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The direct brachial arterial pulse-pressure curve in the evaluation of patients with aortic valvular stenosis
Clinic al communications
The direct
brachial
pulse-pressure of patients
arterial
curve with
in the evaluation
aortic
valvular
stenosis
Abner J. Delman, M.D.* Garet M. Gordon, M.D.** Robert Eisenberg, M.D.*** Doris J. W. Escher, M.D.**** Robert Rosenblum, M.D.***** New York, N. Y.
T
he relationship of the central and peripheral pulse-pressure curves in normal man, in patients with aortic stenosis, and in experimentally produced aortic stenosis has been discussed in the literature.‘e4 However, there has not been a consistent opinion concerning the diagnostic value of the brachial arterial pulsepressure curves in patients with aortic stenosis,5-‘2 despite the fact that in this condition, in contradistinction to the normal state, the direct brachial arterial pressure curve resembles the central arterial pulse contours. 13-15 Since the techniques of left heart catheterization for quantitatively evaluating the gradient across the aortic valve are not without complications,‘6-18 it was thought that an attempt should be made to determine the value of these brachial arterial tracings as a screening test for the presence of aortic stenosis. From
Material
and
methods
The brachial arterial pulse-pressure curves of 80 patients (age range of 2 to 64 years) were recorded and analyzed. These were divided into five groups on the bases of underlying cardiac states, as follows : 1. Severe aortic valvulur stenosis (24 patients-18 acquired and 6 congenital). Those patients with a normal cardiac index (C. I.) with a peak-to-peak or mean systolic gradient of over 50 mm. Hg, or with a decreased cardiac index with a valve area calculated, by the method of Gorlin and Gorlin,lg to be less than 0.75 cm.2. 2. Mild aortic valvulur stenosis (16 patients-9 acquired and 7 congenital). Those patients with gradients less than 50 mm. Hg across the valve with a normal cardiac index, or with a decreased cardiac
the Cardiac Catheterization Laboratory and the Cardiology Service, Medical Division. Mont&ore Hospital, New York, N. Y. Received for publication June 11, 1964. *Adjunct Attending Physician, Cardiology Service, Medical Division, Montefiore Hospital. Address: Montefiore Hospital, 210th St. and Bainbridge Ave., New York, N. Y.. 10067. QNew York Heart Association Trainee 1961-1962. Presently, Assistant Attending Physician. Medical Division, Montefiore Hospital. ***Associate Attending Physician, Pediatric Division, and Research Associate in Pediatric Cardiology, Cardiology Service, Mont&ore Hospital; Assistant Professor of Clinical Pediatrics, Albert Einstein College of Medicine. “***Associate Attending Physician. Cardiology Service, Medical Division, and Physician-in-Charge, Cardiac Catheterization Laboratory. Montefiore Hospital; Lecturer in Medicine, Columbia University. *****Adjunct Attending Physician, Cardiology Service, Medical Division. and Research Associate, Mont&ore Hospital: Teaching Assistant, New York University School of Medicine.
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Volume Number
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Direct BA pulse-pressure curve in evaluation of aortic stenosis
index and a valve area calculated to be greater than 0.75 cm.2. This criterion for valve area in both mild and severe stenosis related only to patients over 16 years of age. 3. Mitral stenosis--normal C. I. (7 patients). Those patients with a cardiac index in the range of 2.8 to 3.6 L./min./M.2 and no evidence of aortic stenosis. 4. Mitral stenosis--low C. I. (11 patients). Those patients with a cardiac index of less than 2.8 L./min./M.2 with no evidence of aortic stenosis. 5. No heart disease (22 patients). Hospitalized patients without clinical evidence of heart disease who were comparable in age to the patients in Groups l-4. Patients with aortic stenosis with significant mitral insufficiency were not included in the study because mitral insufficiency itself will shorten the systolic ejection time.20s21Patients with aortic stenosis and hemodynamically significant aortic insufficiency were also excluded. Significant aortic and mitral insufficiency were determined by accepted clinical, hemodynamic, and angiocardiographic criteria. All of the patients in Groups l-4 and 8 of the patients in Group 5 had concurrently performed right and left heart catheterizations. Gradients across the mitral valve were obtained by the analysis of simultaneous pulmonary artery wedge or direct left atria1 and left ventricular pressures. The direct left atria1 measurements were obtained by the transseptal technique. 22 The left ventricular pressure was obtained either by the retrograde Seldinger method23 using a femoral artery, or by direct percutaneous left ventricular puncture.24 Mean and peak-to-peak systolic gradients across the aortic valve were obtained from the simultaneous left ventricular and brachial arterial pressures. Cardiac output was measured by the direct Fick principle, with analyses of the respiratory gases by the method of Scholander,25 and the blood gasesby the method of Van Slyke and Nei11.26The brachial arterial pulsepressure tracings were recorded with a Cournand needle placed in the right or left brachial artery. All measurements of pressure were recorded on the Electronics for Medicine multichannel recorder using Statham gauge transducers.
583
The following information was obtained from the brachial arterial tracings: (1) the time, in seconds, from the initial rise to the maximum systolic pressure (upstroke time); (2) the rate of rise in the initial slope of the brachial curves, in millimeters of mercury per second (the upstroke velocity); and (3) the time, in seconds, from the initial rise in the brachial arterial pressure curve to the dicrotic notch (systolic ejection time). Results
The data from each group of patients is tabulated in Tables I and II.
Brachial
arterial
upstroke time (Fig. 1).
In the 22 patients without heart disease the brachial arterial upstroke time varied from 0.06 to 0.19 second, with a mean of 0.11 second. Only one patient had an upstroke time greater than 0.14 second. In 23 of the 24 patients with severe aortic stenosis (4 with coexistent mitral stenosis) the upstroke time was equal to or greater than 0.18 second, with a range of 0.18 to 0.30 second. One patient with severe aortic stenosisand mitral stenosis had an upstroke time of lessthan 0.18 second. The mean for the 24 patients was 0.22 second. An upstroke time equal to or greater than 0.18 second was also noted in 8 of the 9 patients with mild acquired aortic stenosis, with a range of 0.18 to 0.25 second. One patient had an upstroke time of 0.11 second. The mean for the 9 patients was 0.19 second. Six of the 7 patients with mild congenital aortic stenosis had upstroke times of less than 0.18 second, with a range of 0.10 to 0.12 second. The seventh patient had an upstroke time of 0.20 second. The mean for the 7 patients was 0.13 second. In the 7 patients with isolated mitral stenosis and normal cardiac indices the upstroke time was 0.075 to 0.18 second, with a mean of 0.12 second. In the 11 patients with isolated mitral stenosis and reduced cardiac indices, the upstroke time was 0.07 to 0.16 second, with a mean of 0.11 second. A reduced cardiac index did not prolong the upstroke time in any group of patients. Brachial upstroke velocity (Fig. 2). The 22 patients without heart disease had a mean upstroke velocity of 999 mm. Hg per second, with a range of 595 to 1,710 mm. Hg per second. In the patients with
Xld
yi? R.D.
Aortic I.M. N.H. T.D. CR. R.A. G.B.
Severe i\ortic R.L. R.S. J.U. G.G. L.D. L.W.
S.S.’ F.B. E.D. A.L. IS.
Severe Aortic L.M. R.P.* N.M. A.E.* M.S.* L.D. W.N. L.C. AC.* P.F. A.E. ;“A
Patient
Table I
i
I
CO (L./min.)
50 54 53 5.5 50
2.6 2.44
4.9 3.9
M, 49 42 F, 57
Stenosis-Acquired F, 54 M, 43 M, 30 F, 37 M, 37 F, 41
1.5 4.2 2.5
1.63 1.44
2.33 2.89 1.39 2.40 2.80
2.3 3.8
I
(L./m&. /M .“)
ICI
3.8 5.4
2.82 2.9 2.78
2.93 1.88
4.40 2.70
5.52 5.8 5.50
2.29 3.47 2.31
4.25 6.76 4.02
Stenosis-Congenital M, 8 M, 2 M, 50 M, 15 F, 34 M, 10
M, M, F, *al, F,
Stenosis-Acquired M, 62 4.05 F, 64 4.34 M, 51 2.60 M, 50 4.38 M, 50 5.13 M, 44 M 55 2.60 M: 36 2.53 M, 51 M, 49 M, 37 2.68 M, M, 4.5 54 5.95 5.4
Srx, .4ge Cur.1
Mean
24 19 47 42 30
10 1.5
54 4.5
E 56 59 40 56 78 64 32 75 62 40 58
40 58
gradient (mm. Hg)
10 22 2.5 16 32 20 40 45 3.5
73 120 86 135 108(OR) 150
40 87 73 97 58 88 65 85 83 65 36 80 6.5 42 70 94 50 40
Peak gradient (mm. Hg) ffd
170/15 177/17 165/15 100/13 134/10 143/12 164/10 150/10 130/8
240/13
150/13 180/4 201/42 230/16
136/18 230/Z 1 150/32 228/28 182/9 189/42 155/4 181/22 225/16 205/13 136/18 180/13 192/17 162/35 190/15 230/15 180/12 180/10
(mm.
160/80 155/Z 140/80 84/40 102/58 123/74 124/75 105/60 95/50
77/57 60/48 115/60 95172 120/80 91/61
96/66 143/83 77/57 131/85 120/66 101/59 90/44 96/70 142/85 141/88 100/64 100/60 127/62 120/81 120/60 126/78 130/64 140/70
p ressure BA (mm. Hd
0 0 0 0 10 0 0 0 10
0 0 0 0 0 0
0 0 0 0 8.2 0 10E.D. 0 0 0 8.2 0 0 1.5 0 0 0 1.5
Mitral? gradient (mm. Hg)
0.38 0.29 0.38 0.28 0.37 0.25 0.30 0.38 0.32
0.27 0.29 0.35 0.33 0.35 0.30
0.37 0.40 0.29 0.43 0.34 0.47 0.36 0.31 0.34 0.33 0.38 0.35 0.38 0.28 0.47 0.37 0.32 0.32
Ejection time (sec.)
0.93 0.78 0.76 0.90 0.71 0.66 0.75 0.60 0.70
0.62 0.48 0.64 0.90 0.73 0.50
0.48 0.90 0.82 0.85 0.72 0.79 1.10 0.68 0.64 0.90 0.95 0.82 1.00 0.43 0.85 0.55 0.90 0.80
Cardiac cycle (sec.)
0.21 0.21 0.20 0.18 0.20 0.20 0.20 0.18 0.11
0.23 0.19 0.20 0.26 0.22 0.20
0.25 0.24 0.21 0.25 0.18 0.27 0.24 0.22 0.21 0.24 0.20 0.20 0.30 0.14 0.30 0.19 0.20 0.18
Upstroke timp (sec.)
650 660 665 650 610 600 750 320 500
665 375 400 380 247 300
375 418 3.50 387 575
260 387
500 379 480
400 510 4.57 525 512 370 310 218
ITpstroke I velocity (mm. / Hg/sec.)
:, g? ,? s sii .a m.
”)I 2 G1 P
2
F r, 3 5
? 3 3 ir: z. 2 e F CQ
3
B GB
“I 00 rp
Aortic SC. R.G. J.M. L.P. M.P. yi:.
Stenosis-Normal F, 34 Ni, 24 M, 31 M, 39 F, 22 F, 30 F, 47
Output 5.24 4.85 7.75 5.24 5.16 5.77 4.90
2.96 2.87 3.71 3.27 3.22 3.64 3.14
2.1 1.8 1.7 1.85 2.44 2.37 2.64 2.13 2.65 1.56 1.71
2.6
*Murmur of aortic insufficiency; at operation and cardiac catheterization, tUnless indicated by E.D. (end-diastolic). figures represent mean diastolic. CO: Cardiac output. CI: Cardiac index. LV: Left ventricular. BA : Brachial $Patients with basilar ejection murmurs.
J.D. 5.K. M.D. J.P. R.P. E.W. AS.
Mitral
Output 3.4 2.8 2.8 3.72 3.66 3.32 4.65 3.25 3.92 2.30 2.72
Stenosis-Congenital F, 13 M, 13 M, 34 5.5 M, 16 M, 13 M, M, 1.5 15
Mitral Stenosis-Low E.G. F, 56 L.A. F, 49 R.F. F, 47 C.G. M, 44 1.L.j F, 52 A.N. F, 54 1.L.i F, 55 K.Q.% F, 45 J.I.% F, 21 J.B. F, 40 J.A. F, 42
Mild
arterial.
insignificant
17 30 10 0 10 30 25
aortic
insufficiency.
134/s 108/S 95/s 112/s 145/10 105/4 lOO/lO
136/8 98/8 95/7 124/O 11618 127/8 100/7 101/4 100/3 79/7 105/6
117/7 145/3 118/S 119/s 115/14 140/17 160/20
138/69 109/59 100/60 11.5/62 HO/85 109/62 104/56
138/64 104159 98/45 130/82 118/69 129/63 106/60 106/58 105/60 84/60 108/65
100/68 115/79 108/61 120/77 105/50 110/70 135/88
6.6 13.0 10.OE.D. 18.0 23.0 25.0 5.5
8.4 16.0 7.5 15.0 12.0 5 .OE.D. 12.0 6.0E.D. 4.0E.D. 19.0 14-15
0 0 0 0 0 0 0
0.28 0.34 0.29 0.30 0.18 0.26 0.31
0.20 0.22 0.32 0.29 0.28 0.26 0.28 0.31 0.30 0.18 0.24
0.30 0.29 0.30 0.28 0.33 0.36 0.32
0.86 0.96 0.76 0.94 0.45 0.60 0.96
0.62 0.83 1.37 0.89 0.70 1.10 0.70 1.00 0.94 0.42 0.66
0.73 0.77 0.80 0.95 0.80 0.90 0.60
0.18 0.09 0.11 0.13 0.10 0.075 0.15
0.07 0.14 0.16 0.15 0.11 0.08 0.11 0.15 0.10 0.08 0.08
0.10 0.20 0.12 0.11 0.12 0.12 0.12
640 948 453 6.58 850 1,000 740
1,030 575 64.5 400 950 800 950 800 443 524 719
6.50 474 675 925 62.5 700 500
586
Delman, Gordon, Eisenherg, Escher, and Xosenhlurn
0.30
severe aortic stenosis, one patient with congenital stenosis had an upstroke velocit,, greater than 600 mm. Hg per second. The range for the 24 patients in this group n-as 218 to 665 mm. Hg per second, with a mean of 437 mm. Hg per second. Seven of the 9 patients with mild acquired aortic stenosis and 5 of the 7 with mild congenital aortic stenosis had upstroke velocities equal to or greater than 600 mm. Hg per second. The range for the 16 patients with mild stenosis was 320 to 925 mm. Hg per second, with a mean of 602 mm. Hg per second. The group with mitral stenosis and normal cardiac indices had a range of 453 to 1,000 mm. Hg per second, with a mean of 756 mm. Hg per second. Only one of these 7 patients had an upstroke velocity of less than 600 mm. Hg per second. However, 4 of 11 patients with mitral stenosis and decreased cardiac indices had upstroke velocities of less than 600 mm. Hg per second. The range for all 11 was 400 to 1,030 mm. Hg per second, with a mean of 694 mm. Hg per second. Systolic ejection time (Figs. 3 and 4).
00
r
Y
ti 0.24 -
-3
_
.
A
-W xxxx .X x
d
0000
db d dbd %
q OM ODD
0.06
i-
NORiAL
MITRAL STENOSIS
AORTIC
AORTIC
TEY
iEE%;
Fig. 2. Upstroke time in normal patients and in patients with mitral stenosis, mild-aortic stenosis, and severe aortic stenosis. The lines through the columns represent means for each group. X: Congenital aortic stenosis. 0: Acquired aortic stenosis. 0: Combined aortic and mitral stenosis.
Table II. Data in random control subjects
Patient
Sex, Age br.1
Diagnosis
ECG
Blood pressure (mm. Hg)
Cardiac size (x-ray)
Cardiac cycle (sec.)
’ Ejection time (sec.)
I
upstroke time , (sec.)
Upstroke velocity (mm. Hg/ sec.)
E.D. S.S. L.B. L.B. L.P. A.M. S.E. A.B. L.C. R.R. A.M. M.O. M.R. L.J.
Tuberculosis Tuberculosis Tuberculosis Tuberculosis Normal Multiple sclerosis Carcinoma of lung Carcinoma of breast Carcinoma of lung Reticular cell sarcoma Carcinoma of stomach Carcinoma of stomach Carcinoma of lung Tuberculosis
M, M, F, F, M, M, M, F, M, M, M, M, M, M,
50 26 24 29 16 60 37 62 63 27 50 73 54 28
Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal
135/80 135/78 110/70 118/62 134/84 190/80 135/72 126/74 125/68 140/90 130/68 162/76 120/63 160/88
Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal
0.53 0.88 0.73 0.70 1.10 0.94 0.68 0.74 0.78 0.45 0.53 0.67 0.48 0.56
0.23 0.28 0.28 0.30 0.27 0.38 0.30 0.27 0.25 0.28 0.22 0.25 0.22 0.24
0.12 0.06 0.09 0.12 0.10 0.19 0.12 0.13 0.09 0.13 0.11 0.11 0.12 0.10
900 1,635 770 668 945 1,710 787 780 1,020 597 1,170 1,240 1,040 1,003
E.C. P.K. M.M. L.P. J.S. H.S. R.E. L.H.
Normal Normal Normal Normal Normal Normal Normal Normal
F, 11 M, 49 F, 8% M, 16 M, 8 F, 5 M, 17 M, 15
Normal Normal Normal Normal Normal Normal Normal Normal
120/70 150/70 140/80 134/80 138/70 104/60 115/60 140/74
Normal Normal Normal Normal Normal Normal Normal Normal
0.90 0.70 0.60 1.00 0.80 0.80 0.90 0.75
0.26 0.22 0.23 0.28 0.26 0.28 0.30 0.24
0.10 0.08 0.09 0.10 0.14 0.08 0.10 0.08
1,100 900 1,000 900 780 1,025 600 1,100
Volume 69 Number 5
Direct BA pulse-pressure
curve in evaluation of aortic stenosis
587
mm . . 2. 4.
x ----7----“18 yzi 8:
--c ‘-----i----i 2ooL NORMAL STENOSlS
STENOSIS (MILD)
8 0.32 R G s
0.26
AORTIC STENOSIS (SEVERE)
Fig. 2. Upstroke velocity in normal patients and in patients with mitral stenosis, mild aortic stenosis, and severe aortic stenosis. The lines through the columns represent means for each group. X: Congenital aortic stenosis. 0: Acquired aortic stenosis. 0: Combined aortic and mitral stenosis. 0: Mitral stenosis, normal cardiac index. A: Mitral stenosis, low cardiac index.
Fig. 3. Ejection time correlated with the preceding R-R interval in normal patients and in patients with mitral stenosis. The dotted line represents the shortest ejection time at a given R-R interval for patients with severe aortic stenosis. 0: Norma1 patients. a: Mitral stenosis, normal cardiac index. A: Mitral stenosis, low cardiac index.
The systolic ejection time decreased with increasing heart rate in patients with and without heart disease.27 Therefore, the systolic ejection time in patients with and without aortic stenosis must be compared at identical ventricular rates. An arbitrary line connecting the shortest systolic ejection time for given rates in severe aortic
Fig. 4. Ejection time correlated with the preceding R-R interval in patients with aortic stenosis. The dotted line represents the shortest ejection time at a given R-R interval for patients with aortic stenosis. W: Severe aortic stenosis. 0: Mild aortic stenosis, acquired. X: Mild aortic stenosis, congenital.
stenosis has been drawn in Fig. 3. From the slope of this line, the shortest systolic ejection time for severe aortic stenosis for any given rate is determined by the formula: Systolic ejection time = 0.092 (R-R interval) + 0.21. Seven of the 40 patients without aortic stenosis had rate-correlated systolic ejection times in the range of those of patients with severe aortic obstruction. One patient with acquired, and 2 patients with congenital, aortic stenosis who had mild disease had ejection times below the arbitrary range drawn for severe disease. Discussion
In a group of 20 patients with severe aortic stenosis, Hancock and Abelman’ noted an upstroke time of 0.14 to 0.24 second, with a mean of 0.20 second. Although they considered this mean to be significantly different from that of their patients without aortic stenosis, there was an overlap in the range of values of their two groups. Older, normal patients tended to have a more prolonged brachial up-
588
Delman, Gordon, Eiscnberg,
Escher, and Rosenblum
stroke time, but this was not so prolonged as that seen in patients with aortic stenosis. Mathews and associates,” reviewing 39 brachial arterial tracings (only 20 catheterized patients), found only one upstroke time of less than 0.15 second in severe aortic stenosis. Hancock and Flemingx plotted brachial upstroke time against aortic valve areas and found no correlation. However, they did note that the upstroke time in patients with aortic stenosis was prolonged. Lees and associateslo and Braunwald and associates,” in reviews of congenital aortic stenosis, negated the importance of the direct brachial pressurepulse curves in the diagnosis of aortic obstructive disease. The results presented in this paper, however, suggest that the brachial arterial upstroke time may be used effectively as a screening index for the absence or presence of severe, acquired, or congenital aortic valvular stenosis. Only one patient without heart disease and one patient with mitral stenosis in a total of 40 patients had an upstroke time of 0.18 second or greater. Only one of 24 patients with severe aortic stenosis had an upstroke time of less than 0.18 second. An upstroke time of less than 0.18 second is highly suggestive of the absence of severe aortic valvular stenosis. An upstroke time greater than 0.21 second was seen only in the group with severe aortic stenosis (12 of 24 patients). In the group with mild aortic stenosis, 8 of 9 patients with acquired stenosis had an upstroke time of 0.18 second or greater; 6 of 7 patients with congenital stenosis had an upstroke time of less than 0.18 second. An upstroke time of less than 0.10 second was seen only in patients without aortic valvular stenosis (8 patients with normal hearts and 6 patients with mitral stenosis). There was no significant correlation between the degree of prolongation of the upstroke time and the cardiac index. A reduced cardiac index did not significantly change the upstroke time in either the group with mitral stenosis, that with mild acquired aortic stenosis, or that with severe aortic stenosis. Wood2” described the brachial arterial upstroke velocity as an index for detecting the presence or absence of aortic stenosis. His normal range was 750 to 1,250 mm.
Hg per second. An upstroke velocity below 750 mm. Hg per second would suggest aortic stenosis, but he cautioned that patients with a decreased cardiac indes ma)also have a decrease in the upstroke velocity. In the present study, the lowest upstroke velocity in normal subjects was 597 mm. Hg per second. Only one of 24 patients with severe aortic stenosis had an upstroke velocity greater than 600 mm. Hg per second. An upstroke velocity greater than 600 mm. Hg per second is highly suggestive of the absence of severe aortic valvular disease. Except for one patient with an aortic valve gradient of 45 mm . Hg, an upstroke velocity of less than 400 mm. Hg per second was seen only in the group with severe aortic stenosis (13 of 24 patients). However, 12 of 16 patients with mild aortic stenosis had upstroke velocities equal to or greater than 600 mm. Hg per second. One of the 2 patients with mild acquired aortic stenosis and an upstroke velocity of less than 600 mm. Hg per second had a reduced cardiac index. Only one of 7 patients with mitral stenosis and a normal cardiac index had an upstroke velocity of less than 600 mm. Hg per second. In patients with mitral stenosis with a decreased cardiac index, 4 out of 11 had an upstroke velocity of less than 600 mm. Hg per second, which confirms Wood’s observations of the relationship of cardiac index to upstroke velocity. An upstroke time greater than 0.21 second and/or an upstroke velocity of less than 400 mm. Hg per second was seen in 16 of the 24 patients with severe aortic stenosis. The rate-correlated systolic ejection time was the best of the three screening tests for the presence of obstruction of the aortic valve, although it did not separate the group with mild aortic stenosis from the group with severe aortic stenosis. Since no one parameter was completely reliable for the evaluation of the severity of aortic stenosis, all three measurements were cross analyzed. The data indicated that the rate-correlated systolic ejection time was a good screening test for the presence of aortic stenosis, regardless of the severity of the disease. Only 3 of 16 patients with mild disease had ejection
Volame Ntwaber
69 5
Direct BA pulse-pressure
times that were below the shortest ratecorrelated ejection time for severe aortic obstructive disease. One of these 3 with a gradient of 20 mm. had an upstroke time greater than 0.18 second (0.20 second) and an upstroke velocity of 600 mm. Hg per second, suggesting the presence of mild aortic stenosis. A second patient, with a gradient of 16 mm. had an upstroke time of 0.18 second and an upstroke velocity of over 600 mm. Hg per second, again suggesting mild aortic stenosis. The third patient had an upstroke time of 0.11 second and an upstroke velocity of over 600 mm. Hg per second, suggesting the absence of any aortic stenosis. A cardiac angiogram showed deformity of the aortic valve. No gradient across the aortic valve was noted. Thirteen patients with mild aortic stenosis had rate-correlated systolic ejection times in the range of those for severe aortic valvular obstruction. A brachial arterial upstroke time of less than 0.18 second and/or an upstroke velocity of over 600 mm. Hg per second ruled out the presence of severe aortic stenosis in 11 of these patients. The other 2 patients, who had gradients of 30 and 45 mm. Hg across the aortic valve, could not be separated from the group with severe aortic stenosis. Seven of the 40 patients without aortic valvular stenosis had rate-correlated systolic ejection times in the range of those for severe aortic valvular obstruction. A brachial arterial upstroke time of less than 0.18 second and/or an upstroke velocity greater than 600 mm. Hg per second ruled out the presence of severe aortic stenosis in all 7 patients. Two of these patients had upstroke times of less than 0.10 second, suggesting the absence of any aortic stenosis. The presence of mild aortic stenosis could not be excluded in the other 5 patients. The 4 of the 11 patients with mitral stenosis and diminished cardiac output who had upstroke velocities of less than 600 mm. Hg per second would not be considered to have aortic stenosis because their upstroke times were less than 0.18 second, and their rate-correlated systolic ejection times were normal. By means of these combined criteria, there was complete separation of the 24 patients with severe aortic stenosis from
curve in evaluation of aortic
stenosis
589
the 40 patients without aortic obstructive disease. By the same criteria, there was good separation of the 16 patients with mild aortic stenosis from the 40 patients without aortic disease. Thirty-five of the 40 patients without aortic stenosis could be separated from the group with mild aortic stenosis. Fifteen of the 16 patients with mild aortic stenosis could be separated from the non-aortic-stenosis group. The one patient with mild aortic stenosis who fell into the non-aortic-stenosis group had a clinically insignificant lesion. Fourteen of the 16 patients with mild aortic stenosis were also clearly separated from the 24 patients with severe aortic stenosis. The 2 patients with “mild” aortic stenosis who fell into the group with severe aortic stenosis had gradients of 30 and 45 mm. Hg across the valve, at rest. Summary
An evaluation of the direct brachial arterial pressure-pulse curve revealed that, by analysis of the rate-correlated systolic ejection time, the upstroke time, and the upstroke velocity, the presence of aortic valvular stenosis, regardless of severity, could be recognized with a high degree of accuracy. In addition, those patients with significant obstruction could be distinguished from those without significant disease. We wish to thank the staff eterization Unit of Montefiore ance in obtaining the cardiac
of the Cardiac Hospital for catheterization
Cathassistdata.
REFERENCES 1.
2.
3. 4.
5.
Katz, L. N., Ralli, E. P., and Cheer, S.: The cardiodynamic changes in the aorta and left ventricle due to stenosis of the aorta, J. Clin. Invest. 5:205, 1928. Tjong, 0. S., and Verheugt, A. P. M.: The central and peripheral arterial pressure pulses in man. A comparative study, Cardiologia 37:361, 1960. Feil, H. S., and Gilder, M. D. D.: The pulse in aortic disease as felt and graphically inscribed, Heart 8:4, 1921. Tjong, 0. S., and Verheugt, A. P. M.: Peripheral and central arterial pressure pulse in the estimation of the severity of aortic stenosis, AM. HEART J. 62:180, 1961. Dexter, L., Harken, D. E., Cobb, L. A., Novack, P., Schlant, R. C., Phimtey, A. O., and Haynes, F. W.: Aortic stenosis, Arch. Int. Med.
101:254,1958. 6. Raber, G., and Goldberg,
H,:
Left
ventricular,
7.
8. 9.
10.
Il.
12.
13.
14.
15.
16.
17.
central aortic, and peripheral pressure pulses in aortic stenosis, Am. J: Card&l. 1:572.~1958. Hancock. E. W.. and .4belman. ‘1\:. G. : A clinical study of brachial artery pulse form, with special reference to diagnosis of aortic valvular disease, Circulation 16:572, 1957. Hancock, E. W., and Fleming, I’. Ii.: Aortic stenosis, Ouart. I. Med. 29:209. 1960. MathewsyM. By, Medd, W. E.‘, and Gorlin, R.: Aortic stenosis: A clinical study, Brit. M. J. 2~759, 1955. Lees, M. H., Hauck, A. J., Starkey, G. W. B., Nadas, ,4. S., and Gross, Ii. E.: Congenital aortic stenosis. Operative indications and surgical results, Brit. Heart J. 24:31, 1962. Braunwald, E., Goldblatt, A., Aygen, M. M., Rokoff. D. S.. and Morrow. A. G.: Congenital aortic stenosis. I. Clinical ‘and hemod&mic findings in 100 patients, Circulation 27:426, 1963. Robinson, B.: The carotid pulse. II. Relation of external recordings to carotid, aortic and brachial pulses, Brit. Heart J. 25:61, 1963. Feil, H. S., and Katz, L. N.: The transformation of the central into the peripheral pulse in patients with aortic stenosis, AM. HEART J. 2:12, 1926-1927. Dow, I’.: The development of the anarrotic and tardus pulse in aortic stenosis, Am. J. Physiol. 131:432, 1940. Wright, J, L., Toscano-Barbaza, E., and Brandenberg, R. 0. : Left ventricular and aortic pressure pulses in aortic valvular disease, Proc. Staff Meet. Mayo Clin. 31:120, 1956. Brockenbrough, E. C., Morrow, ,4. G., Talbert, J., and Braunwald, E.: Percutaneous puncture of the left ventricle, Brit. Heart J. 23:643, 1961. t\drouny, Z. A., Sutherland, D. W., Griswold, H. E., and Ritzmann, I,. W.: Complications
18.
19.
20.
21.
22.
23.
24.
2.5.
26.
27.
28.
\vith transseptal left heart c;ltheteriz~~ti~,tls, .\M. HEART J. 65~~27. 196.3. I~osenblun~. ft., Eisenberg, Ii., ai~d Eschci-. 1). J. W.: Significant complications with the transseptal technique for left heart catheterizations. Unpublished observations. Gorlin, R., and Gorlin, S. G.: Hydraulic formula for calculation of the arca of the stenotic mitral valve, other cardiac valves, and central circulatoryshunts, AM. HEART J. 41:1, 1951. Levine, S. a., and Harvey, P. W.: Clinical auscultation of the heart, ed. 2, Philadelphia, 1959, W. B. Saunders Company, p. 52. McKusick, \‘. A., editor: Symposium on cardiovascular sound. Clinical aspects, Circulation 16:415, 1957. Ross, J.. Jr., Braunwald, E., and Morrow, A. G.: Transseptal left heart catheterization; a new diagnostic method, Prog. Cardiovas. Dis. 2:315, 1960. Seldinger, S. T.: Catheter replacement of needle in percutaneous arteriography: a new technique, Acta Radiol. 39:368, 1953. Brock, R., Milstein, B. B., and Russ, I). N.: Percutaneous left ventricular puncture in the assessment of aortic stenosis, Thorax 11:163, 1956. Scholander, P. F.: Analyzer for accurate estimation of respiratory gases in one-half cubic centimeter sample, J. Biol. Chem. 167:235, 1947. \Tan Slyke, D. D., and Neill, J. M.: The determination of gases in blood and other solutions by vacuum extraction and manometric measurement, J. Biol. Chem. 61:524, 1924. Robinson, B.: The carotid pulse. I. Diagnosis of aortic stenosis by external recordings, Brit. Heart J. 25:51, 1963. Wood, I’.: Aortic stenosis, Am. J. Cardiol. 1553. 1958.
The direct
brachial
pulse-pressure of patients
arterial
curve with
in the evaluation
aortic
valvular
stenosis
Abner J. Delman, M.D.* Garet M. Gordon, M.D.** Robert Eisenberg, M.D.*** Doris J. W. Escher, M.D.**** Robert Rosenblum, M.D.***** New York, N. Y.
T
he relationship of the central and peripheral pulse-pressure curves in normal man, in patients with aortic stenosis, and in experimentally produced aortic stenosis has been discussed in the literature.‘e4 However, there has not been a consistent opinion concerning the diagnostic value of the brachial arterial pulsepressure curves in patients with aortic stenosis,5-‘2 despite the fact that in this condition, in contradistinction to the normal state, the direct brachial arterial pressure curve resembles the central arterial pulse contours. 13-15 Since the techniques of left heart catheterization for quantitatively evaluating the gradient across the aortic valve are not without complications,‘6-18 it was thought that an attempt should be made to determine the value of these brachial arterial tracings as a screening test for the presence of aortic stenosis. From
Material
and
methods
The brachial arterial pulse-pressure curves of 80 patients (age range of 2 to 64 years) were recorded and analyzed. These were divided into five groups on the bases of underlying cardiac states, as follows : 1. Severe aortic valvulur stenosis (24 patients-18 acquired and 6 congenital). Those patients with a normal cardiac index (C. I.) with a peak-to-peak or mean systolic gradient of over 50 mm. Hg, or with a decreased cardiac index with a valve area calculated, by the method of Gorlin and Gorlin,lg to be less than 0.75 cm.2. 2. Mild aortic valvulur stenosis (16 patients-9 acquired and 7 congenital). Those patients with gradients less than 50 mm. Hg across the valve with a normal cardiac index, or with a decreased cardiac
the Cardiac Catheterization Laboratory and the Cardiology Service, Medical Division. Mont&ore Hospital, New York, N. Y. Received for publication June 11, 1964. *Adjunct Attending Physician, Cardiology Service, Medical Division, Montefiore Hospital. Address: Montefiore Hospital, 210th St. and Bainbridge Ave., New York, N. Y.. 10067. QNew York Heart Association Trainee 1961-1962. Presently, Assistant Attending Physician. Medical Division, Montefiore Hospital. ***Associate Attending Physician, Pediatric Division, and Research Associate in Pediatric Cardiology, Cardiology Service, Mont&ore Hospital; Assistant Professor of Clinical Pediatrics, Albert Einstein College of Medicine. “***Associate Attending Physician. Cardiology Service, Medical Division, and Physician-in-Charge, Cardiac Catheterization Laboratory. Montefiore Hospital; Lecturer in Medicine, Columbia University. *****Adjunct Attending Physician, Cardiology Service, Medical Division. and Research Associate, Mont&ore Hospital: Teaching Assistant, New York University School of Medicine.
582
Volume Number
69 5
Direct BA pulse-pressure curve in evaluation of aortic stenosis
index and a valve area calculated to be greater than 0.75 cm.2. This criterion for valve area in both mild and severe stenosis related only to patients over 16 years of age. 3. Mitral stenosis--normal C. I. (7 patients). Those patients with a cardiac index in the range of 2.8 to 3.6 L./min./M.2 and no evidence of aortic stenosis. 4. Mitral stenosis--low C. I. (11 patients). Those patients with a cardiac index of less than 2.8 L./min./M.2 with no evidence of aortic stenosis. 5. No heart disease (22 patients). Hospitalized patients without clinical evidence of heart disease who were comparable in age to the patients in Groups l-4. Patients with aortic stenosis with significant mitral insufficiency were not included in the study because mitral insufficiency itself will shorten the systolic ejection time.20s21Patients with aortic stenosis and hemodynamically significant aortic insufficiency were also excluded. Significant aortic and mitral insufficiency were determined by accepted clinical, hemodynamic, and angiocardiographic criteria. All of the patients in Groups l-4 and 8 of the patients in Group 5 had concurrently performed right and left heart catheterizations. Gradients across the mitral valve were obtained by the analysis of simultaneous pulmonary artery wedge or direct left atria1 and left ventricular pressures. The direct left atria1 measurements were obtained by the transseptal technique. 22 The left ventricular pressure was obtained either by the retrograde Seldinger method23 using a femoral artery, or by direct percutaneous left ventricular puncture.24 Mean and peak-to-peak systolic gradients across the aortic valve were obtained from the simultaneous left ventricular and brachial arterial pressures. Cardiac output was measured by the direct Fick principle, with analyses of the respiratory gases by the method of Scholander,25 and the blood gasesby the method of Van Slyke and Nei11.26The brachial arterial pulsepressure tracings were recorded with a Cournand needle placed in the right or left brachial artery. All measurements of pressure were recorded on the Electronics for Medicine multichannel recorder using Statham gauge transducers.
583
The following information was obtained from the brachial arterial tracings: (1) the time, in seconds, from the initial rise to the maximum systolic pressure (upstroke time); (2) the rate of rise in the initial slope of the brachial curves, in millimeters of mercury per second (the upstroke velocity); and (3) the time, in seconds, from the initial rise in the brachial arterial pressure curve to the dicrotic notch (systolic ejection time). Results
The data from each group of patients is tabulated in Tables I and II.
Brachial
arterial
upstroke time (Fig. 1).
In the 22 patients without heart disease the brachial arterial upstroke time varied from 0.06 to 0.19 second, with a mean of 0.11 second. Only one patient had an upstroke time greater than 0.14 second. In 23 of the 24 patients with severe aortic stenosis (4 with coexistent mitral stenosis) the upstroke time was equal to or greater than 0.18 second, with a range of 0.18 to 0.30 second. One patient with severe aortic stenosisand mitral stenosis had an upstroke time of lessthan 0.18 second. The mean for the 24 patients was 0.22 second. An upstroke time equal to or greater than 0.18 second was also noted in 8 of the 9 patients with mild acquired aortic stenosis, with a range of 0.18 to 0.25 second. One patient had an upstroke time of 0.11 second. The mean for the 9 patients was 0.19 second. Six of the 7 patients with mild congenital aortic stenosis had upstroke times of less than 0.18 second, with a range of 0.10 to 0.12 second. The seventh patient had an upstroke time of 0.20 second. The mean for the 7 patients was 0.13 second. In the 7 patients with isolated mitral stenosis and normal cardiac indices the upstroke time was 0.075 to 0.18 second, with a mean of 0.12 second. In the 11 patients with isolated mitral stenosis and reduced cardiac indices, the upstroke time was 0.07 to 0.16 second, with a mean of 0.11 second. A reduced cardiac index did not prolong the upstroke time in any group of patients. Brachial upstroke velocity (Fig. 2). The 22 patients without heart disease had a mean upstroke velocity of 999 mm. Hg per second, with a range of 595 to 1,710 mm. Hg per second. In the patients with
Xld
yi? R.D.
Aortic I.M. N.H. T.D. CR. R.A. G.B.
Severe i\ortic R.L. R.S. J.U. G.G. L.D. L.W.
S.S.’ F.B. E.D. A.L. IS.
Severe Aortic L.M. R.P.* N.M. A.E.* M.S.* L.D. W.N. L.C. AC.* P.F. A.E. ;“A
Patient
Table I
i
I
CO (L./min.)
50 54 53 5.5 50
2.6 2.44
4.9 3.9
M, 49 42 F, 57
Stenosis-Acquired F, 54 M, 43 M, 30 F, 37 M, 37 F, 41
1.5 4.2 2.5
1.63 1.44
2.33 2.89 1.39 2.40 2.80
2.3 3.8
I
(L./m&. /M .“)
ICI
3.8 5.4
2.82 2.9 2.78
2.93 1.88
4.40 2.70
5.52 5.8 5.50
2.29 3.47 2.31
4.25 6.76 4.02
Stenosis-Congenital M, 8 M, 2 M, 50 M, 15 F, 34 M, 10
M, M, F, *al, F,
Stenosis-Acquired M, 62 4.05 F, 64 4.34 M, 51 2.60 M, 50 4.38 M, 50 5.13 M, 44 M 55 2.60 M: 36 2.53 M, 51 M, 49 M, 37 2.68 M, M, 4.5 54 5.95 5.4
Srx, .4ge Cur.1
Mean
24 19 47 42 30
10 1.5
54 4.5
E 56 59 40 56 78 64 32 75 62 40 58
40 58
gradient (mm. Hg)
10 22 2.5 16 32 20 40 45 3.5
73 120 86 135 108(OR) 150
40 87 73 97 58 88 65 85 83 65 36 80 6.5 42 70 94 50 40
Peak gradient (mm. Hg) ffd
170/15 177/17 165/15 100/13 134/10 143/12 164/10 150/10 130/8
240/13
150/13 180/4 201/42 230/16
136/18 230/Z 1 150/32 228/28 182/9 189/42 155/4 181/22 225/16 205/13 136/18 180/13 192/17 162/35 190/15 230/15 180/12 180/10
(mm.
160/80 155/Z 140/80 84/40 102/58 123/74 124/75 105/60 95/50
77/57 60/48 115/60 95172 120/80 91/61
96/66 143/83 77/57 131/85 120/66 101/59 90/44 96/70 142/85 141/88 100/64 100/60 127/62 120/81 120/60 126/78 130/64 140/70
p ressure BA (mm. Hd
0 0 0 0 10 0 0 0 10
0 0 0 0 0 0
0 0 0 0 8.2 0 10E.D. 0 0 0 8.2 0 0 1.5 0 0 0 1.5
Mitral? gradient (mm. Hg)
0.38 0.29 0.38 0.28 0.37 0.25 0.30 0.38 0.32
0.27 0.29 0.35 0.33 0.35 0.30
0.37 0.40 0.29 0.43 0.34 0.47 0.36 0.31 0.34 0.33 0.38 0.35 0.38 0.28 0.47 0.37 0.32 0.32
Ejection time (sec.)
0.93 0.78 0.76 0.90 0.71 0.66 0.75 0.60 0.70
0.62 0.48 0.64 0.90 0.73 0.50
0.48 0.90 0.82 0.85 0.72 0.79 1.10 0.68 0.64 0.90 0.95 0.82 1.00 0.43 0.85 0.55 0.90 0.80
Cardiac cycle (sec.)
0.21 0.21 0.20 0.18 0.20 0.20 0.20 0.18 0.11
0.23 0.19 0.20 0.26 0.22 0.20
0.25 0.24 0.21 0.25 0.18 0.27 0.24 0.22 0.21 0.24 0.20 0.20 0.30 0.14 0.30 0.19 0.20 0.18
Upstroke timp (sec.)
650 660 665 650 610 600 750 320 500
665 375 400 380 247 300
375 418 3.50 387 575
260 387
500 379 480
400 510 4.57 525 512 370 310 218
ITpstroke I velocity (mm. / Hg/sec.)
:, g? ,? s sii .a m.
”)I 2 G1 P
2
F r, 3 5
? 3 3 ir: z. 2 e F CQ
3
B GB
“I 00 rp
Aortic SC. R.G. J.M. L.P. M.P. yi:.
Stenosis-Normal F, 34 Ni, 24 M, 31 M, 39 F, 22 F, 30 F, 47
Output 5.24 4.85 7.75 5.24 5.16 5.77 4.90
2.96 2.87 3.71 3.27 3.22 3.64 3.14
2.1 1.8 1.7 1.85 2.44 2.37 2.64 2.13 2.65 1.56 1.71
2.6
*Murmur of aortic insufficiency; at operation and cardiac catheterization, tUnless indicated by E.D. (end-diastolic). figures represent mean diastolic. CO: Cardiac output. CI: Cardiac index. LV: Left ventricular. BA : Brachial $Patients with basilar ejection murmurs.
J.D. 5.K. M.D. J.P. R.P. E.W. AS.
Mitral
Output 3.4 2.8 2.8 3.72 3.66 3.32 4.65 3.25 3.92 2.30 2.72
Stenosis-Congenital F, 13 M, 13 M, 34 5.5 M, 16 M, 13 M, M, 1.5 15
Mitral Stenosis-Low E.G. F, 56 L.A. F, 49 R.F. F, 47 C.G. M, 44 1.L.j F, 52 A.N. F, 54 1.L.i F, 55 K.Q.% F, 45 J.I.% F, 21 J.B. F, 40 J.A. F, 42
Mild
arterial.
insignificant
17 30 10 0 10 30 25
aortic
insufficiency.
134/s 108/S 95/s 112/s 145/10 105/4 lOO/lO
136/8 98/8 95/7 124/O 11618 127/8 100/7 101/4 100/3 79/7 105/6
117/7 145/3 118/S 119/s 115/14 140/17 160/20
138/69 109/59 100/60 11.5/62 HO/85 109/62 104/56
138/64 104159 98/45 130/82 118/69 129/63 106/60 106/58 105/60 84/60 108/65
100/68 115/79 108/61 120/77 105/50 110/70 135/88
6.6 13.0 10.OE.D. 18.0 23.0 25.0 5.5
8.4 16.0 7.5 15.0 12.0 5 .OE.D. 12.0 6.0E.D. 4.0E.D. 19.0 14-15
0 0 0 0 0 0 0
0.28 0.34 0.29 0.30 0.18 0.26 0.31
0.20 0.22 0.32 0.29 0.28 0.26 0.28 0.31 0.30 0.18 0.24
0.30 0.29 0.30 0.28 0.33 0.36 0.32
0.86 0.96 0.76 0.94 0.45 0.60 0.96
0.62 0.83 1.37 0.89 0.70 1.10 0.70 1.00 0.94 0.42 0.66
0.73 0.77 0.80 0.95 0.80 0.90 0.60
0.18 0.09 0.11 0.13 0.10 0.075 0.15
0.07 0.14 0.16 0.15 0.11 0.08 0.11 0.15 0.10 0.08 0.08
0.10 0.20 0.12 0.11 0.12 0.12 0.12
640 948 453 6.58 850 1,000 740
1,030 575 64.5 400 950 800 950 800 443 524 719
6.50 474 675 925 62.5 700 500
586
Delman, Gordon, Eisenherg, Escher, and Xosenhlurn
0.30
severe aortic stenosis, one patient with congenital stenosis had an upstroke velocit,, greater than 600 mm. Hg per second. The range for the 24 patients in this group n-as 218 to 665 mm. Hg per second, with a mean of 437 mm. Hg per second. Seven of the 9 patients with mild acquired aortic stenosis and 5 of the 7 with mild congenital aortic stenosis had upstroke velocities equal to or greater than 600 mm. Hg per second. The range for the 16 patients with mild stenosis was 320 to 925 mm. Hg per second, with a mean of 602 mm. Hg per second. The group with mitral stenosis and normal cardiac indices had a range of 453 to 1,000 mm. Hg per second, with a mean of 756 mm. Hg per second. Only one of these 7 patients had an upstroke velocity of less than 600 mm. Hg per second. However, 4 of 11 patients with mitral stenosis and decreased cardiac indices had upstroke velocities of less than 600 mm. Hg per second. The range for all 11 was 400 to 1,030 mm. Hg per second, with a mean of 694 mm. Hg per second. Systolic ejection time (Figs. 3 and 4).
00
r
Y
ti 0.24 -
-3
_
.
A
-W xxxx .X x
d
0000
db d dbd %
q OM ODD
0.06
i-
NORiAL
MITRAL STENOSIS
AORTIC
AORTIC
TEY
iEE%;
Fig. 2. Upstroke time in normal patients and in patients with mitral stenosis, mild-aortic stenosis, and severe aortic stenosis. The lines through the columns represent means for each group. X: Congenital aortic stenosis. 0: Acquired aortic stenosis. 0: Combined aortic and mitral stenosis.
Table II. Data in random control subjects
Patient
Sex, Age br.1
Diagnosis
ECG
Blood pressure (mm. Hg)
Cardiac size (x-ray)
Cardiac cycle (sec.)
’ Ejection time (sec.)
I
upstroke time , (sec.)
Upstroke velocity (mm. Hg/ sec.)
E.D. S.S. L.B. L.B. L.P. A.M. S.E. A.B. L.C. R.R. A.M. M.O. M.R. L.J.
Tuberculosis Tuberculosis Tuberculosis Tuberculosis Normal Multiple sclerosis Carcinoma of lung Carcinoma of breast Carcinoma of lung Reticular cell sarcoma Carcinoma of stomach Carcinoma of stomach Carcinoma of lung Tuberculosis
M, M, F, F, M, M, M, F, M, M, M, M, M, M,
50 26 24 29 16 60 37 62 63 27 50 73 54 28
Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal
135/80 135/78 110/70 118/62 134/84 190/80 135/72 126/74 125/68 140/90 130/68 162/76 120/63 160/88
Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal Normal
0.53 0.88 0.73 0.70 1.10 0.94 0.68 0.74 0.78 0.45 0.53 0.67 0.48 0.56
0.23 0.28 0.28 0.30 0.27 0.38 0.30 0.27 0.25 0.28 0.22 0.25 0.22 0.24
0.12 0.06 0.09 0.12 0.10 0.19 0.12 0.13 0.09 0.13 0.11 0.11 0.12 0.10
900 1,635 770 668 945 1,710 787 780 1,020 597 1,170 1,240 1,040 1,003
E.C. P.K. M.M. L.P. J.S. H.S. R.E. L.H.
Normal Normal Normal Normal Normal Normal Normal Normal
F, 11 M, 49 F, 8% M, 16 M, 8 F, 5 M, 17 M, 15
Normal Normal Normal Normal Normal Normal Normal Normal
120/70 150/70 140/80 134/80 138/70 104/60 115/60 140/74
Normal Normal Normal Normal Normal Normal Normal Normal
0.90 0.70 0.60 1.00 0.80 0.80 0.90 0.75
0.26 0.22 0.23 0.28 0.26 0.28 0.30 0.24
0.10 0.08 0.09 0.10 0.14 0.08 0.10 0.08
1,100 900 1,000 900 780 1,025 600 1,100
Volume 69 Number 5
Direct BA pulse-pressure
curve in evaluation of aortic stenosis
587
mm . . 2. 4.
x ----7----“18 yzi 8:
--c ‘-----i----i 2ooL NORMAL STENOSlS
STENOSIS (MILD)
8 0.32 R G s
0.26
AORTIC STENOSIS (SEVERE)
Fig. 2. Upstroke velocity in normal patients and in patients with mitral stenosis, mild aortic stenosis, and severe aortic stenosis. The lines through the columns represent means for each group. X: Congenital aortic stenosis. 0: Acquired aortic stenosis. 0: Combined aortic and mitral stenosis. 0: Mitral stenosis, normal cardiac index. A: Mitral stenosis, low cardiac index.
Fig. 3. Ejection time correlated with the preceding R-R interval in normal patients and in patients with mitral stenosis. The dotted line represents the shortest ejection time at a given R-R interval for patients with severe aortic stenosis. 0: Norma1 patients. a: Mitral stenosis, normal cardiac index. A: Mitral stenosis, low cardiac index.
The systolic ejection time decreased with increasing heart rate in patients with and without heart disease.27 Therefore, the systolic ejection time in patients with and without aortic stenosis must be compared at identical ventricular rates. An arbitrary line connecting the shortest systolic ejection time for given rates in severe aortic
Fig. 4. Ejection time correlated with the preceding R-R interval in patients with aortic stenosis. The dotted line represents the shortest ejection time at a given R-R interval for patients with aortic stenosis. W: Severe aortic stenosis. 0: Mild aortic stenosis, acquired. X: Mild aortic stenosis, congenital.
stenosis has been drawn in Fig. 3. From the slope of this line, the shortest systolic ejection time for severe aortic stenosis for any given rate is determined by the formula: Systolic ejection time = 0.092 (R-R interval) + 0.21. Seven of the 40 patients without aortic stenosis had rate-correlated systolic ejection times in the range of those of patients with severe aortic obstruction. One patient with acquired, and 2 patients with congenital, aortic stenosis who had mild disease had ejection times below the arbitrary range drawn for severe disease. Discussion
In a group of 20 patients with severe aortic stenosis, Hancock and Abelman’ noted an upstroke time of 0.14 to 0.24 second, with a mean of 0.20 second. Although they considered this mean to be significantly different from that of their patients without aortic stenosis, there was an overlap in the range of values of their two groups. Older, normal patients tended to have a more prolonged brachial up-
588
Delman, Gordon, Eiscnberg,
Escher, and Rosenblum
stroke time, but this was not so prolonged as that seen in patients with aortic stenosis. Mathews and associates,” reviewing 39 brachial arterial tracings (only 20 catheterized patients), found only one upstroke time of less than 0.15 second in severe aortic stenosis. Hancock and Flemingx plotted brachial upstroke time against aortic valve areas and found no correlation. However, they did note that the upstroke time in patients with aortic stenosis was prolonged. Lees and associateslo and Braunwald and associates,” in reviews of congenital aortic stenosis, negated the importance of the direct brachial pressurepulse curves in the diagnosis of aortic obstructive disease. The results presented in this paper, however, suggest that the brachial arterial upstroke time may be used effectively as a screening index for the absence or presence of severe, acquired, or congenital aortic valvular stenosis. Only one patient without heart disease and one patient with mitral stenosis in a total of 40 patients had an upstroke time of 0.18 second or greater. Only one of 24 patients with severe aortic stenosis had an upstroke time of less than 0.18 second. An upstroke time of less than 0.18 second is highly suggestive of the absence of severe aortic valvular stenosis. An upstroke time greater than 0.21 second was seen only in the group with severe aortic stenosis (12 of 24 patients). In the group with mild aortic stenosis, 8 of 9 patients with acquired stenosis had an upstroke time of 0.18 second or greater; 6 of 7 patients with congenital stenosis had an upstroke time of less than 0.18 second. An upstroke time of less than 0.10 second was seen only in patients without aortic valvular stenosis (8 patients with normal hearts and 6 patients with mitral stenosis). There was no significant correlation between the degree of prolongation of the upstroke time and the cardiac index. A reduced cardiac index did not significantly change the upstroke time in either the group with mitral stenosis, that with mild acquired aortic stenosis, or that with severe aortic stenosis. Wood2” described the brachial arterial upstroke velocity as an index for detecting the presence or absence of aortic stenosis. His normal range was 750 to 1,250 mm.
Hg per second. An upstroke velocity below 750 mm. Hg per second would suggest aortic stenosis, but he cautioned that patients with a decreased cardiac indes ma)also have a decrease in the upstroke velocity. In the present study, the lowest upstroke velocity in normal subjects was 597 mm. Hg per second. Only one of 24 patients with severe aortic stenosis had an upstroke velocity greater than 600 mm. Hg per second. An upstroke velocity greater than 600 mm. Hg per second is highly suggestive of the absence of severe aortic valvular disease. Except for one patient with an aortic valve gradient of 45 mm . Hg, an upstroke velocity of less than 400 mm. Hg per second was seen only in the group with severe aortic stenosis (13 of 24 patients). However, 12 of 16 patients with mild aortic stenosis had upstroke velocities equal to or greater than 600 mm. Hg per second. One of the 2 patients with mild acquired aortic stenosis and an upstroke velocity of less than 600 mm. Hg per second had a reduced cardiac index. Only one of 7 patients with mitral stenosis and a normal cardiac index had an upstroke velocity of less than 600 mm. Hg per second. In patients with mitral stenosis with a decreased cardiac index, 4 out of 11 had an upstroke velocity of less than 600 mm. Hg per second, which confirms Wood’s observations of the relationship of cardiac index to upstroke velocity. An upstroke time greater than 0.21 second and/or an upstroke velocity of less than 400 mm. Hg per second was seen in 16 of the 24 patients with severe aortic stenosis. The rate-correlated systolic ejection time was the best of the three screening tests for the presence of obstruction of the aortic valve, although it did not separate the group with mild aortic stenosis from the group with severe aortic stenosis. Since no one parameter was completely reliable for the evaluation of the severity of aortic stenosis, all three measurements were cross analyzed. The data indicated that the rate-correlated systolic ejection time was a good screening test for the presence of aortic stenosis, regardless of the severity of the disease. Only 3 of 16 patients with mild disease had ejection
Volame Ntwaber
69 5
Direct BA pulse-pressure
times that were below the shortest ratecorrelated ejection time for severe aortic obstructive disease. One of these 3 with a gradient of 20 mm. had an upstroke time greater than 0.18 second (0.20 second) and an upstroke velocity of 600 mm. Hg per second, suggesting the presence of mild aortic stenosis. A second patient, with a gradient of 16 mm. had an upstroke time of 0.18 second and an upstroke velocity of over 600 mm. Hg per second, again suggesting mild aortic stenosis. The third patient had an upstroke time of 0.11 second and an upstroke velocity of over 600 mm. Hg per second, suggesting the absence of any aortic stenosis. A cardiac angiogram showed deformity of the aortic valve. No gradient across the aortic valve was noted. Thirteen patients with mild aortic stenosis had rate-correlated systolic ejection times in the range of those for severe aortic valvular obstruction. A brachial arterial upstroke time of less than 0.18 second and/or an upstroke velocity of over 600 mm. Hg per second ruled out the presence of severe aortic stenosis in 11 of these patients. The other 2 patients, who had gradients of 30 and 45 mm. Hg across the aortic valve, could not be separated from the group with severe aortic stenosis. Seven of the 40 patients without aortic valvular stenosis had rate-correlated systolic ejection times in the range of those for severe aortic valvular obstruction. A brachial arterial upstroke time of less than 0.18 second and/or an upstroke velocity greater than 600 mm. Hg per second ruled out the presence of severe aortic stenosis in all 7 patients. Two of these patients had upstroke times of less than 0.10 second, suggesting the absence of any aortic stenosis. The presence of mild aortic stenosis could not be excluded in the other 5 patients. The 4 of the 11 patients with mitral stenosis and diminished cardiac output who had upstroke velocities of less than 600 mm. Hg per second would not be considered to have aortic stenosis because their upstroke times were less than 0.18 second, and their rate-correlated systolic ejection times were normal. By means of these combined criteria, there was complete separation of the 24 patients with severe aortic stenosis from
curve in evaluation of aortic
stenosis
589
the 40 patients without aortic obstructive disease. By the same criteria, there was good separation of the 16 patients with mild aortic stenosis from the 40 patients without aortic disease. Thirty-five of the 40 patients without aortic stenosis could be separated from the group with mild aortic stenosis. Fifteen of the 16 patients with mild aortic stenosis could be separated from the non-aortic-stenosis group. The one patient with mild aortic stenosis who fell into the non-aortic-stenosis group had a clinically insignificant lesion. Fourteen of the 16 patients with mild aortic stenosis were also clearly separated from the 24 patients with severe aortic stenosis. The 2 patients with “mild” aortic stenosis who fell into the group with severe aortic stenosis had gradients of 30 and 45 mm. Hg across the valve, at rest. Summary
An evaluation of the direct brachial arterial pressure-pulse curve revealed that, by analysis of the rate-correlated systolic ejection time, the upstroke time, and the upstroke velocity, the presence of aortic valvular stenosis, regardless of severity, could be recognized with a high degree of accuracy. In addition, those patients with significant obstruction could be distinguished from those without significant disease. We wish to thank the staff eterization Unit of Montefiore ance in obtaining the cardiac
of the Cardiac Hospital for catheterization
Cathassistdata.
REFERENCES 1.
2.
3. 4.
5.
Katz, L. N., Ralli, E. P., and Cheer, S.: The cardiodynamic changes in the aorta and left ventricle due to stenosis of the aorta, J. Clin. Invest. 5:205, 1928. Tjong, 0. S., and Verheugt, A. P. M.: The central and peripheral arterial pressure pulses in man. A comparative study, Cardiologia 37:361, 1960. Feil, H. S., and Gilder, M. D. D.: The pulse in aortic disease as felt and graphically inscribed, Heart 8:4, 1921. Tjong, 0. S., and Verheugt, A. P. M.: Peripheral and central arterial pressure pulse in the estimation of the severity of aortic stenosis, AM. HEART J. 62:180, 1961. Dexter, L., Harken, D. E., Cobb, L. A., Novack, P., Schlant, R. C., Phimtey, A. O., and Haynes, F. W.: Aortic stenosis, Arch. Int. Med.
101:254,1958. 6. Raber, G., and Goldberg,
H,:
Left
ventricular,
7.
8. 9.
10.
Il.
12.
13.
14.
15.
16.
17.
central aortic, and peripheral pressure pulses in aortic stenosis, Am. J: Card&l. 1:572.~1958. Hancock. E. W.. and .4belman. ‘1\:. G. : A clinical study of brachial artery pulse form, with special reference to diagnosis of aortic valvular disease, Circulation 16:572, 1957. Hancock, E. W., and Fleming, I’. Ii.: Aortic stenosis, Ouart. I. Med. 29:209. 1960. MathewsyM. By, Medd, W. E.‘, and Gorlin, R.: Aortic stenosis: A clinical study, Brit. M. J. 2~759, 1955. Lees, M. H., Hauck, A. J., Starkey, G. W. B., Nadas, ,4. S., and Gross, Ii. E.: Congenital aortic stenosis. Operative indications and surgical results, Brit. Heart J. 24:31, 1962. Braunwald, E., Goldblatt, A., Aygen, M. M., Rokoff. D. S.. and Morrow. A. G.: Congenital aortic stenosis. I. Clinical ‘and hemod&mic findings in 100 patients, Circulation 27:426, 1963. Robinson, B.: The carotid pulse. II. Relation of external recordings to carotid, aortic and brachial pulses, Brit. Heart J. 25:61, 1963. Feil, H. S., and Katz, L. N.: The transformation of the central into the peripheral pulse in patients with aortic stenosis, AM. HEART J. 2:12, 1926-1927. Dow, I’.: The development of the anarrotic and tardus pulse in aortic stenosis, Am. J. Physiol. 131:432, 1940. Wright, J, L., Toscano-Barbaza, E., and Brandenberg, R. 0. : Left ventricular and aortic pressure pulses in aortic valvular disease, Proc. Staff Meet. Mayo Clin. 31:120, 1956. Brockenbrough, E. C., Morrow, ,4. G., Talbert, J., and Braunwald, E.: Percutaneous puncture of the left ventricle, Brit. Heart J. 23:643, 1961. t\drouny, Z. A., Sutherland, D. W., Griswold, H. E., and Ritzmann, I,. W.: Complications
18.
19.
20.
21.
22.
23.
24.
2.5.
26.
27.
28.
\vith transseptal left heart c;ltheteriz~~ti~,tls, .\M. HEART J. 65~~27. 196.3. I~osenblun~. ft., Eisenberg, Ii., ai~d Eschci-. 1). J. W.: Significant complications with the transseptal technique for left heart catheterizations. Unpublished observations. Gorlin, R., and Gorlin, S. G.: Hydraulic formula for calculation of the arca of the stenotic mitral valve, other cardiac valves, and central circulatoryshunts, AM. HEART J. 41:1, 1951. Levine, S. a., and Harvey, P. W.: Clinical auscultation of the heart, ed. 2, Philadelphia, 1959, W. B. Saunders Company, p. 52. McKusick, \‘. A., editor: Symposium on cardiovascular sound. Clinical aspects, Circulation 16:415, 1957. Ross, J.. Jr., Braunwald, E., and Morrow, A. G.: Transseptal left heart catheterization; a new diagnostic method, Prog. Cardiovas. Dis. 2:315, 1960. Seldinger, S. T.: Catheter replacement of needle in percutaneous arteriography: a new technique, Acta Radiol. 39:368, 1953. Brock, R., Milstein, B. B., and Russ, I). N.: Percutaneous left ventricular puncture in the assessment of aortic stenosis, Thorax 11:163, 1956. Scholander, P. F.: Analyzer for accurate estimation of respiratory gases in one-half cubic centimeter sample, J. Biol. Chem. 167:235, 1947. \Tan Slyke, D. D., and Neill, J. M.: The determination of gases in blood and other solutions by vacuum extraction and manometric measurement, J. Biol. Chem. 61:524, 1924. Robinson, B.: The carotid pulse. I. Diagnosis of aortic stenosis by external recordings, Brit. Heart J. 25:51, 1963. Wood, I’.: Aortic stenosis, Am. J. Cardiol. 1553. 1958.