and gradientericrosenthal,josephkmontarello,alexcperakis,edwardgcaboyd,...

Br Heart J 1990;63:238-45

Balloon dilatation of the aortic valve in a pulsatileflow model: assessment of the mechanisms and themagnitude and duration of changes in valve areaand gradient

Eric Rosenthal, Joseph K Montarello, Alex C Perakis, Edward G C A Boyd,Michael Rosin, Alan K Yates, Philip B Deverall, Edgar Sowton, Paul V L Curry

AbstractEighteen stenotic aortic valves (17removed at operation) mounted in a pul-satile flow duplicator were dilated with aballoon catheter. Sequential measure-ments showed that the valve areainitially increased from a mean (SD) of052 (0-16) to 0-78 (0-17) cm2. It wai 0-73(0-16) cm2 five minutes after dilatationand this was little changed at four weeks(0 70 (0-15) cm2). Initially the meantransvalvar gradient fell significantlyfrom 54 (27) to 32 (8) mm Hg butincreased to 35 (10) mm Hg at five min-utes and to 40 (11) mm Hg at four weeks.In six valves stretching of the orifice wasthe only mechanism responsible for thechanges while in the remainder therewas tearing through commissures with agreater initial increase in area (0-31 v0-18 cm2) and a smaller decrease in areaat five minutes (0 03 v 0-08 cm2). Frac-tures of calcific deposits in non-commis-sural positions were seen in one valveonly.This laboratory study of isolated aortic

valves showed a significant but smallincrease in valve area after balloondilatation, which was greater when com-missural tearing had occurred. Recoil ofthe stretched orifice was complete at fiveminutes and there was little furtherchange over the next four weeks.

Department ofCardiology, Guy'sHospital, LondonE RosenthalJ K MontarelloA C PerakisE SowtonP V L CurryDepartment ofClinical Physics, Guy'sHospital, LondonE G CA BoydDepartment ofCardiothoracicSurgery, Guy'sHospital, LondonM RosinA K YatesP B DeverallCorrespondence toDr Eric Rosenthal,Department of Cardiology,Guy's Hospital,St Thomas Street,London SE1 9RT.

Accepted for publication8 November 1989

Percutaneous balloon dilatation of the aorticvalve in elderly patients with calcific aorticstenosis deemed to be at high risk from conven-

tional operation was first described as a

palliative procedure by Cribier et al andMcKay et al in 1986.' 2 Their initial encourag-ing reports were soon followed by largerstudies with more impressive results." Otherreports suggested only a very limited effectfrom balloon dilatation6 and provided evidenceof a rapid loss of any haemodynamicimprovement.7 Recent studies showed thatmore than half the patients had died, under-gone valve replacement or redilatation, or had a

recurrence of symptoms at mean follow up

periods of 5-8 months"' and the value of theprocedure remains uncertain.Haemodynamic evaluation of dilatation of

the aortic valve is confounded by severalprocedural factors including myocardial

depression during balloon inflation, haemor-rhage, arrhythmias, and vagal effects. Aorticvalve area estimations by the Gorlin formulamay be unreliable at discriminating smallchanges, especially in patients with low cardiacoutputs, and the timing ofnon-invasive assess-ments has varied between studies.Both the procedural and methodological

limitations to haemodynamic assessment havecontributed to uncertainty about the real andapparent effects of the procedure. Intra-operative simulation was limited to singlemeasurements before and after dilatation6 andlike most in vitro studies"213 did not measureareas and gradients during flow. We performedballoon dilatation in 18 stenotic human aorticvalves mounted in a pulsatile flow duplicatorand measured the sequential changes in areaand gradient without the constraints present inclinical practice.

Patients and methodsVALVESOf the 18 valves, seventeen were removedintact at aortic valve operation and one atroutine necropsy. Fourteen valves were storedin 10% formaldehyde while four were usedfresh from operation and thereafter stored inhomograft valve nutrient solution."4 Pre-operative peak to peak catheter gradients ran-ged from 50 to 130 mm Hg and significantaortic regurgitation was present in only threepatients. Eleven valves were bicuspid, sixtricuspid, and one unicuspid. In two patientspercutaneous balloon dilatation had been per-formed without sustained symptomaticimprovement (table 1).

TEST APPARATUSThe pulsatile flow duplicator'5 consisted of aroller pump connected to a pulsatile controlunit (Stockert Shiley model PFC II; ShileyLtd, Berkshire) that continuously recirculatedsaline from a 10 litre reservoir through thestenotic valves when placed in the test chamber(fig 1). The valves were mounted with silksutures and cyanoacrylic glue on to a truncatedpolyvinyl chloride cone, cut to the diameter ofthe valve ring, and the 40 mm diameter basewas then clamped into the test chamber. Thetest chamber had a translucent end plate witheight radial flow outlet ports arranged sym-metrically around the circumference, allowinga centrally placed video camera (Hitachi GP5E/1E; Hitachi Ltd, Tokyo, Japan) to be

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Balloon dilatation of the aortic valve: assessment of the mechanisms and the magnitude and duration of changes in valve area

11 Video camera

i End viewing plate

=- Supravalvarpressure portCalibration ringValve

Cone

Upper--_Cone retaining plates

Lower

Infravalvar pressureport

Flow corrector plate

Balloon catheter port

Figure I Cross section through the test chambercontaining a valve mounted on to a cone fixed in place bythe cone retaining plates. Saline at 37°C wascontinuously pumped at 4 1/min through the valve in thedirection indicated by the arrows. The saline left thechamber via radial outlet ports placed symmetricallyaround the video camera which had an unobstructed viewof the valve duringflow.

aligned above the valve. The magnified imageof the aortic valve was displayed on a videomonitor and stored on video tape (Racal Store7; Racal Recorders, Southampton). Themaximal aortic valve area was then measuredby planimetry from the monitor screen with a

bitpad (Bit Pad 1 digitiser tablet; Summa-graphics, Fairfield, USA) interfaced to a Com-modore computer (Model 4032; Commodore,USA). A calibration ring set at valvar level wasused for reference. Pressure ports in subvalvarand supravalvar positions allowedmeasurement of the mean transvalvar gradientby substraction of the integrated pressure-timecurves (Hewlett Packard models HP 1209 Aand HP 7754 B). The saline was maintained at37°C (1°C) and delivered at a constant output of4 litres per minute with an ejection period of45 o and repetition rate of 70 per minute. Themodel is capable of delivering up to 5-4 litresper minute but was set at the lower level toreduce the stresses on the valves which were

due to undergo repeated measurements. Weshowed that the valve area of stenotic valves inthis model was maximal at a flow of 3 litres perminute.'5

PROCEDUREThe mounted valve was placed in the test celland saline was circulated for 30 minutes (allow-ing equilibration of temperature and dissolvedgases) before the valve area and mean trans-valvar pressure gradient were measured. A20 mm balloon (Meditech, USA) was advancedanterogradely through the valve over a 0 35inch J guide wire and positioned with thecentre of the balloon inside the valve orifice as

seen from the side view. The balloon wasinflated to 3 atmospheres (303 kPa) (manufac-turer's limit) during continuous video record-ing. When obvious commissural tearingoccurred the balloon was deflated after 30seconds; otherwise inflation was maintained fora full minute. During inflation the circulationwas temporarily stopped to avoid pressureoverload to the circuitry and valve and thecirculation was restarted on deflation. Fiveseconds after the flow had been re-establishedwe measured the valve area and gradient. Thesemeasurements were repeated at 5, 10, 15, 20,25, 30, 60, and 120 minutes while the flow wasmaintained continuously. The valve wasremoved from the chamber and stored in theappropriate medium. At 24, 48, and 72 hoursand at 1, 2, and 4 weeks the valve was returnedto the test chamber and, after 30 minutes offlow, the area and gradient were measured asbefore. In two valves complete data were notobtained and in one video recordings wereinadvertently erased during subsequentrecordings.

RADIOGRAPHYValves were examined by projectionmicroradiography with a Hilger Watts gen-erator (London) before and after balloondilatation. The images produced were 3-5 timesreal size and showed the calcific deposits in finedetail.

DATA ANALYSISChanges in valve area and mean pressuregradient were investigated by an analysis ofvariance for repeated measures with a GenstatPackage on the University of London mainframe computer. The results are expressed asmeans (SD) and a p value <0 01 was con-sidered statistically significant.

ResultsAREA AND GRADIENT CHANGESThere was an increase in valve area anddecrease in the mean pressure gradient acrossall the valves studied (table 1). The aortic valvearea increased from 0-52 (0-16) cm2 to 0-78(0-17) cm2 immediately after balloon dilatation(p < 0 001) but had fallen to 0-73 (0-16) cm2five minutes after the procedure (p < 0 01).Thereafter there were no significant changes invalve area and at four weeks the area measured0-70 (0-15) cm2-35% more than before dilata-tion. The mean transvalvar pressure gradientfell from 54 (27) mm Hg to 33 (8) mm Hgimmediately after the procedure (p < 0.001)rising to 35 (10) mm Hg at five minutes (NS),with a further slight rise to 40 (11) mm Hg atfour weeks (p < 0-01 compared with dilatationafter). Values at times between those reportedwere similar, did not affect the statisticalanalysis, and have been omitted for clarity(fig 2).

MECHANISM OF DILATATIONThe balloon totally occluded the orifice (figs 3and 4) of only five valves (one tricuspid, oneunicuspid, and three bicuspid). In six valves

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Rosenthal, Montarello, Perakis, Boyd, Rosin, Yates, Deverall, Sowton, Curry

Table 1 Patient and valve characteristics and results of balloon dilatation

Aortic valve area (cm2) Mean pressure gradient (mm Hg)

No Age Sex Gradient* AR Type Mechansm Before After S min 4 wk Before After S min 4 wk

1 62 M 80 0 B Stretch 0-67 0-87 677 075 45 38 43 402 68 M 80 1 Bt Stretch (0) 0-69 0-83 0-76 0-72 44 38 40 423 73 M 70t I B Split (0) 0-65 0-82 0-83 0-77 58 36 40 384 54 M 90 1 T Split 0 59 090 0-87 0-85 36 22. 22 265 73 M 50 0 Tt Stretch 0-48 0-73 0-66 0-63 40 29 31 366 82 F I I T Stretch (0) 0-24 0 49 0-42 0 40 67 46 53 587 71 F - 0 Bt Split (0) 0 34 0 70 0-61 0-58 82 36 38 498 47 M 80 1 B Split 0 55 1-06 101 0-82 31 20 20 319 48 M 55 1 T Split 0-60 0-81 0-80 0-81 44 27 27 3310 30 F 80 1 Bt Split 0 39 0 75 0 70 0-66 53 29 29 3611 62 M 65 1 T Split 0-52 0-68 0-64 0-64 53 33 40 4412 69 M 70 2 T Stretch 0-36 0 45 0-40 0 40 42 36 42 4213 35 F 95 2 U Split (O)t 0-51 0-81 0-76 0-76 53 31 31 3314 54 M 70 0 B Split 0-56 0-66 0-65 0-67 53 47 49 4915 61 M 55 2 B Stretch 0 90 1-04 0 97 0-91 29 24 24 3116 55 M 130 1 B Split§ 0-24 0-68 0-67 0 57 149 40 42 7117 76 M 130 1 B Split 0 53 0-76 0-76 0 73 47 33 35 3318 69 M 70t 0 B Split 0 53 1 01 0-92 0 91 49 22 24 28Mean 61 87 0-52 0-78 0 73 0 70 54-2 32-6 35 0 40 0(SD) (0.16) (0.17) (0.16) (0-15) (26.8) (7 9) (9 5) (11.3)

*Peak to peak at diagnostic catheterisation.tSpecimen preserved in homograft nutrient medium.tBalloon dilatation performed in vivo.§Pre-dilatation with 9 0 mm balloon.11Postmortem valve.AR, aortic regurgitation; B, bicuspid; 0, orifice totally occluded; T, tricuspid; U, unicuspid valves.

t a 5 20-%tf minues

Figure 2 Aortic valve areztransvalvar gradient (mm I

Each point represents the m4deviation.

there were substantialthe balloon (up to 600/(three tricuspid and tthe remainder only(< 20% oforifice) wereing of the valve orifice(figs 3, 4, and 5) in six vtwo bicuspid) and thering or splitting in 12Though the valves witimmediate increase i0 18 cm2) and fall in9 mm Hg) than the vstretching, these diffestatistical significance> 1-0 cm2 were seen inwhich had tearing thione heavily calcified vgballoon could not paDilatation with a 9 misequent dilatation witlthe final valve area wNeither of the two (biiclinical balloon dilatatishowed macroscopic 4

(n=18) the procedure but both were easily split invitro. In only one valve was there clearly afracture of non-commissural calcium (fig 8)while fractures of commissural calciumdeposits were found in seven with commissuralsplitting.

**p<0 OOl vs pre-dihlataonsltig

A pcO Ol vs post-dilatationAA pcO.00l vs post-dilatation

Dsuso~~~~~ Discussionr .. . Interventional balloon techniques are cur-

rently applied to a range of cardiovasculardiseases. The favourable results obtained withcoronary angioplasty and dilatation of congen-

Ho2ws Days Weeks ital valve obstructions have lead to the exten-sion of balloon dilatation to mitral and aortic

a (cm2) and mean systolic stenosis in adults. 1617 Mitral valvotomy is a wellig) plotted against time. established surgical technique and balloonean and the bar the standard dilatation in many ways mimics this effective

procedure. In contrast, the poor long termresults of operative aortic valvotomy"8 mean

passages (fig 5) around that many, especially surgeons, doubt theSO of the original orifice) effectiveness of balloon dilatation of suchhree bicuspid) while in heavily calcified valves.insignificant apertures Immediately after aortic valve dilatationpresent (fig 6). Stretch- patients are haemodynamically unstable so thatwas the sole mechanism the interpretation of changes produced by the,alves (four tricuspid and procedure is difficult. In particular, myocardiale was commissural tear- depression during balloon inflation (owing to' valves (figs,*6 and 7). ventricular overload and coronary underper-h splitting had a greater fusion) may lead to underestimation of thein valve area (0-31 v measured gradient. In addition, haemorrhage,valve gradient (28 v arrhythmias, vagal stimulation, and contrast

alves that only showed administration may all affect the haemodyn-rences did not achieve amic indices. The Gorlin formula may under-(table 2). Valve areas estimate aortic valve area in low output states,19

l only three valves all of which are often present in these patients, butrough commissures. In more importantly its sensitivity to smallalve the deflated 20 mm changes in aortic valve area is unknown. In thess through the orifice. days after balloon dilatation haemodilutionm balloon allowed sub- and/or transfusion effects may variably alterh the larger balloon and blood viscosity, cardiac output, and ejectionras more than doubled. dynamics. Thus even the optimal timing for thecuspid) valves in which early non-invasive assessment is uncertain.ion had been performed Reports of apparent increases in calculatedchanges attributable to valve area in the days after balloon dilatation20

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Figure 3 Senile tricuspid valve (No 6) obtained at necropsy with an aortic valve area of 0-24 cm2 (a). The 20mmballoon completely occluded the orifice (b) and on deflation valve area had increased to 0-49 cm' (c). Byfive minutesthere has been some recoil and the area measured 0-42 cm' (d). Unless otherwise indicated allframes in this andsubsequentfigures were taken during systole.

Figure 4 Bicuspid valve (No 2) in which the balloon compktely occluded the orifice (b). Immediately afterwards (c)the valve area had increasedfrom 0-69 cn2 to 0-83 cm2 but atfive minutes (d) it had decreased to 0.76 cm2.

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Figure 5 Tricuspid valve (No 5) in which the inflated balloon (b) did not occlude the orifice and the areas at thecommissural angles totalled 60% of the original orifice area. On deflation the valve leaflets rapidly returned towardstheir original position (c) although the area had increasedfrom 0-48 cm2 to 0 73 cm'. Atfive minutes (d) the area haddecreased to 0-66 cm2.

Figure 6 Tricuspid valve (No 11) showing splitting of afused commissure during balloon inflation (b). The valvearea increasedfrom 0-52 cm' to only 0-68 cm' after dilatation (c) and atfive minutes had recoiled to 0-64 cm2 (d).

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..~.... ....-.-'

Figure 7 Bicuspid valve (No 10) with an orifice area of 0.39 cm' (a). There is tearing of both commissures duringinflation but especially of the commissure at the top left (b). The valve area had increased to 0 75 cm2 (c) and thediastolicframe (d) shows the tear and aflail leaflet (black arrrow).

Table 2 Area and gradient changes (mean (SD) according to niechanism of dilatation

Aortic valve area (cm2)

n Before After S mn 4 wk

All 18 0-52 (0-16) 0-78 (0-17) 0 73 (0-16) 0 70 (0-15)Stretching 6 0-56 (0.24) 0-74 (0 23) 0-66 (0 22) 0-64 (0 20)Splitting 12 0 50 (0-12) 0 80 (0-13) 0-77 (0-12) 0-73 (0-11)

Mean systolic gradient (mm Hg)

n Before After 6 mn 4 wk

All 18 54-2 (26 8) 32-6 (7-9) 35.0 (9-5) 40-0 (11-3)Stretching 6 44-5 (12-4) 35.2 (7 7) 38-8 (10-1) 41-5 (9-1)Splitting 12 59.0 (30 9) 31-3 (8 0) 33-1 (9 0) 39-3 (12-5)

are countered by reports of decreases71' andboth are explained on the basis of changes inleft ventricular function. Cardiac output isvariously reported to be decreased," un-

changed,2' or increased358 immediately afterthe procedure. The procedural effects are likelyto vary considerably between patients, depend-ing on their initial left ventricular function andthe severity and morphology of their stenoticvalve. Variation between centres with theirdiffering techniques, equipment, andexperience may also influence these variableswhile the methodological errors in bothinvasive and non-invasive assessment will varyaccording to the timing of the measurements.Serial measurements in consecutive patientshave not been reported owing to the variablenumbers at any point in follow up and becausefrequent invasive assessment is inappropriate.These considerations prompted our study ofthe immediate and short term effects of valvedilatation in vitro.

We found only small changes after balloondilatation-the magnitude of which was lessthan that reported in several large clinicalseries.38 10 21 In vitro there was almost animmediate recoil of the stretched orifice(whether or not commissural tearing hadoccurred) but after 5 minutes there was littlefurther recoil. Those studies in patients thatshow a rapid loss of the haemodynamic gain7"'are likely to be overestimating the immediatebenefits and their subsequent measurementsare probably a better indication of theimmediate effect. The very small changes seenin these patients may reflect inadequate balloonpositioning but they would also accord with thevalves in which we found no commissuraltearing and where gains in area were smaller. Itmay be that serial assessments would haveshown similar findings in many of the patientsreported to show "restenosis" by Dopplertechniques a few months after dilatation.'0"Postmortem and operative evidence after valvedilatation indicate that commissural tears orfractures persist for some months at least" 2224;it seems that in isolation stretching or"microfractures" or both do not produce last-ing benefit.LIMITATIONSThe valves obtained at operation were includedonly if they were removed in a single piece andwithout damage. Obviously the true aorticvalve annulus was not removed and the sutureline to the unyielding cone was only anapproximation ofthe in vivo annulus. This mayhave influenced the results in two opposingdirections. A more compliant annulus might

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Figure 8 Bicuspid valve (No 18) with splitting through both commissures. There wasfracturing of calciwn in thecommissures but in addition a clearfracture of non-commissural calcium (white arrow) (b). The valve mounting coneappeared as afaint grid with a denser ring where the material wasfolded.

have prevented tearing through the commis-sure to the edge of the specimen and so resultedin a smaller orifice area. But at the same timethe effect of more force on the remaining partsof the orifice may have caused more stretching,tearing of other commissures, or fractures ofcalcific deposits and so produced a largerorifice area. In six of the valves (including thenecropsy specimen with a true annulus) onlystretching was evident and changes were muchsmaller than in the other valves showing com-

missural tearing-so on balance it seems thatthe absence of the annulus might if anythinghave exaggerated the effects. Ideally, we shouldhave studied postmortem valves with theannulus en bloc but during the nine monthstudy period we found only one suitable case atroutine necropsy.The valves were obtained from a represen-

tative group ofpatients undergoing aortic valveoperation who are not typical ofpatients under-going balloon dilatation.38-11 619 Our patientswere thus younger and this accounts for a

higher frequency of men and bicuspid valves.The pattern of calcification is different inbicuspid and tricuspid valves and this maypartly explain why we found fewer fractures incalcific deposits than in some,2 1322-24 thoughby no means all, postmortem or operativestudies.671'We used a 20 mm balloon in this study for a

single (though optimally positioned) inflation.In some valves the balloon seemed to be toolarge and split the "annulus" whereas in thosethat showed stretching alone it may have beentoo small. Most clinical procedures, however,have been with 20 mm or smaller balloons andan increase in the balloon size has not alwaysincreased valve area after clinical recurrences.8

Nevertheless, it is possible that the much largerballoons being used by some more recentlywould have improved the results in some ofourvalves.

Leaflet recoil caused an early fall in valvearea and only later a rise in gradient. Thesupravalvar pressure port in this model is at afixed distance from the retaining plates thathold the cones, and the distance from the valveto the pressure port varied according to thelength of cone left after it was cut down toaccommodate the valve annulus area. Thedistance was nearly always greater than a halfofthe orifice diameter'5-that is the distance atwhich the pressure drop is lowest (vena con-tracta)-so that slight though systematic underreading of the gradients may have reduced theextent of the early changes. The valve area,however, is not the only factor to determine thegradient-orifice geometry and depth are otherfactors.25 The orifice depth is likely to haveincreased as the stretching displaced leafletmaterial and reduced the expected fall in thegradient; recoil of the leaflet thickening wouldthen have offset the rise in gradient. Most ofthevalves were preserved in formalin-a storagemedium used by others for valve dilatationstudies"2 1 26-and the effects of formalin mayprovide an alternative explanation for thegradient changes. We have previously shownthat the valve area and gradient measured overa wide range of flows does not change within amonth of explantation and storage in eitherformalin or nutrient solution."5 Neverthelessformalin storage may have had an effect on thegradient measured across dilated valves,though the four valves used fresh from surgery(and thereafter stored in nutrient solution)behaved in a similar fashion.

CONCLUSIONSWe found significant though rather smallincreases in valve area after balloon dilatationof calcific stenotic aortic valves. Commissuralsplitting seemed to increase the orifice areamore than stretching alone, but fractures ofcalcific deposits unrelated to commissures were

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uncommon. Stretching of the valve orifice wasfollowed by a measurable recoil within the firstfive minutes, irrespective of coexistent com-missural splitting. Thereafter, and in theabsence of any reparative mechanisms thatmight be present in vivo, there were no sig-nificant changes in valve area over the succeed-ing four weeks. Assessment of balloon dilata-tion of the aortic valve in the clinical settingshould be performed only when the patient isstable and all the procedural effects can bediscounted. In that way it might be possibleaccurately to document the real effects of theprocedure. The changes that we saw suggestthat patients who are critically compromised byaortic stenosis may benefit from balloon dilata-tion. In most patients, however, theimprovement in valve area is unlikely to beadequate for definitive treatment.

We thank Peter Liepins (Radiological Sciences Department) forthe valve radiographs, Ron Wilson (Dental ResearchLaboratory) for assistance with the statistical analysis, andSchneider Shiley (UK) for the pulsatile control unit. JKM wassupported by the Lions Heart Research Foundation of SouthAustralia. ACP was sponsored by a grant from the Greek StateScholarship Foundation.

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