an improvement of aortic compliance. In 18 patients, aortic compliance was estimated noninvasively before and after HD with UF using a pulse pressure method based on the Windkessel model. This technique has not been applied before in a dialysis population, and combines carotid pulse contour analysis by applanation tonometry with aortic outflow measurements by Doppler echocardiography. The median UF volume was 2450 ml (range 1000-4000 ml). The aortic outflow volume after HD (39 ml; 32-53 ml) was lower (P ¼ 0.01) than before (46 ml; 29-60 ml). Carotid pulse pressure after HD (42 mmHg; 25-85 mmHg) was lower (P ¼ 0.01) than before (46 mmHg; 35-93 mmHg).Carotid augmentation index after HD (22%; 3-30%) was lower (P ¼ 0.001) than before (31%; 7-53%). Carotidfemoral pulse wave velocity was not different after HD (8.7 m/s; 5.6-28.9 m/s vs 7.7 m/s; 4.7-36.8 m/s). Aortic compliance after HD (1.10 ml/mmHg; 0.60-2.43 ml/ mmHg) was higher (P ¼ 0.02) than before (1.05 ml/mmHg; 0.45-1.69 ml/mmHg). The increase in aortic stiffness in HD patients is partly caused by a reversible reduction of aortic compliance due to volume expansion. Volume withdrawal by HD moves the arterial wall characteristics back to a more favourable position on the nonlinear pressure-volume curve, reflected in a concomitant decrease in arterial pressure and improved aortic compliance.