Recovery from myocardial failure after aortic valve replacement

Recovery from myocardial failure after aortic valve replacement Left ventricular hypertrophy and function were studied in 27 consecutive patients with chronic aortic valve disease before and 6.4 ± 2.2 (S.D.) months after aortic valve replacement with Bjork-Shiley prostheses. Four patients were excluded because of postoperative paravalvular regurgitation. Five patients had aortic stenosis (AS), seven patients AS plus insufficiency (AS-AI), and II patients aortic insufficiency (AI). Left ventricular muscle mass (LVMI), ejection fraction (EF) , mean circumferential fiber shortening rate (VCF), mean normalized systolic ejection rate (MNSER) , and peak systolic wall stress (PSWS) were determined angiographically. LVMI fell significantly after corrective surgery, whereas EF, VCF, and MNSER increased. PSWS decreased after the operation. Comparison of stress ventriculograms before and after surgery in six patients with predominant AS (isoproterenol infusion, 0.3 J.l,g per kilogram of body weight per minute) showed an increase of EF, VCF, and MNSER and a decrease of psws. We conclude that hypertrophy in chronic aortic valve disease regresses after aortic valve replacement, and thereby depressed cardiac function and reserve recover.

Franz Schwarz, M.D., Willem Flameng, M.D., Jochen Thormann, M.D., Michael Sesto, M.D., Friederike Langebartels, M.D., Friedrich Hehrlein, M.D., and Martin Schlepper, M.D., Bad Nauheim and Giessen, West Germany

Left ventricular function of the heart that is chronically hypertrophied owing to pressure or volume overload has been investigated intensively.':" However, to what extent depressed left ventricular function recovers after corrective surgery is largely unknown. In addition, little information is available concerning regression of left ventricular hypertrophy after successful aortic valve replacement. The objectives of the present study were to determine the adaptive myocardial changes which occur after aortic valve replacement with Bjork-Shiley tilting disc valve prostheses. Before and after surgery, left ventricular muscle mass (L VMI) was measured to characterize the degree of left ventricular hypertrophy. The peak systolic wall stress (PSWS) was used as a measurement of the appropriateness of adaptive hypertrophy.?: 7 The ejection-phase parameters served as meaFrom the Kerckhoff Clinic, Max Planck Gesellschaft, Bad Nauheim, and from the Department of Cardiovascular Surgery, Justus Liebig University, Giessen, West Germany. Received for publication Aug. 3, 1977. Accepted for publication Oct. 20, 1977. Address for reprints: Professor F. W. Hehrlein, Department of Cardiovascular Surgery, Klinikstr. 29, 6300 Giessen, West Germany.

854

surements of myocardial function, because such indices should reveal intrinsic changes of left ventricular function in hypertrophied hearts.

Methods Patients. Initially, we studied 27 consecutive patients with isolated aortic valve disease before and after they underwent open-heart surgery for aortic valve replacement. The iliac artery was cannulated for total cardiopulmonary bypass, for which a roller pump and a disposable bubble oxygenator were used. The left ventricle was decompressed with a left ventricular vent. Preservation of the myocardium was attained by cardioplegic arrest of the heart." The aortic' valve was replaced with a Bjork-Shiley tilting disc valve prosthesis. Preoperatively, mitral valve disease was excluded in all patients by analysis of the left atrial pressure curve and by an additional angiographic study of the left ventricle when needed. Preoperativly, five patients had predominant aortic stenosis (AS), seven AS plus aortic insufficiency (AS-AI), and II predominant aortic insufficiency (AI). Excluded from the results presented here are four patients who had paravalvular aortic regurgitation after the operation. One of these patients additionally had complete peripheral occlusion of the

0022-5223/78/0675-0854$01.10/0 © 1978 The C. V. Mosby Co.

Volume 75

Myocardial failure after aortic valve replacement

Number 6 June, 1978

855

Table I. Clinical data Pat. No.

Age (yr.)

Aortic stenosis 45 I 2 38 3 31 4 41 46 5 Mean 40.2 ± S.D. 6.1 P Value

Funct. class Sex

b

I

a

RE score

I

b

a

CT ratio

b

I

a

PPSG (mm.Hg) AR angio,

b

I

a

b

I

a

Months after surgery at sec. study

Size of BS prosthesis

6 5 6 8 7 6.4 1.1

25 21 27

I I I I I 2.6 1.0 0.6 0 <0.01

4 0 4 0 0 0 6 I 7 0 4.2* 0.2 2.7 0.5 <0.05

0.41 0.40 0.46 0.44 0.47 0.41 0.47 0.41 0.58 0.49 0.48 0.43 0.06 0.04 <0.05

14 86 80 0 72 12 116 32 120 12 94.8 14.0 11.5 21.8 <0.001

Aortic stenosis plus insufficiency M III I 6 50 III I 7 34 M IV M 1 8 25 III I M 38 9 IV II 37 M 10 1 II 48 M III II 12 40 M III 3.3 1.3 Mean 38.9 0.5 0.5 ± S.D. 8.5 <0.001 P Value

4 0 9 2 9 0 9 0 10 I 7 I 8 2 8.0t 0.9 2.0 0.9 <0.001

0.51 0.47 0.55 0.52 0.57 0.47 0.64 0.42 0.69 0.57 0.48 0.44 0.58 0.45 0.57t 0.48* 0.07 0.05 <0.01

58 16 106 36 80 10 64 8 52 0 76 0 188 28 14.0 89.1 47.1 13.7 <0.01

3 0 3 0 4 0 4 0 5 I 3 0 3 0 3.6 0.1 0.8 0.4 <0.001

5 6 8 5 12 4 5 6.4 2.8

27 23 25 27 27 27 23

24 4 2 0 28 6 0 4 5 0 4 7.0 9.7

5 0 4 0 4 0 3 0 3 0 3 I 4 0 4 0 4 0 4 1 4 0 3.8 0.2 0.6 0.4 <0.001

II

27 29 29

Aortic insufficiency 13 19 14 50 15 63 16 25 17 26 44 18 19 60 20 50 21 41 22 53 23 51 Mean 43.8 ± S.D. 14.6 P Value Control Mean ± S.D.

M M F

M F

M M M M F

M M M M M M

II III II III III

III III III III III III III II III II III

I II II I I I II I I I

I 2.8 1.3 0.4 0.5 <0.001

45 9

5

2

RBBB RBBB

3 1 6 10

0 0 3 3

RBBB

6 4 6

3 1 1 5.1t 1.6* 2.6 1.3 <0.001 0.40 0.50

0.57 0.56 0.53 0.50 0.56 0.56 0.36 0.39 0.49 0.48 0.56 0.49 0.57 0.51 0.52 0.48 0.53 0.47 0.51 0.47 0.56 0.52 0.53t 0.49t 0.05 0.05 <0.001

0 12 0 0 0 0 0 28 0 15 8 5.7 9.3

ns

I

0

0

I

2

0 0 0 0.2 0.5

0 1 0.8 0.8

27

25

ns

5 5 6 7 6 4 II

5 5 5 6.4 2.4

27

25 27 29 25 25 29 27

0.43 0.03

Legend: a, After surgery. AR, Degree of aortic regurgitation as estimated by aortic root angiography (Grade 0-5). b, Before surgery. BS, Bjork-Shiley. cr, Cardiothoracic. F, Female. Funct., Functional. M, Male. ns, Not significant. Pat. No., Patient number. PPSG, Peak-to-peak left ventricular-to-aonic pressure gradient. p Value, When comparing paired data. RBBB, Right bundle branch block. RE, Romhilt-Estes. S.D., Standard deviation. *p < 0.05 when compared to control. tp < 0.0 I when compared to control. tp < 0.00 I when compared to control.

left anterior descending branch and asynergy of the anterior wall. All other patients were free of any signs of perioperative infarctions or other serious complications during the period of observation. Age, sex, functional class (New York Heart Association), electrocardiogram (Romhilt-Estes score"), cardiothoracic ratio, aortic valve pressure gradient, degree of aortic regurgitation, to time after operation at the second study, and size of Bjork-Shiley valve prostheses are listed for each

patient in Table I. Overt cardiac failure (Class IV) was present in two patients of the group with combined aortic valve disease. All other patients were in Functional Class II or III. Seven of these patients had a cardiothoracic ratio below the upper limit of normal. No patient had obstructive coronary artery disease, as established by selective coronary angiography. Control data were obtained from 10 normal subjects investigated for chest pain but found to have normal coronary

The Journalof Thoracic and Cardiovascular Surgery

856 Schwarz et at.

Table II. Hemodynamic data at rest

Pat. No.

(HR) (b.p.m.) b

I

Aortic stenosis I 72 2 86 3 51 4 86 5 92 Mean 77.4 ± S.D. 16.5

a

b

83 81 78 86 92 84.0 5.3

184 208 192 200 232

ns

P Value

LVSP (mm. Hg)

I

a

126 140 124 152 148 203.2t 138.0 18.4 12.7 <0.01

Aortic stenosis plus insufficiency 208 136 6 75 77 7 204 156 77 77 168 148 8 88 75 168 98 92 136 9 172 155 10 97 79 140 11 86 160 66 74 296 148 12 75 Mean 82.1 80.1 196.6* 145.6t 47.7 8.4 ±S.D. 12.3 6.4 <0.05 ns P Value Aortic insufficiency 13 67 86 14 67 80 15 83 90 16 77 75 17 113 110 18 65 67 19 75 67 20 70 75 21 86 71 22 75 80 23 92 100 Mean 79. I 81.9 ±S.D. 14.1 13.7 P Value

146 160 160 120 152 128 155 160 160 175 160

136 152 184 120 168 120 152 148 160 140 144 147.6t 19.1

152.4t

15.8

AOSP (mm. Hg) b

98 128 120 84 112 108.4 17.6

a

150 98 88 104 120 84 108 107.4 22.4

ns

I

a

b

I

MLAP (mm. Hg)

a

b

20 18 7 14 13 14.4 5.0

14 16 9 4 8 10.2 4.8

28 25 17 8 9 17.4 9.1

120 120 138 128 155 140 120 131.6 13.4

72 76 52 80 56 81 64 80 72 80 52 76 60 60 61. 1* 76.1 8.6 7.4 <0.05

32 22 32 41 28 32 33

112 148 182 120 140 114 152 144 155 140 140 140.6* 20.2

60 80 50 76 62 100 68 68 68 88 52 72 60 76 52 92 72 83 80 84 72 72 63.3 81.0 9.6 9.6 <0.01

6 14 15 10 15 II 20 8 9 14 40 9 25 12 19 16 15 8 10 10 18.4* 10.7 8.9 3.0 <0.05

71.8 10.8

11.2 3.7

ns

146 148 160 120 152 128 155 132 160 160 152 146.6t 13.9

b

LVEDP (mm. Hg)

60 68 72 80 52 70 56 72 70 72 62.0 72.4 4.6 8.7 <0.05

112 140 112 120 136 124.0 13.3 ns

ns

ns

I

AODP (mm. Hg)

I

a

6 5 5 10 7 6.6 2.1

EDVI (ml/sq. M.) b

I

I

a

ns

ns

ns

11 12 9 9 20 14 14 31.4t 12.7 5.7 3.8 <0.001

12 6 15 19 7 30 5 38 22 15 15 17 25 7 23.3t 10.0 4.7 8.7 <0.05

130.8 108.6 161.2 98.4 203.0 68.2 211.6 61.1 228.0 135.8 131.7 77.2 130.2 74.6 170.9t 89.1 42.5 26.5 <0.01

175 132 202 153 228 105 122 277 250 146 77 157 217 125 215.lt 122.9t 41.6 25.7 <0.001

229.1 146.7 168.0 139.7 169.4 170.0 165.9 147.8 173.2 102.4 118.1

216 131 166 225 121 158 158 123 91 105 161 116 208 132 215 127 169 128 162 125 161 107 176.3t 124.3:1: 18.3 36.1 <0.001

II

II

5 10 4 8 5 5 6 13 14 7

9 12.7 6.5

7.7 3.5

14 9 10 9 8 30 12 15

ns

64.7 105.3 60.6 52.3 63.2 69.2 20.7

b

119 69 118 155 93 66 157 105 184 95 141.6t 90.6 22.6 35.7 <0.01

23

72.4 99.0 93.9 66.0 75.0 81.3 14.4

a

LVMI (Gm./sq. M.)

72.9 132.3 91.3 90.0 71.8 126.8 102.7 74.3 74.8 70.8 78.7 157.3t 89.7 3.1 22.1 <0.001

Controls Mean

±S.D.

75.4 11.4

123.2 14.6

123.2 14.6

8.8 3.3

76.7 20.9

72.6 14.2

Legend: a, After surgery. AODP, Diastolic aortic pressure. A?SP, Systolic aortic pressure. b, Before surgery. VCF, Mean circumferential fiber shortening rate.

EDVI, End-diastolic volume, EF, Ejection fraction. HR, Heart rate. L VEDP, Left ventricular end-diastolic pressure. L VMI, Left ventricular muscle mass. LVSP, Left ventricular systolic pressure. MNSER, Mean normalized systolic ejection rate. MLAP, Mean left atrial pressure. Ns, Not significant. Pat. No., Patient number. p Value, When comparing paired data. PSWS, Peak systolic wall stress. S.D., Standard deviation. *p < 0.05 when compared to control. tp < 0.0 I when compared to control. tp < 0.00 I when compared to controls.

arteries on angiography and no evidence of valvular or myocardial heart disease. Procedures. Diagnostic cardiac catheterization studies were performed in all patients. No premedication was used. All patients with aortic valve disease received digoxin before and after the operation. Catheters were positioned in the left ventricle transeptally (No. 8.5 Fr. Brockenbrough catheter) via femoral vein

puncture and in the ascending aorta retrogradely via femoral artery puncture. Pressures were recorded on an oscillomink direct-writing system with P23db Statham transducers before injection of contrast material. Preoperative and postoperative studies were performed with the same equipment and catheter manometer systems. These systems have uniform amplitude response to 15 to 20 Hz with resonant frequencies of more than

Volume 75

Myocardial failure after aortic valve replacement

Number 6 June. 1978

PSWS (dynes . I03/sq. em.)

b

I

a

EF

VCF (cire.lsee.)

(%)

b

I

a

b

Ia

MNSER (vol./see.)

b

I

a

313 269 59 71 363 301 57 61 405 84 273 71 254 212 60 66 300 244 56 79 327.0 259.8 63.2 69.5 33.5 . 11.7 58.4 6.7 <0.05 ns

0.91 1.64 0.78 1.07 1.17 1.30 1.06 1.33 0.94 1.70 0.97t 1.41 0.15 0.26 <0.05

1.82 2.84 1.58 2.03 1.91 2.37 1.94 2.44 1.87 2.93 1.82t 2.52 0.14 0.37 <0.01

400 271 437 268 417 252 350 194 431 349 327 339 506 206 409.7t 268.4 59.2 59.4 <0.01

65 72 53 68 22 68 36 70 21 60 56 60 42 88 42.lt 69.4 16.9 9.4 <0.01

1.36 1.72 0.76 1.28 0.30 1.30 0.67 1.67 0.24 1.14 0.81 1.07 0.53 2.21 0.67t 1.48 0.38 0.40 <0.01

2.32 2.88 1.51 2.23 0.87 2.19 1.33 2.92 0.70 2.13 2.14 1.56 3.14 1.24 1.36t 2.52 0.53 0.44 <0.01

361 210 265 281 397 358 274 242 535 330 300 276 300 296 267 235 412 259 271 208 335 265 337.9 269.1 83.8 46.7 <0.01

63 68 52 63 42 55 54 56 57 64 61 72 38 58 73 66 40 57 72 69 41 57 53.9t 62.3* 12.6 6.0 <0.01

0.99 1.44 1.03 1.13 0.76 1.16 0.76 0.88 1.04 1.13 1.23 1.49 0,42 1.00 1.26 1.16 0.60 1.13 1.28 1.49 0.52 1.15 0.90t 1.20 0.31 0.20 <0.01

1.85 2.52 1.93 2.17 1.56 2.08 1.59 1.87 2.04 2.29 2.26 2.67 1.15 2.00 2.15 2.06 1.25 1.84 2.08 2.52 1.28 2.19 1.74t 2.20 0.39 0.27 <0.001

293.0 59.2

68.7 6.9

1.31 0.19

2.36 0.28

50 Hz. Left ventricular end-diastolic pressure (LVEDP) was measured following the A wave. Single-plane 35 mm. cineangiograms of the left ventricle were filmed at 48 frames per second in the 30 degree right anterior oblique (RAO) projection after 50 ml. of Urografin 76 had been injected (Brockenbrough catheter). During left ventricular injection through the Brockenbrough catheter placed across the mitral valve, no mitral regurgitation was seen in normally conducted beats. Simultaneously, the electrocardiogram and the aortic pressure pulse were recorded at a paper speed of 100 mm. per second. In all patients, aortic root angiograms were performed to estimate the degree of aortic

857

regurgitation.!" Thereafter, coronary angiography was carried out by the Judkins technique. In six patients with aortic valve disease and in the control subjects, a stress angiogram was carried out after waiting a period of 25 minutes.!' Isoproterenol, 0.3 /Lg per kilogram of body weight per minute, was infused via antecubital vein. During the infusion period, left ventricular systolic pressure (LVSP), LVEDP, and aortic pressure were recorded continuously. When pressures and heart rate had stabilized, the Brockenbrough catheter was withdrawn from the left ventricle into the left atrium, and left ventricular angiography was repeated by left atrial injection. Calculations. Left ventricular volumes were determined via the area-length method'P by use of the largest and smallest angiographic silhouettes. Correction factors for magnification and pincushion distortion were obtained from a grid filmed in the plane occupied by the left ventricle;" The earliest well-opacified cardiac cycle following injection was chosen for analysis. Premature ventricular contractions and post-extrasystolic beats were not analyzed. In the preoperative and postoperative angiographic studies, heart rates were compared and found to be not significantly different (Table II). The long axis (L) was measured and the minor equator (M) was calculated. Calculated volumes (V e) were corrected to true volumes (VJ according to the formula of Kasser and Kennedy": VI = V c x 0.788

+ 8.4 mI.

Using this formula, we found a close agreement of stroke volumes (SV) determined simultaneously by angiography and by the thermodilution technique':' in 15 patients without heart disease: SV angio. = 44.8 ± 10.9 (S.D.) ml./sq. M.

and SV thermo. = 45.4 ± 10.9 (S.D.) ml./sq. M.

Paired analysis revealed no significant difference between the two methods (p > 0.05). Our values for angiographically determined stroke volume are similar to those of others. 15. 16 The ejection fraction (EF) was determined thus: SV EF = EDV x 100%

where SV = stroke volume and EDV = end-diastolic volume. The mean circumferential fiber shortening rate (VCP) was calculated by the equation: VCF =

where M D

MD - M s

MD

= diastolic

..

.

x ejection time

minor equator and M,

= sys-

The Journal of Thoracic and Cardiovascular Surgery

858 Schwarz et at.

LVMI

A.

EF MNSER aortic stenosis

__-"",,-_

':.;......

:I

""~" ....~:. :. .: .: ~: ~)

<

ns

.01

EF • 22 MNSER '0.87

<.01

aortic stenosis + insufficiency 80

3

•

60

•

t ~." <.001

<.01

<.01

80

t·7 ~: t.~. ~.~ 60

200

100

•

f

2

--------<.001

b

Fig. 2. End-diastolic (interrupted lines) and end-systolic silhouettes (dotted lines) of Patient 8. Cardiac function (EF and MNSER) was severely depressed before surgery (A) and recovered to normal levels after aortic valve replacement (B). Wall thickness is indicated by the shaded area. EF, Ejection fraction (percent). MNSER, Mean normalized systolic ejection rate (end-diastolic volume per second).

V M = (V c+

w -

V') 1.05, _4 M h2 V c+w-"j1T(2"+ )

1

20 < .01

a

EF -68 MNSER-2.19

allows an accurate measurement of wall thickness, because there is an excellent correlation between measurements from frontal and RAO projections." Furthermore, the left coronary angiogram was made in the same RAO projection, and the anatomic localization of the left anterior descending coronary artery allowed the exclusion of overlap of the right ventricle. Left ventricular muscle mass (LVMI) was determined according to the method of Rackley and associates" by the equation:

aortic insufficiency 300

: r

b

< .001

a

b

a

Fig. 1. Hemodynamic data before (b) and after (a) aortic valve replacement in patients with aortic stenosis (upper panel), patients with aortic stenosis plus insufficiency (middle panel) and patients with aortic insufficiency (lower panel). Changes in left ventricular mass index (LVMI-grams per square meter), ejection fraction (EF-percent) and mean normalized systolic ejection rate (MNSER-end-diastolic volume per second) are shown. Normal range (mean value ± 2 standard deviations) is indicated by vertical lines. Closed circles = mean values.

tolic minor equator. The mean normalized systolic ejection rate (MNSER) was calculated by division of the ejection fraction by the ejection time (in milliseconds) as measured from the aortic pressure signal. Thickness of the left ventricular free wall at end diastole was measured in the RAO projection. This method

L h (2"+ )

where V M = left ventricular mass, Vc + w = volume on left ventricular chamber plus wall, V' = volume of chamber only, h = left ventricular wall thickness at end diastole, M = minor equator, L = long axis, and 1.05 = specific gravity of myocardium. We used the modified equation introduced by Trenouth and associates." These authors assumed that the wall thickness (h) at the apex and at the base is one half that of the free wall where it is measured on the angiogram. They proposed:

Vc+w=~1T(M+W(~+~) 3

2

2

2

For comparison between groups, EDV and left ventricular mass were normalized by dividing by body surface area. Circumferential (equatorial) wall stress was calculated by the formula of Falsetti and associates": Wall stress

=

PM (2L2 - M2) (L2 + Mh)

4h

Volume 75

Myocardial failure after aortic valve replacement

Number 6 June, 1978

LVSP 200

AS 100

200

AS

+

A 1 100

200

AI 100

LVEOP

M LAP

859

E OVI

..

.. ..

40

• <.05

•• <.01 ••• <.001

200

D •

before after SURGERY

Fig. 3. Mean values of left ventricular systolic pressure (LVSP-miIIimeters of mercury), left ventricular end-diastolic pressure (LVEDP-miIIimeters of mercury), mean left atrial pressure (MLAP-miIIimeters of mercury) and end-diastolic volume (EDVI-miIIiliters per square meter) before and after aortic valve replacement. Average normal values are shown by closed squares. Data are depicted for aortic stenosis (upper panel), aortic stenosis plus insufficiency (middle panel), and aortic insufficiency (lower panel).

We used the method of Gaasch and associates'" to calculate peak systolic wall stress (PSWS), despite some controversy in the literature'?' 21 regarding the calculation ofPSWS. This method contains three assumptions: ( I) that peak wall stress occurs at approximately the same time as maximum left ventricular pressure, (2) that about one third of the stroke volume has been ejected at this point, and (3) that the change in eccentricity (LIM) with respect to the change in volume is linear. End-systolic wall thickness was calculated from end-systolic volume and left ventricular mass. Thickness at PSWS was determined by assuming a linear change of wall thickness throughout ejection as proposed by Gault and associates." According to Gaasch and colleagues," left ventricular end-diastolic dimensions and wall thickness are combined as Xed, then

2 Xed = M .o:(2:..:L:--2_----'-M.::...<... ) 2 4h (L + Mh) where M, L, and h are measured at end diastole. Accordingly Xes can be defined. PSWS then can be calculated as p 2Xed + Xes 3 where P = LVSP (l03dynes/sq. em.). We compared the PSWS values calculated by the method of Gaasch and associates" to the maximal wall stresses (max.WS) calculated by frame-by-frame analysis" in 12 patients with aortic valve disease, and we found no significant difference (p > 0.05) using both methods (PSWS = 427 ± 78 and max.WS = 416 ± 75 dynes 103/sq.

The Journalof Thoracic and Cardiovascular Surgery

860 Schwarz et al.

A.

/'

CONTROL

_

//

before surgery

<. -,

,:

"

""\

EF.~~""---,

:

MNSER·1.56 '----

after surgery

c. (:::::":,,\ -,

", .......

EFs 6 0

•••••••

.

MNSER·214 '---

~ ';

1

...=

:

j

Fig. 4. End-diastolic (interrupted lines) andend-systolic (dotted lines) silhouettes of Patient II, who had predominant

aortic stenosis, before surgery at rest (A) and during isoproterenol (ISO) infusion (B) as well as after surgery at rest (e) and during isoproterenol infusion (D). Improvement of cardiac reserve is evident between. D and B. EF, Ejection fraction (percent). MNSER, Mean normalized systolic ejection rate (end-diastolic volume per second).

cm.). Linear regression analysis demonstrated a close correlation: max.WS = 23.6 ± 0.92 PSWS, r = 0.951, S.E.M. = 7.3. Results Functional class (N.Y.H.A.), Romhilt-Estes score, and cardiothoracic ratio had improved significantly 6 months after aortic valve replacement (Table I). However, several patients with AS-AI (Nos. 10 and 12) and with AI (Nos. 14, 15 and 19, Table I) complained still of dyspnea during stress after the operation; one of them (No. 15) had an unimproved cardiothoracic ratio. In patients with AI an abnormal Romhilt-Estes score (p < 0.05) was seen after the operation. In patients with AS-AI the cardiothoracic ratio remained elevated (0.48 as compared to 0.43 in control subjects, p < 0.05). This was also true in patients with AI (0.49, P < 0.01). Residual aortic valve pressure gradients after surgery were between zero and 36 mm. Hg (Table I). The effect of valve replacement on LVMI, ejection fraction, and mean normalized systolic ejection rate (MNSER) in patients with AS and patients with AS-AI is shown in Fig. I. In patients with AS, L VMI decreased (p < 0.01), ejection fraction remained unchanged (p > 0.05), and MNSER increased (p < 0.01). In patients with AS-AI, the decrease of L VMI was even more pronounced (p < 0.001), and the depressed ejection fraction and MNSER increased (p < 0.01) to normal levels (Table II).

Fig. I shows L VMI, ejection fraction, and MNSER in patients with AI; all of these variables improved significantly. As listed in Table II, LVMI returned to normal in patients with AS only, but not in patients with AS-AI (p < 0.01) or those with AI (p < 0.001). Ejection fraction in AI remained slightly depressed after the operation (p < 0.05), but VCF and MNSER did not (p > 0.05). PSWS before surgery was normal in patients with AS (p > 0.05) and those with AI (p > 0.05) but was elevated in those with AS-AI (p < 0.01). It decreased in all groups (p < 0.05, P < 0.01) to normal range (p > 0.05, if compared to control values). Fig. 2 represents the ventriculographic outlines of Case 8. Before the operation (A), cardiac function as estimated by ejection fraction and MNSER was drastically depressed and the degree of hypertrophy was excessive (228 grams per square meter). Eight months after the operation (B), cardiac function was normal and LVMI was drastically reduced (105 grams per square meter). All individual data including LVSP, aortic pressure (systolic/diastolic), and heart rate are listed in Table II. Fig. 3 compares the average values of LVSP, L VEDP, mean left atrial pressure, and EDVI before and after valve replacement. The L VSP decreased in patients with AS (p < 0.001) and AS-AI (p < 0.05) but remained unchanged in those with AI (p > 0.05). After the operation L VSP was still elevated in patients with AS-AI (p < 0.01) and in those with AI (p < 0.01). The LVEDP, which was elevated in patients with AS-AI and AI, decreased significantly (AS-AI: p < 0.001, AI: p < 0.05) and reached normal range. The mean left atrial pressure was significantly elevated in patients with AS-AI (p < 0.01) before the operation and decreased after valve replacement (p < 0.05) to normal range. EDVI was elevated in those with AS-AI and in those with AI (both P < 0.00 I, if compared to control values); it decreased after valve replacement (AS-AI: p < 0.01, AI: p < 0.001) and thus became normal (p > 0.05 if compared to control values). In six patients with predominant AS (three with additional AI), a stress ventriculogram was obtained before and after the operation. Fig. 4 shows the ventriculographic outlines of Case II before surgery at rest (A) and during isoproterenol infusion (B) and after surgery at rest (C) and during isoproterenol infusion (D). After valve replacement, most marked improvement is demonstrated when silhouettes obtained during isoproterenol infusion are compared (B and D). Fig. 5 shows individual ejection fraction and MNSER values of control subjects as compared to

Volume 75

Myocardial failure after aortic valve replacement

Number 6 June. 1978

REST 80

.

t

*u..W

60

r.

• --iL

.

•

De

ISO

...

T

0

e

861

i 0

T

•

-.L

•

----0-

•

40

•

2 P<·Ol

!

o >

ns

p<.05

..

4

~

i

a: W

en

Z :;E

3

~

•

. .... ..

fil

•

~

2

ns

+

•

• ns

B

A

. 0

•

= controls = AS = AS+AI

0

~

•

0

P< .01

-i-

• p<.Ol

B B

<.05

A

= before

A = after

Fig. 5. Ejection fraction (EF) and mean normalized systolic ejection rate (MNSER) of six patients with predominant aortic stenosis before (B) and after (A) surgery are compared to controls. Data were obtained at rest (REST) and during isoproterenol infusion (ISO). Valve replacement restored function at rest as well as cardiac reserve.

those of patients with AS before and after surgery. The data points during isoproterenol infusion (right panels) show a clearer differentiation between control subjects and patients with AS before surgery without the overlap which exists at rest (left panels). Furthermore, the improvement of cardiac performance during isoproterenol infusion (right panels) signifies recovery of cardiac reserve. Heart rate, L VSP, L VEDP, aortic pressure (systolic/diastolic), mean left atrial pressure, EDVI, PSWS, and ejection-phase parameters during infusion of isoproterenol are listed in Table III. Discussion Critique of methods. To calculate PSWS, we followed the method of Gaasch and colleagues." It is clear that PSWS and maximum left ventricular pressure

do not occur exactly at the same time in each patient; it was shown by Gault and colleagues" that in normal subjects PSWS may occur soon after the onset of ejection, whereas in patients with left ventricular disease PSWS is sustained at a relatively high level throughout most of systole. However, we found a close correlation between PSWS values determined according to the method of Gaasch and colleagues'" and PSWS values determined by frame-by-frame analysis. Furthermore, our values in normal subjects are similar to those reported by others.": 22-24 To assess cardiac function in normal and hypertrophied hearts, we used the ejection-phase indices which express function per unit of muscle." Furthermore, the ejection fraction has been shown to have prognostic significance in the surgical treatment of valvular heart disease;" The peak circum-

The Journal of

862 Schwarz et al.

Thoracic and Cardiovascular Surgery

Table III. Hemodynamic data during isoproterenol infusion

Pat. No. Aortic stenosis I 4 5 6 7 11 Mean ± S.D.

b

± S.D.

I

a 116 158 150 133 150 143 142 15

125 130 135 108 140 150 131 14

P Value

Control Mean

LVEDP (mm. Hg)

HR (b.p.m.)

ns 137.3 11.7

b

I

AOSP (mm. Hg) a

b

I

AODP (mm. Hg) a

b

240 152 312 180 320 180 188 168 216 192 184 160 260t 172t 15 55 <0.01

120 72 88 128 96 128 136 120 140 105 128 80 127 96t 23 7 <0.05

48 60 68 64 52 48 57t 9

130.8 14.9

130.8 14.9

72.7 8.2

I

LVEDP (mm. Hg)

a

b

56 68 60 64 64 60 62t 4

33 8 10 10 14 10 14 9

ns

I

MLAP (mm. Hg)

a

b

22 10 16 4 24 6 14 8

16 9 3 15 28 10 14* 9

ns 6.5 2.8

I

EDVI (ml/sq. M.)

a

b

13 4 14 4 18 5 10 6

50.7 65.9 71.3 153.3 143.1 92.9 96.2 42.6

ns 4.2 1.3

I

a 78.5 47.7 59.3 63.9 93.7 63.7 67.8 16.1

ns 63.8 16.9

For legend see Table II. *p < 0.05 whencompared to control. tp < 0.01 when compared to control. tp < 0.001 when compared to control.

ferential (equatorial) wall stress representing the relation between hemodynamic burden and adaptive hypertrophy was normal in patients with AS and AI but elevated in patients with AS-AI before the operation. Hood and associates? found a normal PSWS in patients with compensated volume overload, but an increased PSWS in those with decompensated volume and in those with mixed pressure and volume overload. Gould and co-workers'" described a significantly increased PSWS in patients with severe AI. Grossman and colleagues;" on the other hand, found no significant difference between PSWS in control subjects and in patients with volume and pressure overload. Results of aortic valve replacement. The most important finding of our study is that severe myocardial failure (i.e., low ejection fraction and high wall stress) with congestive symptoms (i.e., high mean left atrial pressure) normalizes completely within 6 months after operation. To our knowledge, improvement of cardiac function after aortic valve replacement was shown only by indirect methods such as heart size determination, pulmonary artery pressure measurements, echocardiography, and clinical status of the patients.">" In this study containing a large consecutive series of patients, recovery from myocardial failure and restoration of cardiac reserve after aortic valve replacement were shown by direct measurements of myocardial contractile behavior. Several patients, however, although exhibiting a considerable degree of hypertrophy, had only minimal depression of left ventricular function be-

fore the operation; this condition probably represented a stage of still-compensated hypertrophy. In addition, these patients had an almost normal cardiothoracic ratio before the operation and were only in Class II or III. Proper timing of valve replacement is a major problem in aortic valve disease. The exact point at which cardiac dysfunction is associated with irreversible tissue damage is still unknown." In this respect, we believe that surgery should be performed before the clinical symptoms and cardiothoracic ratio begin to deteriorate considerably. We feel that the postoperative improvement of cardiothoracic ratio and of ejection-phase parameters in patients with values in the upper limits of normal implies beginning deterioration of left ventricular function preoperatively and thus justifies our decision of operative treatment. In contrast, in most patients with AS-AI, a severe impairment of myocardial function is indicated by increased mean left atrial pressure and severe depression of ejection-phase parameters. This myocardial failure may be explained at least partially by the degenerative structural changes of the myocardium which have been described in severe chronic left ventricular hypertrophy.F" 34 Kennedy and co-workers 35 reported a reduction of EDVI and left ventricular mass after homograft aortic valve replacement, without any change of the preoperative normal ejection fraction. Gault and colleagues" found no change of VCF but a decrease of PSWS after aortic valve replacement with Starr-Edwards prostheses in four patients who had aortic regurgitation and depressed myocardial contrac-

Volume 75

Myocardial failure after aortic valve replacement

Number 6 June, 1978

PSWS (dynes I03/sq. em.)

b

276 393 371 567 428 323 393* 101

253.1 52.5

I

ns

a

336 214 276 218 306 314 277' 51

EF

VCF (cire./see.)

(%)

b

I

a

b

I

a

MNSER (vol./see.)

b

I

a

78 85 61 84 71 83 77 81 47 74 37 75 62* 80 17 5 <0.05

1.77 2.12 1.52 2.36 1.60 2.59 1.90 2.60 1.15 2.05 0.78 2.42 1.45t 2.36 0.42 0.23 <0.01

2.89 3.38 2.90 3.82 2.84 3.62 3.35 4.05 2.35 3.52 1.68 3.94 2.67t 3.72t 0.58 0.26 <0.01

80.6 3.7

2.45 0.18

4.03 0.19

tility. The discrepancy between the latter observations and our results may be partially related to the fact that Bjork-Shiley valves produce lower pressure gradients (fewer outflow tract obstructions) than Starr-Edwards prostheses.:" Nevertheless, three of our patients (Nos. 4, 7, and 12, Table I) had notable pressure gradients after Bjork-Shiley valve implantation, especially those in whom small sizes of disc prostheses were used. The pressure difference at rest over Model A 23 BjorkShiley aortic prostheses was 12 mm. Hg in a series of 90 cases reported by Bjork and associates." With increasing flow, the pressure gradient increased to more than 30 mm. Hg. An important influence of time after surgery on recovery of myocardial function in AI has been described.P In our patients this time factor was not recognizable, because all patients were studied within 12 months after operation. Recatheterization after several years may reveal different results, since deterioration has been known to recur after a phase of improved cardiac function following successful aortic valve replacement. 29 Normal cardiac function after aortic valve replacement with Starr-Edwards prostheses was found by Hultgren and associates;" who reported the greatest decrease of heart size in patients with heart failure prior to surgery. Moderate abnormalities during exercise were described after aortic valve replacement with Cutter-Smeloff prostheses." Isoproterenol, a beta stimulating drug which has been widely used in the evaluation of patients with valvular stenosis.P" 40 produced a depression of cardiac reserve in six patients with predominant AS; this reserve was restored after surgery. The improvement was most impressive in Cases 7 and 11, as demonstrated in

863

Figs. 4 and 5. From the study of Bolen and colleagues," we have learned that evaluation of ventriculograms during stress often is more useful than evaluation at rest for detecting impaired function in aortic valve disease. Our results seem to confirm this statement. REFERENCES

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3

4

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6 7

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12

13

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15

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