328A ABSTRACTS – Poster JACC February 1997

the annulus and papillav muscle (PM), consistent with chordal tension limit-ing excursion. We therefore examined the MV by 2D eohocardiogrephy in 58patients with LVdyefunotion (36with IMLC and 22 without) vs 21 normal con-trols. Results: In most patients with IMLC vsthose without, 1) the AL showedabnomnalbending in systole, 2) AL opening was restrictedto the annulus-PMline, and 3) the opening excursion angle u of the AL was markedly reduced.Conclusions: In most patients with IMLC, abnormal systolic and diastolicleaflet mnfiguration and reatriotedmotion auggest abnormal leaflet tetheringcreated by geometric changes in the mitral-LV complex.

m101836 Isthe Vena Contracta Area forStenoticandRegurgitantOrificeaDependentonHemodynamicVarieblea?An In VitroStudyusingLaserInducedFluorescenceImaging

R. Shandas, N. Trujillo, E.A. Gill, J. Kwon, C.G. DeGrolf, L. Valdes-Cruz.The Children’s Hospital, University of Colorado Health Sciences CentecDenver, CO, USA

Although the vena contracta area (VCA) of atenotic and regurgitant jets hasbeen shown toreprasentthe true measureof diaeaseseverity, there isnogoldatanderd for quantifying VCA. This has presented problems when attemptingto aaseas VCA dependence on hemodynamics (pressure, flow, pulsatility)aa well as the ability of Doppler methods such as the mntinuity equationand proximal jet imaging to accurately reflect VCA. Using a precise in vitroIaaer induced fluorescence (LIF) imaging system to illuminate perpendicularcross-sectional regions immediately distal to rigid orifices of various sizes(0.2-4.9 cmz) and shapes (circular, slit, Y-shaped), we were able to isolateand measure VCA (Figure) for steady (25-150 cckec) and pulsatile (20-100Cc/beat;60 bpm) flows. VCA ragion (minimum cross-sectional jet area) wasfound between 0.1 cm and 0.5 cm distal to all orifices at all flow rates. VCAwas found to depend on a pressure to viscous force ratio. Low pressureto viscous force ratios (increased viscous effects) caused VCA to approachanatomic areas while increasing the ratio (decreasingviscous effects)causedan asymptotic decrease in VCA towards a constant value (79% + 3.3% ofanatomic area). VCA did not change significantly over the pulsatile cycle(Graph).

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m101837 AbeenceofSevereThickeningoftheMitralVelvein MitrelValveProlapaePatientswhoDieSuddenly

A. Pandey, E.K. Louie, T.L. McKiernan, S. Bharati. The Hear?Institute forChildren, Christ Hospital, Oak Lawn, IL, USA, Loyola Uni~ Medical CentecMaywood, IL, USA

Prior eohocsrdiographic atudies report that a mitral leaflet width >5 mmidentifies a subaet of mitral valve prolapse (MWJ pts at increased riskfor audden death. We directly measured intrinsic leaflet thicknaas in 24autopsiad hearts (12 MVP,12 controls with normal mitral valves, NL) selectedfrom a consecutive series of 376 victims of unexplained sudden death. Anobaewer, blinded to the pathologic assignment of MVP, performed in situtriplicate measurements of leaflet body thickness (THb), leaflet coaptationmargin thickness (THc), and leaflet closure line thickness including chordalattachments (THch) for anterior (AMV) and posterior (PMV) mitral leaflets(measured in mm to 0.01 mm precision with a digital caliper):

AMV PMV

THb THc THch THb THc THch

MVP 0.8 + 0.2 0.9 * 0.3 2.0 + 0.6 0.s ● 0.2 0.9 ● 0.4 1.7 * 0.8NL 0,6 k 0.1 0.6 + 0.2 1.6 + 0.7 0.5 i 0.1 0.5 * 0.1 0.9 * 0.2P <0,01 ns ns <0,005 <0.01 <0005

Though portions of AMV and PMV were significantly thicker for MVPcompared to NL, the maximum measurements from either leaflet for MVPwere only: THb = 1.2 mm, THc = 1.9 mm, and THch = 3.2 mm. Conclusions:Although intrinsic thickness of the mitral valve is increased in MVP relativeto NL, the maximum leaflet thicknesses observed were considerably leesthan the 5 mm threshold proposed by echocardiographic studies aa a markerfor sudden death. Our study shows that marked ’increases in intrinsic leafletthickness are not a prerequisite for sudden death in mitral valve prolapsepatients.

mEl Basic Electrophysiology: Autonomic Effectsand Mechanisms of Arrhythmias

Tuesday,March 18, 1997, 3:00 p.m.–5:OOp.m.AnaheimConventionCenter,Hall EPresentationHour:4:00 p.m.–5:OOp.m.

-[ MuacleNerveSymPatheticActivitYC0ntr0k3BloodPressureduringVasovagalPreayncope

D.L. Jardine, S.1.Bennett, R. Frethey, H. Ikram, LG. Crozier. ChristchurchHospital, NewZaa/and

Previous case reports have demonstrated a fall in muscle sympathetic neweactivity [MNSA] during the presyncopal phase of vasovaaal svnco!Je WS1.We hypothesized that blood pressure would correlate dir&tly with MNSA atthis time irrespective of parasympathetic activity [PA].

Eighteen patients with recurrent VS were compared during eatiy 8@head-up tilt to 17 controls all of whom tolerated tilt for 45 min. Mean bloodpressure [MBP], MNSA, heart rate [HR], high frequency heart rate variability[HFHRV], and baroreceptor sensitivity [BS] were continuously monitored.During early tilt, BP was maintained and MNSA increased [both groups p <0.01] while PA activity fell [HFHRV, BS p < 0.01]. Presyncope, defined asthe time of the first sustained fall in MBP during tilt [p < 0.05], began at amean time of 15.2 + 3 min and lasted 170 + 10 sec. During presyncope,MBP and MNSA decreased in direct correlation [p < 0.001] while HFHRVand BS remained low. HR also correlated with MNSA [p < 0.001] suggestingthat sympathetic withdrawal rather than parasympathetic activity mediateavasovagal syncope.

\ 1019-78 I Beta-AdrenergicMediaticJnofMechenoelectricalFeedback

B.B. Lerman, K. Todaka, E. Engelstein, D. Burkhoff. New YorkHospital-Cornell Medical Centec New York, NY USA

It has been previously shown that augmented preload increases myooardialexcitability by shortening action potential duration (APD). The mechaniamgoverning this phenomenon is unknown. Since shortening of APD is madi-ated by K+ depolarizationcurrents which are sensitive to cAMP, we hypoth-esized that load-dependent changes in myooerdial excitability are mediatedby stimulation of cAMP. We therefore studied the effects of propranolol onload-induced changes in electrical excitability in 7 isolated ejecting caninehearts. Monophaaic APD (MAPDso)and electrical excitability (relative [RRP]and abaolute [ARP] refractory periods derived from strength-intetval curves)were determined at low and high loads before and after p-blockade.

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m101980 Yohimbine Facilitates Induction of VentricularTschycardia of Purkinje Origin in the IschemicCanine Heart

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m101997 Early Afterdepolarizations and AftercontractionsInduced by Isoproterenol in Canine VentricularMyocytes are Fast-Pacing Dependent!

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