Author + information
- Received June 15, 1992
- Revision received December 14, 1992
- Accepted December 18, 1992
- Published online June 1, 1993.
- ↵∗Address for correspondence: Ole Rossvoll, MD, Section of Cardiology, Department of Medicine, University Hospital, N-7006 Trondheim, Norway.
Objectives.This study was conducted to investigate whether pulmonary venous flow variables measured by transthoracic Doppler ultrasound can help identify patients with elevated left ventricular end-diastolic or filling pressures, or both.
Background. A widened left atrial pressure A wave occurs when left ventricular end-diastolic pressure is increased. Increased duration of pulmonary venous flow reversal at atrial systole might therefore be a marker for elevated end-diastolic pressure. Decreased systolic pulmonary venous flow is shown to be related to increased left ventricular filling pressure in studies using transesophageal Doppler echocardiography.
Methods. Left ventricular pressures at late diastole were measured by fluid-filled catheters in 50 consecutive patients undergoing diagnostic cardiac catheterization. Pulmonary venous and mitral flow velocities were recorded by transthoracic pulsed Doppler ultrasound.
Results. Adequate recordings were obtained ia 45 patients. Pulmonary venous flow reversal exceeding the duration of the mitral A wave predicted left ventricular end-diastolic pressure >15 mm Hg with a sensitivity of 0.85 and a specificity of 0.79. This difference in flow duration correlated well with the increase in ventricular pressure (r = 0.70, p < 0.001) at atrial systole and the end-diastolic pressure (r = 0.68, p < 0.001). The systolic fraction of pulmonary venous flow was markedly decreased (< 0.4) in all patients with a pre-A pressure (left ventricular pressure before atrial systole) >18 mm Hg.
Conclusions. Pulmonary venous flow reversal exceeding the duration of the mitral A wave indicates an exaggerated increase in left ventricular late diastolic pressure. Pulmonary venous systolic fraction <0.4 suggests markedly increased ventricular filling pressure.
↵∗ Present address: King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia.
☆ This study was supported by grants from the Norwegian Research Council for Science and Humanities and the Norwegian Council of Cardiovascular Diseases.
- Received June 15, 1992.
- Revision received December 14, 1992.
- Accepted December 18, 1992.