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J Am Coll Cardiol, 2007; 49:899-908, doi:10.1016/j.jacc.2006.07.075
(Published online 8 February 2007). © 2007 by the American College of Cardiology Foundation |
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* Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota
Division of Cardiovascular Diseases, Mayo Clinic, Scottsdale, Arizona
Department of Aerospace Engineering and Mechanics, University of Minnesota, Minneapolis, Minnesota
Manuscript received April 19, 2006; revised manuscript received June 30, 2006, accepted July 10, 2006.
* Reprint requests and correspondence: Dr. Marek Belohlavek, Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905 (Email: belohlavek.marek{at}mayo.edu).
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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