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(Circulation. 2008;118:373-380.)
© 2008 American Heart Association, Inc.

Imaging

Mechanisms of Preejection and Postejection Velocity Spikes in Left Ventricular Myocardium

Interaction Between Wall Deformation and Valve Events

Espen W. Remme, MSc, Dr ing; Erik Lyseggen, MD, PhD; Thomas Helle-Valle, MD; Anders Opdahl, MD; Eirik Pettersen, MD; Trond Vartdal, MD; Asgrimur Ragnarsson, MD; Morten Ljosland, MD; Halfdan Ihlen, MD, PhD; Thor Edvardsen, MD, PhD; Otto A. Smiseth, MD, PhD

From the Institute for Surgical Research (E.W.R., E.L., T.H.-V., A.O., E.P., T.V., T.E., O.A.S.), Rikshospitalet University Hospital and University of Oslo, and Department of Cardiology (A.R., H.I., T.E.), Rikshospitalet University Hospital, Oslo, Norway; and Department of Heart and Lung Disease, Østfold Hospital, Fredrikstad, Norway (M.L.).

Correspondence to Otto Smiseth, Department of Cardiology, Rikshospitalet, N-0027 Oslo, Norway. E-mail Otto.Smiseth{at}rikshospitalet.no

Received July 21, 2006; accepted May 19, 2008.

Background— Normal left ventricular myocardium demonstrates distinct spikes in the velocity trace before and after left ventricular ejection. We tested the hypothesis that the preejection and postejection velocity spikes reflect early systolic shortening and late systolic lengthening that are interrupted by mitral and aortic valve closure, respectively.

Methods and Results— In 11 anesthetized dogs, timing of valve closure was determined by pressure variables; left ventricular dimensions were determined by sonomicrometry. Myocardial shortening started 20±10 ms (mean±SD; P<0.001) before mitral valve closure and was interrupted at the time of mitral valve closure (time difference, 4±7 ms). Similarly, myocardial lengthening started 31±15 ms (P<0.001) before aortic valve closure and was interrupted at the time of aortic valve closure (time difference, 0±3 ms). Prevention of mitral (n=4) and aortic (n=4) valve closure by stenting the valves abolished the preejection and postejection velocity spikes, respectively. Echocardiographic measurements of patients (n=15) with severe mitral regurgitation showed that the preejection velocity spike was reduced after prosthetic valve replacement (43±25 versus 32±15 mm/s; P=0.036), indicating that preejection shortening was larger with a leaking valve. Similarly, late systolic lengthening was reduced in patients (n=15) with severe aortic regurgitation after prosthetic valve replacement; minimum postejection velocity spike was increased from –32±11 to –17±11 mm/s; P=0.0003). Asynchronous onset of contraction/relaxation and atrioventricular interaction were investigated as alternative mechanisms of the velocity spikes in dogs and patient groups but were found implausible.

Conclusions— This study supports the hypothesis that normal left ventricular preejection and postejection velocity spikes are attributed to valve closures that interrupt early systolic shortening and late systolic lengthening, respectively.

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