Hemodynamic Changes Following Correction of Severe Aortic Stenosis Using the Cutter-Smeloff Prosthesis By SIMON J. K. LEE, M.D., M. HARAPHONGSE, M.D., J. C. CALLAGHAN, M.D., R. E. ROSSALL, M.D., AND R. S. FRASER, M.D. SUMMARY Twelve patients with pure or dominant stenosis were studied before and after aortic valve replacement (Cutter-Smeloff). The changes in cardiac output and A-V 02 difference were small and insignificant, but exercise stroke volume increased from 72 to 96 ml after the surgery. The aortic peak systolic gradient was 92 + 29 mm Hg before and 4 + 9.8 mm Hg after surgery. The PA wedge pressure, taken as a measure of the LV diastolic pressure, decreased from 18 mm Hg to 12 mm Hg at rest and 30 mm Hg to 16 mm Hg on exercise. The PA pressures also decreased from 37/18 (mean, 26) to 28/11 (17) mm Hg at rest, and 61/31 (43) to 41/17 (27) mm Hg on exercise, but the PA and PA wedge pressures maintained their tendency to increase in a linear manner with oxygen con- sumption (Vo2) on exercise after surgery. As a result of decreased wedge pressure, the pulmonary vascular resistance also decreased significantly afterward. The adequacy of cardiac output at rest and on exercise expressed by cardiac output as the linear function of Vo2 improved toward the normal (values before operation, CO = 2.78 + 0.0069 V02, r = 0.84; after operation, CO = 3.80 + 0.0062 V02, r = 0.91). The exercise fac- tor (ACO/AzVo2) or the regression coefficient, however, was similar before and after surgery. The hemodynamic result was satisfactory although some abnormalities of the left ventricular function persisted after operation. Additional Indexing Words: Left ventricular function Exercise HEMODYNAMIC studies have been re- ported following replacement of the aortic valve using the Starr-Edwards prosthe- sis,1-3 and various parameters of cardiac function have been found to improve although significant abnormalities may persist in some From the Division of Cardiology, Department of Medicine, University of Alberta and University Hospital, Edmonton, Alberta, Canada. This study was supported by a grant-in-aid of the Alberta Heart Foundation. This study was carried out during Dr. Lee's tenure of a Senior Research Fellowship from the Canadian Heart Foundation. Received April 8, 1970; revision accepted for publication June 16, 1970. Circulation, Volume XLII, October 1970 Exercise factor patients. To increase the effective lateral orifice of the ball-valve prosthesis, Cartwright and associates4 made modifications to the original prosthesis and these modifications have been widely accepted.5 The purpose of this communication, therefore, is to report circulatory changes at rest and exercise before and after aortic valve replacement using the Cutter-Smeloff prosthesis. Only patients with pure or dominant aortic stenosis were includ- ed in this study to assess the result of the decreasing pressure load of the left ventricle rather than the volume load as in aortic regurgitation. Of special interest was a study of the circulatory adaptation to strentuous exercise after surgery. 719 by guest on September 1, 2017 http://circ.ahajournals.org/ Downloaded from
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Hemodynamic Changes Following Correction ofSevere Aortic Stenosis Using the Cutter-Smeloff
Prosthesis
By SIMON J. K. LEE, M.D., M. HARAPHONGSE, M.D., J. C. CALLAGHAN, M.D.,
R. E. ROSSALL, M.D., AND R. S. FRASER, M.D.
SUMMARYTwelve patients with pure or dominant stenosis were studied before and after aortic
valve replacement (Cutter-Smeloff). The changes in cardiac output and A-V 02
difference were small and insignificant, but exercise stroke volume increased from 72to 96 ml after the surgery. The aortic peak systolic gradient was 92 + 29 mm Hg beforeand 4 + 9.8 mm Hg after surgery.The PA wedge pressure, taken as a measure of the LV diastolic pressure, decreased
from 18 mm Hg to 12 mm Hg at rest and 30 mm Hg to 16 mm Hg on exercise. ThePA pressures also decreased from 37/18 (mean, 26) to 28/11 (17) mm Hg atrest, and 61/31 (43) to 41/17 (27) mm Hg on exercise, but the PA and PA wedgepressures maintained their tendency to increase in a linear manner with oxygen con-
sumption (Vo2) on exercise after surgery. As a result of decreased wedge pressure, thepulmonary vascular resistance also decreased significantly afterward. The adequacy ofcardiac output at rest and on exercise expressed by cardiac output as the linear functionof Vo2 improved toward the normal (values before operation, CO = 2.78 + 0.0069V02, r = 0.84; after operation, CO = 3.80 + 0.0062 V02, r = 0.91). The exercise fac-tor (ACO/AzVo2) or the regression coefficient, however, was similar before and aftersurgery. The hemodynamic result was satisfactory although some abnormalities of theleft ventricular function persisted after operation.
Additional Indexing Words:Left ventricular function Exercise
HEMODYNAMIC studies have been re-ported following replacement of the
aortic valve using the Starr-Edwards prosthe-sis,1-3 and various parameters of cardiacfunction have been found to improve althoughsignificant abnormalities may persist in some
From the Division of Cardiology, Department ofMedicine, University of Alberta and UniversityHospital, Edmonton, Alberta, Canada.
This study was supported by a grant-in-aid of theAlberta Heart Foundation.
This study was carried out during Dr. Lee's tenureof a Senior Research Fellowship from the CanadianHeart Foundation.
Received April 8, 1970; revision accepted forpublication June 16, 1970.
Circulation, Volume XLII, October 1970
Exercise factor
patients. To increase the effective lateralorifice of the ball-valve prosthesis, Cartwrightand associates4 made modifications to theoriginal prosthesis and these modificationshave been widely accepted.5 The purpose ofthis communication, therefore, is to reportcirculatory changes at rest and exercise beforeand after aortic valve replacement using theCutter-Smeloff prosthesis. Only patients withpure or dominant aortic stenosis were includ-ed in this study to assess the result of thedecreasing pressure load of the left ventriclerather than the volume load as in aorticregurgitation. Of special interest was a studyof the circulatory adaptation to strentuousexercise after surgery.
11. G.W. 44 Syncope, No LVH, Same Cutter, #2 11M CHF strain
12. F.M. 40 Dyspnea, No LVH, Normal Cutter, #2 17M angina strain
Abbreviation: PND = paroxysmal nocturnal dyspnea.
MethodsPatients StudiedThe clinical summary is listed in table 1. All 12
patients had clinical and hemodynamic findingsconsistent with severe valvular aortic stenosis.Patients with dominant aortic regurgitation or
coexisting mitral valve disease or patients whodeveloped significant aortic regurgitation aftersurgery were excluded from this series. Allpatients were in sinus rhythm and no patient hadelectrocardiographic evidence of myocardial in-farction before or after operation. The postopera-tive studies were done between 6 and 22 moafter surgery (average 13 mo). All patients exceptone (case 7) were female, and their averageage was 47 years (range, 26 to 65).
TechnicsCardiac catheterization was performed after a
light breakfast following premedication withsecobarbital (Seconal) 100 mg by mouth. Forthe left heart catheterization a no. 7 NIH or no.7.5 Sones catheter was introduced into the rightbrachial artery via cutdown, and a no. 6Cournand catheter was used for the venouscatheterization. The aortic pressure gradient was
measured by withdrawing the catheter from theleft ventricle into the aorta while the pressure wascontinuously recorded. The midthoracic level wastaken as the reference point for zero pressure.Oxygen uptake was estimated by collecting theexpired gas in Douglas bags with analysis of gasfor oxygen (E2, Beckman 02 analyzer) and CO2(Capnograph-Goddart). Cardiac output was es-timated using the Fick principle, and the arterialand pulmonary artery blood samples wereanalyzed for oxygen by the method of Van Slykeand Neil. Supine leg exercise was performedusing a constant load bicycle ergometer(Fleisch), and measurements of cardiac outputand pressures were made during the fourth andsixth minute of steady-state exercise. The secondexercise with a higher workload was carried outafter several minutes of rest. Pressure wasrecorded using P23Db transducers and a photo-graphic recorder (DR-8, Electronics for Medi-cine). The pulmonary vascular resistance indexwas expressed as the ratio of the pressuredifference across the pulmonary vascular bed inmm Hg (mean PA pressure minus pulmonarywedge pressure) over the cardiac output inL/min. The total pulmonary vascular resistance
Pulmonary artery pressures at rest and on exercise before and after surgery. Clear bar=preoperative; crossed bar = postoperative.
was calculated by dividing the mean PA pressure(mm Hg) by cardiac output (L/min) .For aortic valve replacement total cardiopul-
monary bypass and a disposable bubble oxygena-tor (Travenol) were used.6 Coronary perfusionwas used in most patients.
ResultsAll patients complained of one or more of
the following: dyspnea, chest pain on exer-tion, or syncope before operation (table 1).After surgery, eight patients were entirelysymptom-free while four had only mildresidual symptoms including dyspnea, dizzi-ness, or fatigue. Before operation, 11 patientshad electrocardiographic evidence of leftventricular hypertrophy with increased QRSvoltage and ST and T-wave changes, and onepatient had only increased QRS voltage. Theelectrocardiograms improved definitely in sev-Circulation, Volume XLII, October 1970
en patients; they were unchanged in four, andleft bundle-branch block appeared after sur-gery in one.The hemodynamic data obtained are listed
in table 2, and the paired comparison of thedata at rest and comparable levels of exerciseis made in table 3 and figures 1 and 2.
Pressures
Resting pulmonary artery pressure (37/18;mean, 26 mm Hg) and mean PA wedgepressure (18 mm Hg) were slightly elevatedbefore operation. In the absence of mitralvalve disease, the increase in wedge pressureis due to the elevated left ventricular end-diastolic pressure (LVEDP) which was23± 10 mm Hg. Following surgery, thepulmonary artery (28/11; mean, 17 mm Hg)and the wedge pressures (12 mm Hg) had
decreased (table 3). During exercise, how-ever, a greater fall in these pressures was
found following surgery: PA mean pressure
decreased from 61/31 (43) mm Hg to 41/17(27) mm Hg and mean wedge pressures from30 to 16 mm Hg. The pulmonary vascularresistance (PVR) index decreased at rest from1.65 to 1.23, and on exercise, from 1.45 to 1.08after surgery. The resting aortic pressure
increased after surgery, from 98/57 (76) to115/61 (83) mm Hg and the changes insystolic (18%) and mean pressure (8%) are
significant (P < 0.05). Before operation, theaverage peak systolic pressure gradient was 92(±+ 29) mm Hg. Following surgery, thegradient was measured in eight patients withthe Cutter-Smeloff prosthesis including thosepatients not included in this series, with a
mean value of 3.9 (±+ 10) mm Hg.
Other Data
Resting oxygen consumption ( Vo2) de-creased by 10% (fig. 2) from 245 to 218ml/min7 while cardiac output increased by 9%(4.73 to 5.14 L/min); thus, the arteriovenousoxygen difference decreased from 5.21 to 4.32vol% (18%). During the postoperative study,the average Vo2 for the first exercise (El) washigher by 12% (997 ml/min compared to 887ml/min), indicating that the intensity ofexercise was slightly greater. Similarly, cardiacoutput increased on exercise after operationfrom 8.58 to 10.35 L/min. The increase incardiac output was 21% while V02 increasedonly 12%. Thus, the arteriovenous 02 differ-ence decreased from 10.33 to 9.63 vol%.A more obvious change was found in stroke
volume (SV) following surgery: resting SV,61+21 ml compared to 72+29 ml (+18%)and exercise SV, 74 32 ml compared to96 28 ml ( + 30%). The resting heart ratedecreased slightly (6 beats/min). Althoughthe first exercise was slightly heavier (12%)during the postoperative study, the exerciseheart rate decreased by 8 beats/min, inkeeping with the improved stroke volume.The relationship between exercise Vo2 and
CO is depicted in figure 3. Cardiac outputincreased in a linear fashion with Vo2 before
Cardiac output, arteriovenous oxygen difference, strokevolume to wedge pressure (SV/WP) before and aftercrossed bar = postoperative.
(CO 2.782 + 0.0069 Vo2, r =0.84, P < 0.001)and after the surgery (CO= 3.7995 + 0.0062Vo2, r = 0.907, P < 0.001). Thus, the regressionof cardiac output on Vo2 improved towardnormal, and it was almost identical to thatfound in patients with normal cardiovascularsystems of similar age (30 to 64 years) studiedby us: CO = 3.83 + 0.0061 Vo2, r -0.90, n =52(11 males and 12 females). The pulmonaryartery systolic (PAS) and the wedge pressure(PAW) increased progressively with exercisebefore surgery: PAS = 31.27 + 0.031 Vo2, r =0.463, P < 0.05; PAW = 13.47 + 0.0149 Vo2, r =0.618, P <0.001. After surgery, however, thepressure increase due to exercise was signifi-cantly less: PAS = 28.2 + 0.0135 Vo2, r = 0.55,
12
zig
4,1
SV
10
8
6
cL
(A4
sssstssn
.I |
_hSVN,IP
volume, and the ratio of strokesurgery. Clear bar = preoperative;
- - BVEGVRDDONALD
LEE-- HULTGRWJ
--.-ROSS
0.2 06to2 List
1O 1.4
Figure 3Cardiac output in relation to oxygen consumption atrest and on exercise.
also decreased significantly. We suggest thatthis is due to decreased systolic pressure andalso to the changes in the myocardial compli-ance, possibly because of diminished leftventricular wall thickness.
Before operation, the wedge pressure had atendency to increase in a linear fashion withthe degree of exercise, that is, with exerciseVo2 (r = 0.618). A similar correlation wasfound in the patients with severe aorticstenosis studied previously7 (LA or PAWpressure was 10.8 + 0.0199 Vo2, r =0.594,P <0.01). The reason for the increasing end-diastolic pressure and the apparent decreasein the myocardial compliance during exercisehas not been established, but it is likely due tothe increasing systolic pressure and therelative myocardial ischemia which may de-velop from the increased myocardial oxygendemand. Following surgery, the wedge pres-sure decreased both in the intercept and in theslope of the regression (from 0.0149 to0.0064) but still maintained its tendency toincrease with exercise (fig. 4), indicating theresidual abnormalities of the left ventricularfunction.The pulmonary artery systolic pressure, as a
linear function of the exercise Vo2, alsodecreased in intercept and in the regressioncoefficient (from 0.030 to 0.013), which mustbe due to the reduction in the wedge pressureand the pulmonary vascular resistance aftersurgery. The paired comparison of pulmonaryvascular resistances decreased by 25% at restand on exercise after surgery, as a result ofdecreased wedge pressure, and the totalpulmonary resistance (PA mean pressure, mmHg/CO, L/min) also decreased by 38% at restand 32% during exercise (5.39 to 3.36 and 4.13to 2.81). The degree of hyperventilation(ventilation/Vo2) during exercise is an objec-tive measurement of dyspnea, and among thehemodynamic parameters studied it wasfound to be most closely related to the totalpulmonary vascular resistance8 (r = 0.816).Hence, the disappearance of dyspnea onexertion, noted by most of these patients,appears to be related to this decrease inpulmonary vascular resistance.
The average peak systolic gradient mea-sured in eight patients after operation was 3.9(±+ 10) mm Hg; no gradient was found in sixpatients, and it was 28 mm Hg and 3 mm Hgin the remaining two patients. Therefore, theresidual abnormalities of the left ventricularfunction do not appear to be due to theinadequate valve orifice. Our result is signifi-cantly different from that of McHenry and as-sociates9 who found an average gradient of 19(+ 8) mm Hg in seven patients with the sameprosthesis. In 60 patients with the Starr-Ed-wards prosthesis reported on by others," 2,10-12the average gradient was 13.9 (+ 11.1) mmHg.As found by others, the changes in cardiac
output following surgery are rather small(table 2, fig. 2). Hultgren and associates3found an increase in resting cardiac index of16% and a decrease in arteriovenous oxygendifference of 19%, while Bristow' and Ross2and their co-workers have reported an in-crease in resting cardiac index of only 4% and3%, respectively. In the present study, thearteriovenous oxygen difference as a measureof the adequacy of cardiac output decreasedby 18% at rest and by 7% during exercise. Therather small magnitude of these changes isprobably due to the fact that only a fewpatients were in true heart failure with lowcardiac output before surgery. Although thechanges in cardiac output were small, theincrease in stroke volume was greater at rest(18%) and especially during exercise (30%).This suggests increased myocardial contrac-tion or fiber shortening, since the end-diastolicvolume or the initial fiber length should nothave increased afterward. This appears to bethe result of decreased afterload on the leftventricle. It has been shown that exercisestroke volume is a more sensitive indicator ofcardiac performance than cardiac output,'3-15as the inadequate cardiac output can becompensated by an increase in heart rate.Thus, the 30% increase in exercise strokevolume, from 74 ml to 96 ml, indicates a trueimprovement in the ability to increase cardiacoutput during exercise. The maximum strokevolume is reached with a moderate degree of
exercise and remains relatively constant withthe maximum exercise,'3-16 In 11 patients whowere studied on two levels of exercise afteroperation, the stroke volumes were 84 + 17 mland 85 + 16 ml on the first and secondexercises, in keeping with the findings innormal individuals. Assuming the maximumheart rate is not altered due to surgery, the34% increase in exercise stroke volume is equalto the increase in the maximum cardiac outputof this magnitude.As in normal individuals,'3-1' cardiac output
at rest and on submaximal exercise showed alinear increase with oxygen consumptionbefore (r = 0.84, P < 0.001) and after surgery(r = 0.91, P < 0.001). Although the interceptwas higher after the surgery, the regressioncoefficient did not change (0.0069 comparedto 0.0062); this indicates that the exercisefactor was unchanged. Before operation, inspite of the high systolic pressure gradient(92 + 29 mm Hg), all patients were able toachieve an increase in cardiac output withexercise, as was found in a previous report7;therefore, a truly fixed cardiac output in aorticstenosis must be rare.The relationship between cardiac output
and V02 in the present series has beencompared with that in normal subjects studiedby Donald,17 Holmgren,13 and Bevegard'4 andtheir associates, as well as the patients studiedafter aortic valve replacement (Starr-Ed-wards) by Hultgren3 and Ross2 and their co-workers. There is essentially no differenceamong the three groups of patients with aorticvalve replacement (fig. 3). The regression inpatients who have had valve replacement issignificantly lower in the intercept when com-pared to the young normal individuals'3' 14, 17but is the same as that found in the normalindividuals of similar age studied by us. It isinteresting to note that the regression coeffi-cients are similar in all these studied: Donald'sgroup, 0.00566; Beveg'ard's group, 0.0061; Lee'sgroup, 0.0061 (normals) and 0.00623 (post-operative patients); Hultgren's group, 0.00649;and Ross's group, 0.0058. These values indicatethat the exercise factor, that is, the increase incardiac output for a given increase in oxygenCirculation, Volume XLII, October 1970
consumption,2 is the same in all groups. Thecharacteristic of the low cardiac output state,therefore, is the lower intercept of this regres-sion rather than the reduced exercise factor.
Following surgery, the ratio of the strokevolume and the pulmonary artery wedgepressure (SVIPAW), as an index of the leftventricular function, improved by 57% at rest(4.45 to 7.05) and 105% during exercise (2.96to 6.08). In normal individuals, supine legexercise has been found to increase stroke vol-ume without changing PA wedge pressure,13-15resulting in an increase in the SV/WP index.However, in the patients with aortic stenosisconsidered here, this index decreased withexercise by 34% (4.45 to 2.96) before operationand 14% (7.05 to 6.08) afterward, which sug-gests residual dysfunction of the left ventricle.It is likely that those patients with severelydepressed left ventricular function before sur-gery may continue to have it afterward; infact, the SV/WAP ratios during exercise beforeand after surgery did show a significant posi-tive correlation (P < 0.001): postoperative SV/PAW = 3.575 + 0.844 SV/PAW, r = 0.614. Theclinical implication of this finding is that thevalve surgery should be carried out beforesevere left ventricular failure ensues, as suchpatients may fail to improve significantly after-ward.From 1966 to 1969 inclusive, the Cutter-
Smeloff aortic prosthesis has been used in 166patients at the University of Alberta Hospital,and no incidence of prosthesis failure due toball degeneration has been encountered todate. Bloodwell and associates5 also have re-ported no such complication in a series of635 patients. This complication appears to berare in the Cutter-Smeloff aortic prosthesis, asonly three such cases have been reported thusfar.18 It may be more common in the Starr-Edwards prosthesis.'9 20 This absence ofcomplication, in our opinion, is due to therelatively smaller diameter of the ball in theCutter-Smeloff prosthesis than in the othervalve, which allows more space for expansionbetween the ball and the cage if the ballshould swell.
Previously we reported three cases of failureof the mitral Cutter-Smeloff prosthesis21 dueto "sticking" of the ball in the seating ring as aresult of minimum swelling of the ball. Thefact that the same phenomenon has not beenencountered with the aortic prosthesis is likelydue to the lesser force with which the aorticball descends during diastole, while the mitralball strikes the ring with a greater forceduring systole; therefore, although we havestopped using the mitral prosthesis, the aorticCutter-Smeloff prosthesis remains our choice.
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Clinical and hemodynamic results of aorticvalve replacement with a ball-valve prosthesis.Circulation 29 (suppl I): I-36, 1964
2. Ross J, MORROW A, MASON D, ET AL: Leftventricular function following replacement ofthe aortic valve. Circulation 33: 507, 1966
6. SINGH NS, CALLAGHAN JC: The follow-up of 80consecutive aortic valve replacements. AnnSurg 6: 40, 1968
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13. HOLMGREN A, JONSSON B, SJOSTRAND T: Circula-tory data in normal subjects at rest and duringexercise in recumbent position with specialreference to the stroke volume at differentworkloads. Acta Physiol Scand 49: 343,1960
14. BEVEGXRD S, HOLMGREN A, JONSSON B: Theeffect of body position and circulation at restand during exercise, with special reference tothe influence of the stroke volume. ActaPhysiol Scand 49: 279, 1960
15. BEVEGIRD S, HOLMGREN A, JONSSON B: Circula-tory study in well-trained athletes at rest andduring heavy exercise, with special reference tostroke volume and the influence of bodyposition. Acta Physiol Scand 49: 279, 1960
16. ASTRAND PO, CUDDY TE, SALTIN B, ET AL:Cardiac output during submaximal and maxi-mal work. J Appl Physiol 19: 268, 1964
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18. McHENRY MM, SMELOFF EA, FONG W, ET AL:Critical obstruction of prosthetic heart valvesdue to lipid absorption by silastic. J ThoracCardiovasc Surg 59: 413, 1970
19. ALLEN P, ROBERTSON R: The significance ofintermittent regurgitation in aortic valve pros-thesis. J Thorac Cardiovasc Surg 54: 549,1967
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