title: Relationship of pulmonary vein flow to left ventricular short-axis epicardial displacement in diastole: model-based prediction with in vivo validation.
abstract: 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.
authors.affiliation: Department of Internal Medicine, Cardiovascular Biophysics Laboratory, Washington University School of Medicine, St. Louis, MO 63110, USA.
authors.forename: Matt M
authors.initials: MM
authors.lastname: Riordan
authors.forename: Sándor J
authors.initials: SJ
authors.lastname: Kovács
mesh_terms: 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