Why the study?
Does increasing preload via lower body positive pressure alter transmitral and pulmonary venous flow velocities differently depending on the underlying heart disease (dilated vs hypertrophied)?
Does increasing preload via lower body positive pressure alter transmitral and pulmonary venous flow velocities differently depending on the underlying heart disease (dilated vs hypertrophied)?
Transmitral and pulmonary venous flow velocities respond differently to increased preload depending on the underlying cardiac pathology, indicating lower left ventricular functional reserve in dilated hearts.
Requires pathology-specific diastolic assessment under preload variation; hypothesis-generating for LV reserve differences and needs prospective validation.
Changes in transmitral flow (TMF) and pulmonary venous flow (PVF) velocities during increases in preload were compared in patients with a higher peak atrial systolic velocity than peak early diastolic velocity (A/E > 1) for the TMF velocity to determine differences in hemodynamic response. Fifteen patients with dilated hearts, 22 with hypertrophied hearts and 15 control patients were studied. TMF and PVF velocities were recorded by transesophageal pulsed Doppler echocardiography before and during application of lower body positive pressure. The value for peak early diastolic velocity increased, while the isovolumic relaxation time decreased with increases in preload in all groups. The value for peak atrial systolic velocity decreased in the dilated-heart group, but increased in the hypertrophied-heart and control groups. The peak second systolic and early diastolic PVF velocities increased in the dilated- and hypertrophied-heart groups, but did not change in the control group. The peak atrial systolic PVF velocity and the difference in duration of the atrial systolic PVF and TMF velocities increased in the dilated- and hypertrophied-heart groups, and its changing rate was highest in the group with dilated hearts. These results suggest that both peak early diastolic and atrial systolic TMF velocities increase during increases in preload through the Frank-Starling mechanism in hypertrophied hearts. Furthermore, the left ventricular functional reserve was lower in the dilated-heart group. Thus, TMF and PVF velocities respond differently during increases in preload, depending on the underlying heart disease.
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Yamada et al. (1998) studied this question.
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