TY - JOUR
T1 - Left Ventricular Isovolumic Flow Sequence During Sinus and Paced Rhythms. New Insights From Use of High-Resolution Doppler and Ultrasonic Digital Particle Imaging Velocimetry
AU - Sengupta, Partho P.
AU - Khandheria, Bijoy K.
AU - Korinek, Josef
AU - Jahangir, Arshad
AU - Yoshifuku, Shiro
AU - Milosevic, Ilija
AU - Belohlavek, Marek
N1 - Funding Information:
This work was supported by grant HL68573 and, in part, by grants HL68555 and HL70363 from the National Institutes of Health. Nothing in this article implies endorsement of any product or manufacturer mentioned in this article.
PY - 2007/2/27
Y1 - 2007/2/27
N2 - Objectives: We sought to clarify the role of isovolumic intervals during a cardiac cycle by in vivo visualization of left ventricular (LV) intracavitary flow dynamics. Background: Asynchronous LV deformation during isovolumic contraction (IVC) and isovolumic relaxation (IVR) might represent a transient feature of myocardial wall mechanics that reverses the direction of blood flow. Methods: In 10 beating porcine hearts, the changes in LV intracavitary flow were recorded at baseline and after LV epicardial and right atrial pacing with high-resolution Doppler and contrast echocardiography. Two-dimensional vector flow fields were generated offline from B-mode contrast images with particle imaging velocimetry. Results: During IVC, flow from the LV apex accelerated toward the base, whereas blood from the base was redirected toward the outflow through formation of an anterior vortex. Conversely, during IVR, flow was initially directed toward the apex and then briefly reversed toward the base. Epicardial pacing from the LV base altered the stages of flow redirection during the pre-ejection period and delayed mitral valve closure (28 ± 14 ms vs. 61 ± 13 ms, p < 0.001) and aortic valve opening (77 ± 18 ms vs. 111 ± 18 ms, p = 0.004). Conclusions: Isovolumic intervals are not periods of hemodynamic stasis but, rather, phases with dynamic changes in intracavitary flow. Experimentally induced aberrant epicardial electrical activation alters stages of flow redirection and prolongs the pre-ejection period. Normal electromechanical activation through the His-Purkinje system in mammalian hearts maintains an inherent synchrony with the sequence of intracavitary flow redirection.
AB - Objectives: We sought to clarify the role of isovolumic intervals during a cardiac cycle by in vivo visualization of left ventricular (LV) intracavitary flow dynamics. Background: Asynchronous LV deformation during isovolumic contraction (IVC) and isovolumic relaxation (IVR) might represent a transient feature of myocardial wall mechanics that reverses the direction of blood flow. Methods: In 10 beating porcine hearts, the changes in LV intracavitary flow were recorded at baseline and after LV epicardial and right atrial pacing with high-resolution Doppler and contrast echocardiography. Two-dimensional vector flow fields were generated offline from B-mode contrast images with particle imaging velocimetry. Results: During IVC, flow from the LV apex accelerated toward the base, whereas blood from the base was redirected toward the outflow through formation of an anterior vortex. Conversely, during IVR, flow was initially directed toward the apex and then briefly reversed toward the base. Epicardial pacing from the LV base altered the stages of flow redirection during the pre-ejection period and delayed mitral valve closure (28 ± 14 ms vs. 61 ± 13 ms, p < 0.001) and aortic valve opening (77 ± 18 ms vs. 111 ± 18 ms, p = 0.004). Conclusions: Isovolumic intervals are not periods of hemodynamic stasis but, rather, phases with dynamic changes in intracavitary flow. Experimentally induced aberrant epicardial electrical activation alters stages of flow redirection and prolongs the pre-ejection period. Normal electromechanical activation through the His-Purkinje system in mammalian hearts maintains an inherent synchrony with the sequence of intracavitary flow redirection.
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U2 - 10.1016/j.jacc.2006.07.075
DO - 10.1016/j.jacc.2006.07.075
M3 - Article
C2 - 17320749
AN - SCOPUS:33750958159
SN - 0735-1097
VL - 49
SP - 899
EP - 908
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 8
ER -