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Haemodynamic response during low-dose dobutamine infusion in patients with chronic systolic heart failure: comparison of echocardiographic and invasive measurements

  1. Michael Egstrup1,*
  2. Ida Gustafsson2
  3. Mads Jønsson Andersen3,
  4. Caroline Nervil Kistorp4
  5. Morten Schou3
  6. Christian Ditlev Tuxen5 and
  7. Jacob Eifer Møller3
Author Affiliations


  1. 1Department of Cardiology and Endocrinology, Frederiksberg University Hospital, Nordre Fasanvej 59, Frederiksberg 2000, Denmark


  2. 2Department of Cardiology, Herlev University Hospital, Herlev Ringvej 75, Herlev 2730, Denmark


  3. 3Department of Cardiology, Rigshospitalet, Blegdamsvej 9, Copenhagen 2100, Denmark


  4. 4Department of Endocrinology, Herlev University Hospital, Herlev Ringvej 75, Herlev 2730, Denmark


  5. 5Department of Cardiology, Bispebjerg University Hospital, Tuborgvej 235, Copenhagen 2400, Denmark

  1. *Corresponding author. Tel: +45 22 64 15 40; fax: +45 38 16 40 29, Email:michaelegstrup@dadlnet.dk
  • Received June 19, 2012.
  • Revision received September 21, 2012.
  • Accepted October 12, 2012.

Abstract

Aims To investigate whether left ventricular (LV) systolic shortening velocity (s′), diastolic lengthening velocity (e′), and non-invasively estimated LV filling pressure (E/e′) during low-dose dobutamine echocardiography (LDDE) reflect invasive measures of cardiac output and pulmonary capillary wedge pressure (PCWP) in stable patients with chronic systolic heart failure.
Methods and results Fourteen patients with heart failure (aged 65 ± 8 years, LVEF 36 ± 8%) underwent simultaneous tissue Doppler echocardiography and invasive measurements of cardiac output and PCWP by right heart catheterization at rest and during dobutamine infusion at rates of 10 and 20 µg/kg/min. Cardiac output increased from rest to peak dobutamine (4.9 ± 1.2 to 6.6 ± 2.0 L/min, P < 0.001) and correlated with the peak systolic tissue velocity (s′) at rest (R = 0.61, P = 0.02) and during dobutamine stimulation (R = 0.79, P < 0.001). Increases in early diastolic mitral inflow (E, 74.9 ± 29.0–90.8 ± 29.5 cm/s) and LV lengthening (e′, 6.5 ± 2.4–8.2 ± 2.8 cm/s) velocities were observed during LDDE leaving the E/e′ ratio unchanged. Although a mean PCWP was also unchanged from rest to peak dobutamine (16.6 ± 8.3–14.2 ± 9.2, P = 0.25), E/e′ and PCWP only correlated at rest (R = 0.64, P = 0.014).
Conclusion The LV systolic shortening velocity is closely associated with cardiac output during LDDE in CHF patients. Dobutamine stimulation increases early diastolic mitral inflow and lengthening velocities, but theE/e′ ratio does not reflect the PCWP during LDDE, which warrants some caution in converting changes in E/e′ into changes in LV filling pressure. The sample size is, however, small and the observation need to be confirmed in a larger population.

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