TY - JOUR
T1 - Relationship of pulmonary vein flow to left ventricular short-axis epicardial displacement in diastole
T2 - Model-based prediction with in vivo validation
AU - Riordan, Matt M.
AU - Kovács, Sándor J.
PY - 2006
Y1 - 2006
N2 - Previous studies in healthy humans have established that the (≈850 ml) volume enclosed by the pericardial sac is nearly constant over the cardiac cycle, exhibiting a transient ≈5% decrease (≈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 (Δ) (i.e., magnitude of "crescent effect" in the radial direction). We measured Δ 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 Δ 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 Δ 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 Δ as a regional (radial) parameter of diastolic function.
AB - Previous studies in healthy humans have established that the (≈850 ml) volume enclosed by the pericardial sac is nearly constant over the cardiac cycle, exhibiting a transient ≈5% decrease (≈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 (Δ) (i.e., magnitude of "crescent effect" in the radial direction). We measured Δ 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 Δ 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 Δ 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 Δ as a regional (radial) parameter of diastolic function.
KW - Constant-volume heart
KW - Left atrial conduit volume
UR - http://www.scopus.com/inward/record.url?scp=33748419496&partnerID=8YFLogxK
U2 - 10.1152/ajpheart.01339.2005
DO - 10.1152/ajpheart.01339.2005
M3 - Article
C2 - 16603684
AN - SCOPUS:33748419496
SN - 0363-6135
VL - 291
SP - H1210-H1215
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 3
ER -