Prosthetic Aortic Stenosis

A Method to Prevent Its Occurrence by Measurement of Aortic

Size from Preoperative Aortogram

By RONALD P. SENINGEN, M.D., BERNADINE H. BULKLEY, M.D., AND

WILLIAM C. ROBERTS, M. D.

SUMMARYA cause of early death after aortic valve replacement with a caged-ball prosthesis is obstruction to left ven-

tricular outflow because the prosthesis is too large for the aortic root. Of 68 patients dying within twomonths of aortic valve replacement, death in ten, each of whom had had intractable low cardiac output afteroperation, was attributed at necropsy to prosthetic aortic stenosis, despite the use of small sized (8A Starr-Edwards) prostheses in seven of them. The diameters of the aorta at the sinotubular junction, determinedfrom the preoperative cineangiograms, in the seven patients with prosthetic stenosis were < 30 mm in all.Poppet clearances, defined as the differences between poppet and aortic root diameters, ranged from 4 to 12mm (avg. 9). In contrast, the diameters of the aortas at the sinotubular junctions in eight control patients(unobstructed prosthetic aortic valves and early death from other causes) were > 30 in all but one, and thepoppet clearances ranged from 12 to 19 mm (avg. 15). Thus, prosthetic aortic stenosis is likely to developafter aortic valve replacement with rigid-framed caged ball valves if the preoperative aortograms discloseaortic diameters at the sinotubular junctions to be < 30 mm. In such patients, either the aorta must bewidened for a caged-ball prosthesis or a central flow valve must be used.

Additional Indexing Words:Aortic valve Cardiac valve replacement Cardiac operation

WHENEVER THE MITRAL or aortic valve isreplaced with a caged-ball prosthesis, some

degree of stenosis is nearly always produced by theprosthesis. 1-5 The obstruction is usually relativelymild, but on occasion the degree of stenosis isconsiderable.15 Anatomic features of fatal prostheticmitral and prosthetic aortic stenosis have beendescribed6"'0 but fatal prosthetic stenosis has not beendocumented hemodynamically in the earlypostoperative period. If the prosthetic stenosis is ex-tremely severe, cardiac function may not be restoredin the operating room after valve replacement. Also,cardiac catheterization is infrequently performed dur-ing the first few days after operation. As a conse-quence, diagnosis of fatal prosthetic obstruction hasbeen made almost exclusively" at necropsy.To help predict and perhaps prevent its occurrence,

the sizes of the aortic roots measured by preoperativeangiogram were compared to the sizes of the im-planted prosthetic aortic poppets in patients with

From the Department of Diagnostic Radiology, Clinical Center,and the Section of Pathology, National Heart and Lung Institute,National Institutes of Health, Bethesda, Maryland 20014.

Received October 16, 1973; revision accepted for publicationJanuary 3, 1974.

Address for reprints: William C. Roberts, M.D., Chief, Section ofPathology, National Heart and Lung Institute, National Institutesof Health, Bethesda, Maryland 20014.

necropsy-diagnosed prosthetic aortic obstruction, andthese measurements were compared to those innecropsy patients with replaced aortic valves butwithout prosthetic obstruction.

Patients Studied and Methods

Of 68 patients dying within two months of aortic valvereplacement, death in ten was attributed at necropsy toprosthetic stenosis. Of the 10, seven who had preoperativeaortic cineangiograms form the basis of this report (tables 1and 2). Preoperatively, 5 patients had pure aortic regurgita-tion and 2 had aortic stenosis. Death occurred in theoperating room in 1 patient, and in 6, from 1 to 8 days (avg.4) after valve replacement. Size 8A to 11A (avg. 8.6) Starr-Edwards prostheses were used. In each of the latter 6patients, death was attributed to the low cardiac output syn-drome.* At necropsy, the prosthesis in each appeared to betoo large for the aorta. At least 2 of the 3 struts of the cagecame into contact with the wall of aorta which protrudedinto the cage and prevented adequate movement of the pop-pet (figs. 1 and 2).

*All patients had at one time direct systemic systolic pressures of< 90 mm Hg. Each also had evidence of underperfusion of at leastone organ system: brain (disorientation or seizures); bowel (pain orbleeding); kidney (oliguria); lung (alveolar infiltrates = alveolarhemorrhage [shock lung]); liver (hyperbilirubinemia); and skin(peripheral cyanosis or coldness). The hypotension and organ-perfusion inadequacy responded poorly or not at all to therapy, in-cluding vasopressors. These signs of low organ perfusion were con-firmed by necropsy examination in all patients.

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Table 1Data in Patients Studied

S+e 1 LV-SA LA-LV tOperva Size/Model Diaeer DiarneterPatient Age MIVR PSG MDG A MR Operaton (mm,) Cleafance(yea,$) {mnH} {r g 0-42 10-4) to Death Prostei

SE

Po..

e f aota at {nnRg) 1+14 RH 0)4) ,d0osh P,cithesi, o+Poppet S-T9JneiWITH PROSTHETIC STENOSIS

1. A67-207 F/51 + 51 12 4+ 2+ 7 8A 1200 15 20 52RA72-235 F/45 + 5 11 2+ 0 BA 2300 15 23 S3. A65133 M/Z5 + 18 0 24 3. BA 1000 15 23 a44A683 Mf29 + 0 0 4+ 1+ 3 11A2300 18 26 a5. A73-39 F155 + 0 17 3+ 0 OR 8A 2320 15 26 116 A68-67 F/37 + 0 10 4+ 0 2 4A 2300 15 27 127 A67-311 M/42 0 0 0 4+ 2+ a 4A 1200 17 29 12

WITHOUT PROSTHETIC STENOSIS84A73-4 M/59 0 0 7 4+ 2+ 50 11A 2320 14 30 129. A71-149 f/52 0 0 0 4+ 1+ 44 1A 2320 10 28 13

10. A71-63 F154 + + 0 3+ 3+ 13 9A 2310 16 30 1411. A72-124 F/57 + 35 5 3+ 1+ 2 9A 2320 16 30 1412. A71 94 M/41 + 26 is 2+ 3+ 5ii 9A 2310 16 30 1413 A67-18 M/33 0 100 0 0 0 OR 8A 1200 15 30 1514.A64-40 M/45 + 0 19 3+ 0 OR 8A 1Z00 15 33 1815RA64-107 M/36 + 0 7 3+ 2+ OR RA lWSO 15 34 19

Abb+e,,iati++s: AR aonic reg+r+gitatio. LA left LV -Ieft vMntricle;hDG+ m4eandia c+g 4 nt.b MRH miI rgitpt oMVR m+itralvalve repIacement; PSG peak Wstolic gradient: SA .ysy+onl +... SE09.,Edo4o, S-T+sinotububI.

Of the remaining 58 necropsy patients who died < 2mnllths after aortic valve replacement, 8 were selected ascontrols on the basis of their havinig measurable aortic rootcinicangiograms (i.e., grids present on the frames), similarpreoperative lesions and similar sized prostheses (Starr-Edwards) as those in the 7 patients with prosthetic stenosis.Preoperatively, 5 patients had ptore aortic regurgitation, and3 had aortic stenosis. Death occurred in the operating roomin 3 patients and from 2 to 56 days (avg. 33) after valvereplacement in the other 5 patients. Size 8A to 11Aprostheses (avg. 8.7) were uitilized. Death was due totechnical mishaps in 4 patients, unexplained low cardiacouitptut in 2, uinexplained sudden death in 1, and non-cardiaccauises in 1. At necropsy, the aortic poppets moved freely inthe cages and never did more than 1 of the 3 struts of theprosthesis contact the aortic wall (fig. 3).

TFhe hearts in the 7 patients with prosthetic stenosisweighed 310 to 1040 g (avg. 670), and those in the 8 con-trols, 500 to 1100 g (avg. 630). None of the 15 patients hadhad the Marfan or Marfan-like syindrome, anid none had hada portior of ascendinig aorta resected.

(:iuca,(iortograrmi EvalucationThe cliameters of the aortic roots were measured from

preoperative cineaortograms, corrected for geometricmagnification, in all 15 patients. The internal diameter ofeach aorta was measured at the sinotubular junction (themost proximal portions of the tubular aortas or the mostcephalad externsions of the sinuses of Valsalva), and at a level2 em above the sinotubular junction (fig. 4). Bothmeasturements were taken from the same cine frame at max-imal systolic aortic distention. These measuirements wereperformed vithout prior knowledge of the clinical orneeropsy findinigs. TFhe diameters of the aortic prostheticpopI)pets (supplied by Edwards' Laboratories) were com-

Table 2Prosthetic Aortic Stenosis

Di41No. c

Patients

1. Stenotic 7

prosthetic

aortic valve

11. Non-stenoticprostheticaortic valve(controls)

pared to the dliameters of the aortas and the differences(maximal clearances) were recorded (tables 1 anid 2).

Comments

Malfunction of an implanted prosthesis is a com-mon cause of death in the early postoperative periodafter cardiac valve replacement.6'-' Of 133 patientsdying early ( < 2 mo) after replacement of one ormore cardiac valves with caged ball prostheses(mainly Starr-Edwards), 34% died from prostheticdysfunction.'0 Of the 68 necropsy patients with aorticprostheses, death in 10 resulted because the prosthesiswas too large for the aorta into which it had been in-serted. All 10 patients with prosthetic aortic stenosishad evidence of inadequate cardiac outputpostoperatively. Prosthetic stenosis in all 10 patientswas diagnosed only at necropsy.

Studies in the patients with prosthetic stenosisdemonstrated that measurement of aortic size frompreoperative aortograms can predict those patientswho are at high risk of developing prosthetic aorticstenosis. The critical diameter of the ascending aortaat the sinotubular junction is about 30 mm. Thismeasurement was < 30 mm (avg. 25) in each of the 7patients xvith fatal prosthetic aortic stenosis but inonly 1 of the 8 control patients with normally func-tioning aortic prostheses of similar size (avg. 31).

Figure 1

Prosthetic aortic stenosits. Shown here are photographs of rigid-meter9(mm) Diameter4(mm) Sizeof Diameter (mm) Maximal fr(ontied caged-bll (trtle prostheses irt patiettts "2 (a, afl)5 (b) and l3

at S-T above S-T prdsl popesz ceae (c, (/`).Ti(taortpir t entet thougt sntall (SA, Starr-SI abo+e 0 1 ~(tarrEdwarEds uti1lized (91+1)0unction jAnction fdatds). are too large for the aortas irito wlticht tliy Iad bent20-29 29-39 8A11A 15-18 4-12 Placed. Thte strtuts of the cages contact the aortic walls which(25) (33) (8.6) (16) ig) protrude hetweeti thle stritts to contact the poppets and restrict their

2t311oenment. Duirirng simulated vcietricuclar systole (e') the poppet is20-34 29-39 8A-11A 15-18 12-19(31) (36) (8.7) (16) (15) preWentedfrortt asceinding completely to the apex of the cage by the

intrudhng aortic wtnall. A maltch head projects from the narrowedProsthletic orifice. R. atid L. right and left coronary arteries.

ruitlatton volititte ,',I lay 19.t74

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PROSTHETIC AORTIC STENOSIS

Figure 2

Prostetic (iortic stenlosis in patient '4. The ascending aorta at 2 cm(ilOVC (a), at 1 cn ao)cc (b)), and at the sinotabular jutnction itself(c)

Moreover, prosthetic stenosis occurred in 5 of the 7patients despite the use of small sized (8A) prostheses.Thus, some aortas are simply not large enough foreven these small rigid-framed caged ball prostheses.Aortic diameters measured 2 cm above thesinotubular junctions did not correlate with thedevelopment of prosthetic aortic stenosis. Hence, atoperation the aorta above the sinuses of Valsalva mayappear of adequate size to readily accommodate arigid-framed prosthesis, but at the same time, the sizeof aorta at the sinotubular junction may be too smallto accept the prosthesis.

Thus, measuirement of the diameter of aorta fromthe preoperative cineaortogram at the level of thesinotubular junction can be used to predict thosepatients in whom prosthetic stenosis is likely todevelop after aortic valve replacement with a rigid-framed caged-ball prosthesis. Those patients with aor-tic diameters < 30 mm are at high risk, and in suchpatients widening of the aorta should be considered ifcaged-ball prostheses are implanted or central flowtype prostheses should be used. Knowledge of thismeasu.rement recently proved helpful in a patient un-dfergoing aortic valve replacement. The diameter ofaorta at the sinotubular junction measured 29 mm onthe preoperative eineaortogram. After valve replace-

Figure 3

Two exaniplcs of unon-stenotic aortic prostheses. The aortic walls donot contact the p)oppets or the struts of the protheses, (anid poppetiiiovement is oninipeded.

(Cii iuation Xo/umc xI.I\, mayltt )19

SINOTUBULA2RJUNCTION

SINUS OF VALSALVA

Figure 4

Cineaortograin in the right anterior oblique view withcorrespondintg line drawing. Measurement A represents the initernalaortic diamneter at the junction of the sinus of Valsalva and tubularaorta (sinlotuibiidar jun11ction); nieasurement B, the itnternal aorticdianieter 2 cm above the sinotuhular jtunction.

ment the heart functioned poorly, prosthetic aorticstenosis was suspected, and the aortic root waswidened with a patch. The heart then functioned wellafter discontinuation of cardiopulmonary bypass andthe postoperative course was smooth.

In addition to the measurements performed in the15 patients described herein, the diameters of aorta at,and just above, the sinotubular junctions weremeasured from preoperative cineaortograms in 8other patients, all of whom underwent cardiaccatheterization about 6 months after aortic valvereplacement with Starr-Edwards prostheses. The sizesof the aortic prostheses in these 8 patients, however,averaged 11.1: in 5, size llA prostheses were used; in2, size 12A; and in 1, size JOA. The diameters of aortaat the sinotubular junctions in these 8 patients rangedfrom 32 to 38 mm (avg 36), and the poppet clearancesfrom 15 to 20 mm (avg 17). The peak systolic pressuregradients between left ventricle and systemic artery atthe 6-month postoperative catheterization studieswere < 25 mm Hg in each of the 8 patients. Althoughthese patients are not comparable to our necropsypatients, these data clearly indicate that the diametersof the sinotubular junctions and the poppet clearancesare considerably smaller in the patients with fatalprosthetic aortic stenosis than in the patients withoutsignificant prosthetic aortic stenosis.

References

1. \1()Iiioxw AC, O)ii1iAm NH, ELKINS RC, BRAxUNWAii) E:Prosthetic replacement of the mitral valve Preoperativeclinical and hemodvnamic assessments itl 100 patients Cir-etilation 35: 962, 1967

2. Ki(0 T EIR FE, FAU(CII C, MOLURD)J1NiS A HonI)Axi R, S ARR A,CGISWOILD HE: Hemodynamic studies in patienits with cloth-covered composite-seat Starr-Edwards valve prostheses. jThorac Cardiovase Surg 60: 879, 1970

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3. GLANcY DL, O'BRIEN KP, REIS RL, EPSTEIN SE, MORRow AG:Hemodynamic studies in patients with 2M and 3M Starr-Edwards prostheses: Evidence of obstruction to left atrialemptying. Circulation 39 & 40 (suppl I): 1-113, 1969

4. WINTER TQ, REIS RL, GLANCY DL, ROBERTS WC, EPSTEIN SE,MORROW AG: Current status of the Starr-Edwards cloth-covered prosthetic cardiac valves. Circulation 45 & 46 (supplI): 1-14, 1972

5. HAWE A, FRY RL, ELLIS FH JR: Late hemodynamic studies aftermitral valve surgery. J Thorac Cardiovasc Surg 65: 351, 1973

6. ROBERTS WC, MORROW AG: Mechanisms of acute left atrialthrombosis after mitral valve replacement. Pathologic find-ings indicating obstruction to left atrial emptying. Am J Car-diol 18: 497, 1966

7. ROBERTS WC, MORROW AG: Anatomic studies of hearts

containing caged-ball prosthetic valves. Johns Hopkins MedJ 121: 271, 1967

8. ROBERTS WC, MORROW AG: Causes of early postoperativedeath following cardiac valve replacement. J Thorac Car-diovasc Surg 54: 422, 1967

9. ROBERTS WC, MORROW AG: Causes of death and otheranatomic observations after cardiac valve replacement. AdvCardiol 7: 226, 1972

10. ROBERTS WC, BULKLEY BH, MORROW AG: Pathologic anatomyof cardiac valve replacement. A study of 224 necropsypatients. Progr Cardiovasc Dis 15: 539, 1973

11. SHEPHERD RL, GLANCY DL, STINSON EB, ROBERTS WC:Hemodynamic confirmation of obstruction to left ventricularinflow by a caged-ball prosthetic mitral valve. J Thorac Car-diovasc Surg 65: 252, 1973

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RONALD P. SENINGEN, BERNADINE H. BULKLEY and WILLIAM C. ROBERTSAortic Size from Preoperative Aortogram

Prosthetic Aortic Stenosis: A Method to Prevent Its Occurrence by Measurement of

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1974 American Heart Association, Inc. All rights reserved.

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