Mechanisms of preejection and postejection velocity spikes in left ventricular myocardium: interaction between wall deformation and valve events.
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.


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.
Remme
Espen W
EW
Institute for Surgical Research, Rikshospitalet, Oslo, Norway.
Lyseggen
Erik
E
Helle-Valle
Thomas
T
Opdahl
Anders
A
Pettersen
Eirik
E
Vartdal
Trond
T
Ragnarsson
Asgrimur
A
Ljosland
Morten
M
Ihlen
Halfdan
H
Edvardsen
Thor
T
Smiseth
Otto A
OA
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D001021:Aortic Valve; D016022:Case-Control Studies; D004285:Dogs; D015150:Echocardiography, Doppler; D005260:Female; D006350:Heart Valve Prosthesis; D006351:Heart Valves / Q000000981:diagnostic imaging / Q000502:physiology*; D006352:Heart Ventricles / Q000000981:diagnostic imaging; D006801:Humans; D019563:Mechanics; D008875:Middle Aged; D008943:Mitral Valve; D008944:Mitral Valve Insufficiency / Q000000981:diagnostic imaging / Q000503:physiopathology; D013599:Systole; D016277:Ventricular Function, Left / Q000502:physiology*