Relationship of pulmonary vein flow to left ventricular short-axis epicardial displacement in diastole: model-based prediction with in vivo validation.
Previous studies in healthy humans have established that the (approximately 850 ml) volume enclosed by the pericardial sac is nearly constant over the cardiac cycle, exhibiting a transient approximately 5% decrease (approximately 40 ml) from end diastole to end systole. This volume decrease manifests as a "crescent" at the ventricular free wall level when short-axis MRI images of the epicardial surface acquired at end systole and end diastole are superimposed. On the basis of the (near) constant-volume property of the four-chambered heart, the volume decrease ("crescent effect") must be restored during subsequent early diastolic filling via the left atrial conduit volume. Therefore, volume conservation-based modeling predicts that pulmonary venous (PV) Doppler D-wave volume must be causally related to the radial displacement of the epicardium (Delta) (i.e., magnitude of "crescent effect" in the radial direction). We measured Delta from M-mode echocardiographic images and measured D-wave velocity-time integral (VTI) from Doppler PV flow of the right superior PV in 11 subjects with catheterization-determined normal physiology. In accordance with model prediction, high correlation was observed between Delta and D-wave VTI (r=0.86) and early D-wave VTI measured to peak D-wave velocity (r=0.84). Furthermore, selected subjects with various pathological conditions had values of Delta that differed significantly. These observations demonstrate the volume conservation-based causal relationship between radial pericardial displacement of the left ventricle and the PV D-wave-generated filling volume in healthy subjects as well as the potential role of the M-mode echo-derived radial epicardial displacement index Delta as a regional (radial) parameter of diastolic function.
Riordan
Matt M
MM
Department of Internal Medicine, Cardiovascular Biophysics Laboratory, Washington University School of Medicine, St. Louis, MO 63110, USA.
Kovács
Sándor J
SJ
D003326:Coronary Circulation / Q000502:physiology; D003971:Diastole / Q000502:physiology*; D004452:Echocardiography; D015150:Echocardiography, Doppler; D006352:Heart Ventricles / Q000033:anatomy & histology / Q000473:pathology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000473:pathology / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D008875:Middle Aged; D008944:Mitral Valve Insufficiency / Q000473:pathology / Q000503:physiopathology; D008955:Models, Cardiovascular; D008962:Models, Theoretical; D010496:Pericardium / Q000033:anatomy & histology / Q000473:pathology / Q000502:physiology*; D011667:Pulmonary Veins / Q000033:anatomy & histology / Q000473:pathology / Q000502:physiology*; D016276:Ventricular Function