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Importance of the “atrial kick” in determining the effective mitral valve orifice area in mitral stenosis
VALVULAR HEART DISEASE
Importanceof the “Atrial Kick” in Determining the EffectiveMitral ValveOrifice Area in Mitral Stenosis PASCAL
NICOD, MD, L. DAVID HILLIS, MD, MICHAEL D. WINNIFORD, and BRIAN G. FIRTH, MD, DPhil
Atrial fibrillation with a rapid ventricular response in patients with mitral stenosis (MS) is often accompanied by pulmonary congestion and reduced cardiac output owing to a diminished diastolic filling period and the loss of the end-diastolic left ventricular (LV) pressure increment. To test the hypothesis that loss of atrial contraction (atrial kick) also results in a decrease in effective mitral valve orifice area, 6 patients with pure, isolated MS were studied in sinus rhythm during atrial pacing and simultaneous atrioventricular pacing. Atrial pacing at 140 beats/min caused no significant change from baseline in cardiac output or mitral valve area, but there was a decrease in LV end-diastolic volume and ejection fraction as well as an increase in left atrial pressure and mean diastolic gradient. Simultaneous atrioventricu-
MD,
lar pacing (to eliminate atrial kick) induced a decrease in cardiac output (4.4 f 0.9 vs 5.2 f 0.8 liters/min at 110 beats/min, 4.2 f 0.9 vs 5.1 f 0.9 liters/min at 140 beats/min; p <0.05) and LV end-diastolic volume (77 f 27 vs 93 f 29 ml at 110 beats/min, 54 f 17 vs 65 f 19 ml at 140 beats/min; p <0.05), an increase in left atrial pressure (28 f 3 vs 20 f 5 mm Hg at 110 beats/min, 30 f 4 vs 25 f 5 mm Hg at 140 beats/min; p <0.05), and a decrease in mitral valve area (1.2 i 0.4 vs 1.4 f 0.5 cm* at 110 beats/min, 1.2 f 0. vs 1.4 f 0.4 cm* at 140 beats/min; p <0.05). Thus, loss of atrial kick may cause pulmonary congestion and reduced cardiac output in patients with MS, partly because of a decrease in effective mitral valve area. (Am J Cardiol 1986;57:403-407)
T
he occurrence of atria1 fibrillation with a rapid ventricular response in patients with mitral stenosis (MS] may be accompanied by symptoms of pulmonary congestion, owing to a reduced diastolic filling period or the loss of the end-diastolic left ventricular (LV) pressure increment because of the loss of atria1 contraction (atria1 kick]. Although previous investigators have
shown an increase in transmitral valve gradient and left atria1 pressure when the diastolic filling period is reduced during sinus tachycardia or atria1 pacing in patients with MS,lm3the importance of atria1 kick in these patients is controversial. Previous hemodynamic evaluations, performed before and after reversion of atria1 fibrillation to sinus rhythm, showed that sinus rhythm causes an increase or no change in cardiac output as well as an increase or decrease in left atria1 pressure.4-g Likewise, in studies using atria1 pacing and simultaneous atrioventricular pacing [to suppress atria1 kick], cardiac output increased or remained unchanged during atria1 pacing, in contrast to atrioventricular pacing. *JO Other studies in which different techniques were used indicate an important role for the atria in maintaining cardiac output.ll-l3 We undertook the present study to attempt to clarify the importance of an increase in heart rate and the loss of atria1
From the Department of Internal Medicine (Cardiology Division], University of Texas Health Science Center, Dallas, Texas. Dr. Nicod’s present address: Cardiology Division, University of California, 225 West Dickinson Street, San Diego, California 92103. Manuscript received April 8, 1985; revised manuscript received July 17,1985, accepted July 18,1985. Address for reprints: Brian G. Firth, MD, DPhil, Cardiology Division, L5.134, University of Texas Health Science Center, 5323 Harry Hines Boulevard, Dallas, Texas 75235. 403
404
ATRIAL
KICK IN MITRAL
STENOSIS
kick in patients with MS. In so doing, we tested the hypothesis that the loss of atria1 kick may decrease the effective mitral valve orifice area, thereby aggravating the hemodynamic derangement.
Methods Patient selection: The patient population consisted of 6 patients (2 men, 4 women, aged 37 f 9 years [mean f standard deviation]) referred for catheterization for the assessment of MS. All patients were in sinus rhythm and had pure MS without mitral regurgitation or involvement of other valves. All patients gave informed consent. Cardiac catheterization: A No. 7Fr thermodilution Swan-Ganz catheter was introduced via the right brachial vein and passed to the pulmonary artery. A No. 8Fr Brockenbrough catheter was passed from the right femoral vein to the left atrium by the standard transseptal technique .14Two No. 6Fr bipolar pacing catheters were introduced via the left femoral vein and positioned in the high right atrium and right ventricular apex. A No. 8Fr micromanometer-tipped pigtail catheter (Millar Instruments] was advanced from the right femoral artery to the left ventricle. Technique for multigated equilibrium gated blood pool scintigraphy: Multigated equilibrium blood pool imaging was performed using a technique combining both in vivo and in vitro labeling of red blood cells with 30 mCi of technetium-99m pertechnetate.15 Data were collected using a standard gamma scintillation camera (Ohio Nuclear Series 100) equipped with an all-purpose, parallel-hole collimator interfaced with a dedicated on-line computer system [Ohio Nuclear VIP 550). Energy discrimination was provided by a 20% window centered on the 140-keV photopeak. The studies were acquired in a left anterior oblique projection with caudal angulation adjusted to provide the best separation of the 2 ventricles and of the left atrium and ventricle. The LV ejection fraction, end-diastolic and end-systolic volumes were calculat-
*r
ed according to a nongeometric, count-related technique previously described. l6 Since each patient served as his or her own control, no attempt was made to correct for photon attenuation on an individual basis. Study protocol: The following hemodynamic variables were measured during sinus rhythm and after 1 minute of atria1 pacing (at 110 and 140 beats/min) and simultaneous atrioventricular pacing [at 110 and 140 beats/min): left atria1 pressure, LV pressure, cardiac output (by thermodilution] in triplicate, and LV volumes and ejection fraction (by radionuclide ventriculography). All hemodynamic measurements were performed during the 3 to 5 minutes required for scintigraphic data acquisition at each pacing level. At the conclusion of the hemodynamic study, an LV angiogram in the 30’ right anterior oblique projection, an aortic root angiogram (to exclude aortic regurgitation] and coronary arteriography were performed. In 3 patients, an LV angiogram was performed during atrioventricular simultaneous pacing at 110 beats/min to exclude pacing-induced mitral regurgitation. The mean mitral diastolic pressure gradient was calculated during sinus rhythm and at each pacing level from the average of 5 consecutive beats, from which the effective mitral valve orifice area was calculated according to the formula of Gorlin and Gorlin.17 Statistical analysis: All results are expressed as mean f standard deviation. For each variable, the data during the 5 acquisition periods were compared with a repeated-measures analysis of variance to determine whether some were different from others, after which the Newman-Keuls multiple comparison procedure was performed .18For all analyses, a p value
Results All patients had pure MS, no aortic or mitral regurgitation, and no coronary artery narrowing. One patient had fluoroscopic evidence of minimal mitral valve calcification. No patient developed second-de-
*
6
I
*
I I ----a_----a-, .----a--aaaaaaa, P 1.6
5
---a-_
1.2
4 I
)c
2.4
7
I-
I I
0.8
----a-_
I
, Imaaa---------P
32l0
n Atrial Pacing 0 AV Simultaneous Pacing += p< 0.05 for atria1 vs AV simultaneous
I Baseline
pacing
I IlO/min
I 1401
Baseline min
FIGURE 1. Effects of atrial pacing and atrioventricular (AV) simultaneous pacing at 110 and 140 beats/min on cardiac output.
1101 min
1401
min
FIGURE 2. Effects of atrial pacing and atrioventricular (AV) simultaneous pacing at 110 and 140 beats/min on effective mitral valve orifice area.
February 15, 3986
TABLE I
Effects of Atrial and Atrioventricular
Pt
1
HR (beats/min)
100 110
Pacing Mode
co (literslmin)
Simultaneous
Pacing on
LA (mm Hg)
LVEDP (mm Hg) 13 11 9 12 11
LA-LV Gradient (mm Hg)
THE AMERICAN
emo~yna~ic
JOURNAL
OF CAWIOLOGY
and Sciniigraphic
MV Area
Volume 57
405
Variables
LVEDV
LVESV
(cm’)
(ml)
(ml)
LVEF
Mean DFT (ms)
17 18 22 16
ia
1.1 1.3 1.2 1.0 0.9
128 123 87 105 71
62 61 50 55 39
0.51 0.51 0.41 0.47 0.44
306 248 172 250 la3
15 16 21 13 16
1.1 1.1 1.1 1.1 1.0
126 104 71 a3 55
49 36 34 34 24
0.60 0.61 0.51 0.57 0.55
338 224 148 233 176
11 12 18 13 20
2.1 2.3 2.1 1.9 1.8
62 44 32 27 23
19 13 IO
8
0.66 0.67 0.63 0.67 0.61
250 162 131 196 126
15 16 21 16 14
1.1 1.1 1.1 0.9 1.0
93 85 60 86 48
36 34 24 43 24
0.60 0.58 0.58 0.49 0.49
292 242 170 258 186
140 110 140
Sinus A A AV AV
5.3 5.6 5.2 4.1 3.7
26 26 30 33 36
2
82 110 140 108 134
Sinus A A AV AV
4.7 4.5 4.0 3.7 3.6
20 23 25 29 32
3
90 112 140 112 140
Sinus A A AV AV
6.1 6.1 a.3
22 14 22 28 25
92 110 140 110 140
Sinus A A AV AV
4.3 4.6 4.4 3.8 3.6
23 27
5
76 108 136 108 136
Sinus A A AV AV
3.3 4.2 4.5 3.7 3.4
23 23 30 28 30
12 6 9 10 7
IO 17 20 11 12
1.0 1.1 1.1 1.1 1.0
92 83 64 69 56
21 27 24 23 25
0.75 0.66 0.60 0.65 0.54
3ao 223 178 250 191
6
86 112 140 112 140
Sinus A A AV AV
6.7 5.9 6.1 5.1 5.4
21 18 22 28 31
4 4 2 3 4
15 14 21 14 19
1.6 1.6 1.8 1.4 1.5
137 118 77 93 68
51 56 40 43 36
0.62 0.52 0.47 0.52 0.46
352 226 139 227 151
Mean f SD
88 4 6a llOf2b 139 f 2c llOf2b 138 f 3c
Sinus A A AV AV
lOf5a 7 f 3a 7 * 4a 9 * 3a a i 3a
14 3~ 3a 16% 2a 21 f lb 14f2a 17 f 3a
4
5.8 5.4
5.1 5.2 5.1 4.4 4.2
f f f f -I
16 9 10 11 IO
16 15
ia
1.2a 0.8a 0.9a 0.9b 0.9b
21 20 25 28 30
f f f f f
3a 5a 5b 3c 4~
1.3 1.4 1.4 1.2 1.2
f k f f *
0.4ab 0.5a 0.4a 0.4bc 0.4c
106 93 65 77 54
f 29a zk29b L!Zl9c 4 27d f 17e
40 & 38 !C 30 f 34 & 26%
17a 18ab 14bc 17ab Ilc
0.62 0.59 0.53 0.56 0.52
f f f f f
o.oaa 0.07ab o.oac 0.08bc 0.06~
320 224 156 236 169
+ i: f f f
47a 23b 2Oc 23b 25~
Note: Absolute EDV and ESV may be in error due to a constant attenuation factor assumed for the radionuclide studies in all patients, but relative changes in any given individual are appropriate. Means marked with the same letter (a,b,c,etc) are statistically indistinguishable (p ZO.05); in turn, means marked with different letters are statistically distinguishable (p <0.05). A = atrial pacing; AV = atrioventricular simultaneous pacing: CO = cardiac output; DFT = diastolic filling time; EF = ejection fraction; HR = heart rate; LA = left atrial; LV = left ventricular; LVEDV = LV end-diastolic volume; LVESV = LV end-systolic volume; MV = mitral valve; SD = standard deviation.
gree atrioventricular block during atria1 pacing. In 3 patients in whom an LV angiogram was recorded during simultaneous atrioventricular pacing, pacing-induced mitral regurgitation was not present. Atria1 pacing: During atria1 pacing at 110 and 140 beats/min, cardiac output (Fig. 1) and mitral valve area (Fig. S] were similar to values at baseline (Table I], but at 140 beats/min left atria1 pressure (Fig. 3) and mean transmitral gradient [Table I] increased significantly. At the same time, LV end-diastolic volume and ejection fraction decreased. Atrioventricular simultaneous pacing: Compared with atria1 pacing, simultaneous atrioventricular pacing induced a decrease in cardiac output (Fig. 1, Table I] and effective mitral valve orifice area [Fig. 2, Table I]. Left atria1 pressure was higher during simultaneous atrioventricular pacing than during atria1 pacing at the same rate (Fig. 3). Representative pressure recordings from patient 5 are displayed in Figure 4.
Discussion In our patients with pure MS, atria1 pacing at 140 beats/min did not alter cardiac output from baseline sinus rhythm, but output was maintained during rapid atria1 pacing at the expense of an increased left atria1 pressure and transmitral pressure gradient (Table I]. These findings are similar to those reported previousl~.l-~ In addition, rapid atria1 pacing caused a decrease in LV end-diastolic volume and ejection fraction, the latter probably reflecting diminished preload rather than reduced contractility. Importance of atria1 kick in patients with mitral stenosis: The loss of atria1 kick during simultaneous atrioventricular pacing was associated with a decrease in cardiac output, effective mitral valve orifice area, and LV end-diastolic volume, in contrast to atria1 pacing at a similar rate. At the same time, left atria1 pressure increased, but transmitral valve pressure gradient
406
ATRIAL
KICK IN MITRAL
STENOSIS
*
10/’ I OL
Atrial Pacing 0 AV Simultaneous Pacing += p< 0.05 for atrial vs AV simultaneous n
I Baseline
, IlO/min
pacing I 1401
min
FIGURE 3. Effects of atrial pacing and atrioventricular (AV) simultaneous pacing at 110 and 140 beats/min on left atrial pressure.
was unchanged [at 110 beats/min) or reduced (at 140 beats/min). These data suggest that atria1 kick may be important in patients with MS. The ability of atria1 kick to maintain cardiac output in these patients was similar at 110 and 140 beats/min. Our observations are in agreement with those of Thompson et al,l but differ from those of Carleton et al.1° The decrease in LV enddiastolic volume during simultaneous atrioventricular pacing (compared with atria1 pacing at the same rate)
110 beats /minute
suggests that the decrease in cardiac output may be a result of decreased LV preload. Limitations of the study: This study has several limitations. First, we used simultaneous atrioventricular pacing to eliminate atria1 kick and to attempt to simulate atria1 fibrillation. Actually, simultaneous atrioventricular pacing probably simulates a junctional rhythm more closely than atria1 fibrillation. Although left atria1 cannon waves may contribute to the high mean pressure during this rhythm, the left atrial-LV diastolic pressure gradient is less during simultaneous atrioventricular pacing than during atria1 pacing at a similar rate (Table I). Second, in these 6 patients, the effective mitral valve areas during sinus rhythm were 1.0 to 2.1 cm2 (average 1.3 f 0.4) (Table I], and only 1 had fluoroscopic evidence of valvular calcification. Thus, most of these subjects had mild or moderate MS without calcification; as a result, they were likely to have relatively pliable valves capable of allowing an atria1 augmentation of LV filling. We do not know if similar events would occur in patients with heavily calcified and severely stenosed valves. Third, the formula of Gorlin and Gorlin17 uses the mean transmitral pressure gradient during diastole and the mean diastolic flow across the valve. Although this formula ideally should use instantaneous rather than average pressure-flow relations, it is not clinically feasible to measure instantaneous mitral valve flow. Therefore, alterations in the instantaneous pressureflow relation during simultaneous atrioventricular
140 beats/minute
FIGURE 4. Representative left atrial (LA) and left ventricular (LV) pressure recordings during atrial pacing and simultaneous atrioventricular pacing at 110 and 140 beats/min from patient 5. Note that the LA-LV diastolic pressure gradient is greater during atrial than during simultaneous atrioventricular pacing.
I
/ 0 1 Second
I
II
I
I ” I Second-
I
February 15, 1986
pacing (in contrast to atria1 pacing] may, in part, explain the difference in the calculated mitral valve orifice areas. Clinical implications: The loss of atria1 kick during atria1 fibrillation may be accompanied by a decrease in the effective mitral valve orifice area. Such changes in calculated valve area have been described during exercise in patients with aortic stenosis.lg Our observations are supported by those of Nakhjavan et a1,2who noted that the effective mitral valve area may vary with different hemodynamic conditions in patients with MS. Thus, the hemodynamic deterioration sometimes seen in patients with MS when atria1 fibrillation develops may be a result of 3 factors: a reduction in the diastolic filling period, a loss of atria1 kick, and a diminution in the effective mitral valve orifice area. Our findings await confirmation by a hemodynamic study in patients with MS who are evaluated in atria1 fibrillation and sinus rhythm with a short intervening time interval. Acknowledgment: The technical assistance of Randy Christian, Sara Hawkins, Nancy Smith and R. Scott Lyons is gratefully acknowledged. The expert secretarial assistance of Belinda Lambert and Rose Ruiz is greatly appreciated.
References 1. Thompson ME, Shaver JA, Leon DF. Effect of tachycardia on atrial transport in mitral stenosis. Am Heart r 1977;94:297-306. 2. Nakhiavan FK, Katz MR. Shedrovilzkv H. Maranhao V. Goldberg H. Hemodinamic effect of exercise, catecholamine stimulation and tachy&dia in mitral stenosis and sinus rhythm at comparable heart rates. Am 1 Cardiol
THE AMERICAN
JOURNAL
OF CARDIOLOGY
Volume 57
407
1969;23359-666.
3. Manchanda SC, Ramesh L, Roy SB. Hemodynamic effects of atriai pacing in rheumatic mitral stenosis. Br Heart J 1974;36:636-640. 4. Co&s RJ, McKenna DH, Crumpton CW. Rowe GC. Hemodynamic effects after conversion of arrhythmias. J CJin Invest 1968;47:1774-1786, 5. Shapiro W, Klein G. Alterations in cardiac function immediately following electrical conversion of atrial fibrillation to normal sinus rhythm. Circulation 1968;38:1074-1084. 8. Morris JJ, Entman M, North WC, Kong Y, McIntosh A. The changes in cardiac output with reversion of atrial fibrillation to sinus rhythm. Circulation 1965;31:670-678. 7. Graettinger JS, Carleton RA, Muenster JJ. Circulatory consequences of changes in cardiac rhythm produced in patients by transthorocic directcurrent shock. f CJin Invest 1964;43:2296-2392. 8. Killip T, Baer RA. Hemodynamic effects after reversion from atrial fibrillation to sinus rhythm by precordial shock. J CJin Invest 1966;45:658-671. 9. Rodman T, Pastor BH, Figueroa W. Effect on cardiac output of conversion from atrial fibrillation to normal sinus mechanism. Am J Med 1966; 41:249-258. 10. Carleton RA, Graettinger JS. The hemodynamic role of the atria with or without mitral stenosis. Am J Med 1967;42:532-538. 11. Heidenreich FP, Thompson ME, Shaver ]A, Leonard JJ.Left atrial transport in mitral stenosis. Circulation 1969;40:545-554. 12. Stott DK, Marple DGF, Bristow JD, Kloster FE, Griswold HE. The role of left atriai transport in aortic and mitral stenosis. Circulation 1970; 41:1031-1041. 13. Curry CL, Behar VS, McIntosh HD, Morris JJ,Kong Y. AtriaJ contraction in mitral stenosis. Circulation 1968;36:suppl IRIII-64. 14. Brockenbrough FC, Braunwald E. A new technique for left ventricular angiocordiography and transseptal catheterization. Am J CardioJ 1966; 6:1062-1064. 15. Froelich RJ. Callahan RJ, Leppo J. McKusick KA, Strauss HW. Time course of in vivo labeling of red blood ceils. J NucJ Med 1980;21:44. 16. Dehmer GJ, Lewis SE, Hillis LD, Twieg D, Falkoff M, Parkey RW, Willerson JT. Nongeometric determination of left ventricular volumes from equilibrium blood pool scans. Am J Cordial 1980;45:293-300. 17. Gorlin R, Gorlin SG. Hydraulic formula for calculation of the area of the stenotic mitral valve, other cardiac valves and central circulatory shunts. I. Am Heart J 1951;41:1-29. 18. Zar JH. Biostatistical Analysis. Engfewood Cliffs, NJ: Prentice-Hall, Inc., 197159-69. 19. Bathe RJ, Wang Y, Jorgensen CR. Hemodynamic effects of exercise in isolated valvufar aortic stenosis. Circulation 1971;44:1003-1013.
Importanceof the “Atrial Kick” in Determining the EffectiveMitral ValveOrifice Area in Mitral Stenosis PASCAL
NICOD, MD, L. DAVID HILLIS, MD, MICHAEL D. WINNIFORD, and BRIAN G. FIRTH, MD, DPhil
Atrial fibrillation with a rapid ventricular response in patients with mitral stenosis (MS) is often accompanied by pulmonary congestion and reduced cardiac output owing to a diminished diastolic filling period and the loss of the end-diastolic left ventricular (LV) pressure increment. To test the hypothesis that loss of atrial contraction (atrial kick) also results in a decrease in effective mitral valve orifice area, 6 patients with pure, isolated MS were studied in sinus rhythm during atrial pacing and simultaneous atrioventricular pacing. Atrial pacing at 140 beats/min caused no significant change from baseline in cardiac output or mitral valve area, but there was a decrease in LV end-diastolic volume and ejection fraction as well as an increase in left atrial pressure and mean diastolic gradient. Simultaneous atrioventricu-
MD,
lar pacing (to eliminate atrial kick) induced a decrease in cardiac output (4.4 f 0.9 vs 5.2 f 0.8 liters/min at 110 beats/min, 4.2 f 0.9 vs 5.1 f 0.9 liters/min at 140 beats/min; p <0.05) and LV end-diastolic volume (77 f 27 vs 93 f 29 ml at 110 beats/min, 54 f 17 vs 65 f 19 ml at 140 beats/min; p <0.05), an increase in left atrial pressure (28 f 3 vs 20 f 5 mm Hg at 110 beats/min, 30 f 4 vs 25 f 5 mm Hg at 140 beats/min; p <0.05), and a decrease in mitral valve area (1.2 i 0.4 vs 1.4 f 0.5 cm* at 110 beats/min, 1.2 f 0. vs 1.4 f 0.4 cm* at 140 beats/min; p <0.05). Thus, loss of atrial kick may cause pulmonary congestion and reduced cardiac output in patients with MS, partly because of a decrease in effective mitral valve area. (Am J Cardiol 1986;57:403-407)
T
he occurrence of atria1 fibrillation with a rapid ventricular response in patients with mitral stenosis (MS] may be accompanied by symptoms of pulmonary congestion, owing to a reduced diastolic filling period or the loss of the end-diastolic left ventricular (LV) pressure increment because of the loss of atria1 contraction (atria1 kick]. Although previous investigators have
shown an increase in transmitral valve gradient and left atria1 pressure when the diastolic filling period is reduced during sinus tachycardia or atria1 pacing in patients with MS,lm3the importance of atria1 kick in these patients is controversial. Previous hemodynamic evaluations, performed before and after reversion of atria1 fibrillation to sinus rhythm, showed that sinus rhythm causes an increase or no change in cardiac output as well as an increase or decrease in left atria1 pressure.4-g Likewise, in studies using atria1 pacing and simultaneous atrioventricular pacing [to suppress atria1 kick], cardiac output increased or remained unchanged during atria1 pacing, in contrast to atrioventricular pacing. *JO Other studies in which different techniques were used indicate an important role for the atria in maintaining cardiac output.ll-l3 We undertook the present study to attempt to clarify the importance of an increase in heart rate and the loss of atria1
From the Department of Internal Medicine (Cardiology Division], University of Texas Health Science Center, Dallas, Texas. Dr. Nicod’s present address: Cardiology Division, University of California, 225 West Dickinson Street, San Diego, California 92103. Manuscript received April 8, 1985; revised manuscript received July 17,1985, accepted July 18,1985. Address for reprints: Brian G. Firth, MD, DPhil, Cardiology Division, L5.134, University of Texas Health Science Center, 5323 Harry Hines Boulevard, Dallas, Texas 75235. 403
404
ATRIAL
KICK IN MITRAL
STENOSIS
kick in patients with MS. In so doing, we tested the hypothesis that the loss of atria1 kick may decrease the effective mitral valve orifice area, thereby aggravating the hemodynamic derangement.
Methods Patient selection: The patient population consisted of 6 patients (2 men, 4 women, aged 37 f 9 years [mean f standard deviation]) referred for catheterization for the assessment of MS. All patients were in sinus rhythm and had pure MS without mitral regurgitation or involvement of other valves. All patients gave informed consent. Cardiac catheterization: A No. 7Fr thermodilution Swan-Ganz catheter was introduced via the right brachial vein and passed to the pulmonary artery. A No. 8Fr Brockenbrough catheter was passed from the right femoral vein to the left atrium by the standard transseptal technique .14Two No. 6Fr bipolar pacing catheters were introduced via the left femoral vein and positioned in the high right atrium and right ventricular apex. A No. 8Fr micromanometer-tipped pigtail catheter (Millar Instruments] was advanced from the right femoral artery to the left ventricle. Technique for multigated equilibrium gated blood pool scintigraphy: Multigated equilibrium blood pool imaging was performed using a technique combining both in vivo and in vitro labeling of red blood cells with 30 mCi of technetium-99m pertechnetate.15 Data were collected using a standard gamma scintillation camera (Ohio Nuclear Series 100) equipped with an all-purpose, parallel-hole collimator interfaced with a dedicated on-line computer system [Ohio Nuclear VIP 550). Energy discrimination was provided by a 20% window centered on the 140-keV photopeak. The studies were acquired in a left anterior oblique projection with caudal angulation adjusted to provide the best separation of the 2 ventricles and of the left atrium and ventricle. The LV ejection fraction, end-diastolic and end-systolic volumes were calculat-
*r
ed according to a nongeometric, count-related technique previously described. l6 Since each patient served as his or her own control, no attempt was made to correct for photon attenuation on an individual basis. Study protocol: The following hemodynamic variables were measured during sinus rhythm and after 1 minute of atria1 pacing (at 110 and 140 beats/min) and simultaneous atrioventricular pacing [at 110 and 140 beats/min): left atria1 pressure, LV pressure, cardiac output (by thermodilution] in triplicate, and LV volumes and ejection fraction (by radionuclide ventriculography). All hemodynamic measurements were performed during the 3 to 5 minutes required for scintigraphic data acquisition at each pacing level. At the conclusion of the hemodynamic study, an LV angiogram in the 30’ right anterior oblique projection, an aortic root angiogram (to exclude aortic regurgitation] and coronary arteriography were performed. In 3 patients, an LV angiogram was performed during atrioventricular simultaneous pacing at 110 beats/min to exclude pacing-induced mitral regurgitation. The mean mitral diastolic pressure gradient was calculated during sinus rhythm and at each pacing level from the average of 5 consecutive beats, from which the effective mitral valve orifice area was calculated according to the formula of Gorlin and Gorlin.17 Statistical analysis: All results are expressed as mean f standard deviation. For each variable, the data during the 5 acquisition periods were compared with a repeated-measures analysis of variance to determine whether some were different from others, after which the Newman-Keuls multiple comparison procedure was performed .18For all analyses, a p value
Results All patients had pure MS, no aortic or mitral regurgitation, and no coronary artery narrowing. One patient had fluoroscopic evidence of minimal mitral valve calcification. No patient developed second-de-
*
6
I
*
I I ----a_----a-, .----a--aaaaaaa, P 1.6
5
---a-_
1.2
4 I
)c
2.4
7
I-
I I
0.8
----a-_
I
, Imaaa---------P
32l0
n Atrial Pacing 0 AV Simultaneous Pacing += p< 0.05 for atria1 vs AV simultaneous
I Baseline
pacing
I IlO/min
I 1401
Baseline min
FIGURE 1. Effects of atrial pacing and atrioventricular (AV) simultaneous pacing at 110 and 140 beats/min on cardiac output.
1101 min
1401
min
FIGURE 2. Effects of atrial pacing and atrioventricular (AV) simultaneous pacing at 110 and 140 beats/min on effective mitral valve orifice area.
February 15, 3986
TABLE I
Effects of Atrial and Atrioventricular
Pt
1
HR (beats/min)
100 110
Pacing Mode
co (literslmin)
Simultaneous
Pacing on
LA (mm Hg)
LVEDP (mm Hg) 13 11 9 12 11
LA-LV Gradient (mm Hg)
THE AMERICAN
emo~yna~ic
JOURNAL
OF CAWIOLOGY
and Sciniigraphic
MV Area
Volume 57
405
Variables
LVEDV
LVESV
(cm’)
(ml)
(ml)
LVEF
Mean DFT (ms)
17 18 22 16
ia
1.1 1.3 1.2 1.0 0.9
128 123 87 105 71
62 61 50 55 39
0.51 0.51 0.41 0.47 0.44
306 248 172 250 la3
15 16 21 13 16
1.1 1.1 1.1 1.1 1.0
126 104 71 a3 55
49 36 34 34 24
0.60 0.61 0.51 0.57 0.55
338 224 148 233 176
11 12 18 13 20
2.1 2.3 2.1 1.9 1.8
62 44 32 27 23
19 13 IO
8
0.66 0.67 0.63 0.67 0.61
250 162 131 196 126
15 16 21 16 14
1.1 1.1 1.1 0.9 1.0
93 85 60 86 48
36 34 24 43 24
0.60 0.58 0.58 0.49 0.49
292 242 170 258 186
140 110 140
Sinus A A AV AV
5.3 5.6 5.2 4.1 3.7
26 26 30 33 36
2
82 110 140 108 134
Sinus A A AV AV
4.7 4.5 4.0 3.7 3.6
20 23 25 29 32
3
90 112 140 112 140
Sinus A A AV AV
6.1 6.1 a.3
22 14 22 28 25
92 110 140 110 140
Sinus A A AV AV
4.3 4.6 4.4 3.8 3.6
23 27
5
76 108 136 108 136
Sinus A A AV AV
3.3 4.2 4.5 3.7 3.4
23 23 30 28 30
12 6 9 10 7
IO 17 20 11 12
1.0 1.1 1.1 1.1 1.0
92 83 64 69 56
21 27 24 23 25
0.75 0.66 0.60 0.65 0.54
3ao 223 178 250 191
6
86 112 140 112 140
Sinus A A AV AV
6.7 5.9 6.1 5.1 5.4
21 18 22 28 31
4 4 2 3 4
15 14 21 14 19
1.6 1.6 1.8 1.4 1.5
137 118 77 93 68
51 56 40 43 36
0.62 0.52 0.47 0.52 0.46
352 226 139 227 151
Mean f SD
88 4 6a llOf2b 139 f 2c llOf2b 138 f 3c
Sinus A A AV AV
lOf5a 7 f 3a 7 * 4a 9 * 3a a i 3a
14 3~ 3a 16% 2a 21 f lb 14f2a 17 f 3a
4
5.8 5.4
5.1 5.2 5.1 4.4 4.2
f f f f -I
16 9 10 11 IO
16 15
ia
1.2a 0.8a 0.9a 0.9b 0.9b
21 20 25 28 30
f f f f f
3a 5a 5b 3c 4~
1.3 1.4 1.4 1.2 1.2
f k f f *
0.4ab 0.5a 0.4a 0.4bc 0.4c
106 93 65 77 54
f 29a zk29b L!Zl9c 4 27d f 17e
40 & 38 !C 30 f 34 & 26%
17a 18ab 14bc 17ab Ilc
0.62 0.59 0.53 0.56 0.52
f f f f f
o.oaa 0.07ab o.oac 0.08bc 0.06~
320 224 156 236 169
+ i: f f f
47a 23b 2Oc 23b 25~
Note: Absolute EDV and ESV may be in error due to a constant attenuation factor assumed for the radionuclide studies in all patients, but relative changes in any given individual are appropriate. Means marked with the same letter (a,b,c,etc) are statistically indistinguishable (p ZO.05); in turn, means marked with different letters are statistically distinguishable (p <0.05). A = atrial pacing; AV = atrioventricular simultaneous pacing: CO = cardiac output; DFT = diastolic filling time; EF = ejection fraction; HR = heart rate; LA = left atrial; LV = left ventricular; LVEDV = LV end-diastolic volume; LVESV = LV end-systolic volume; MV = mitral valve; SD = standard deviation.
gree atrioventricular block during atria1 pacing. In 3 patients in whom an LV angiogram was recorded during simultaneous atrioventricular pacing, pacing-induced mitral regurgitation was not present. Atria1 pacing: During atria1 pacing at 110 and 140 beats/min, cardiac output (Fig. 1) and mitral valve area (Fig. S] were similar to values at baseline (Table I], but at 140 beats/min left atria1 pressure (Fig. 3) and mean transmitral gradient [Table I] increased significantly. At the same time, LV end-diastolic volume and ejection fraction decreased. Atrioventricular simultaneous pacing: Compared with atria1 pacing, simultaneous atrioventricular pacing induced a decrease in cardiac output (Fig. 1, Table I] and effective mitral valve orifice area [Fig. 2, Table I]. Left atria1 pressure was higher during simultaneous atrioventricular pacing than during atria1 pacing at the same rate (Fig. 3). Representative pressure recordings from patient 5 are displayed in Figure 4.
Discussion In our patients with pure MS, atria1 pacing at 140 beats/min did not alter cardiac output from baseline sinus rhythm, but output was maintained during rapid atria1 pacing at the expense of an increased left atria1 pressure and transmitral pressure gradient (Table I]. These findings are similar to those reported previousl~.l-~ In addition, rapid atria1 pacing caused a decrease in LV end-diastolic volume and ejection fraction, the latter probably reflecting diminished preload rather than reduced contractility. Importance of atria1 kick in patients with mitral stenosis: The loss of atria1 kick during simultaneous atrioventricular pacing was associated with a decrease in cardiac output, effective mitral valve orifice area, and LV end-diastolic volume, in contrast to atria1 pacing at a similar rate. At the same time, left atria1 pressure increased, but transmitral valve pressure gradient
406
ATRIAL
KICK IN MITRAL
STENOSIS
*
10/’ I OL
Atrial Pacing 0 AV Simultaneous Pacing += p< 0.05 for atrial vs AV simultaneous n
I Baseline
, IlO/min
pacing I 1401
min
FIGURE 3. Effects of atrial pacing and atrioventricular (AV) simultaneous pacing at 110 and 140 beats/min on left atrial pressure.
was unchanged [at 110 beats/min) or reduced (at 140 beats/min). These data suggest that atria1 kick may be important in patients with MS. The ability of atria1 kick to maintain cardiac output in these patients was similar at 110 and 140 beats/min. Our observations are in agreement with those of Thompson et al,l but differ from those of Carleton et al.1° The decrease in LV enddiastolic volume during simultaneous atrioventricular pacing (compared with atria1 pacing at the same rate)
110 beats /minute
suggests that the decrease in cardiac output may be a result of decreased LV preload. Limitations of the study: This study has several limitations. First, we used simultaneous atrioventricular pacing to eliminate atria1 kick and to attempt to simulate atria1 fibrillation. Actually, simultaneous atrioventricular pacing probably simulates a junctional rhythm more closely than atria1 fibrillation. Although left atria1 cannon waves may contribute to the high mean pressure during this rhythm, the left atrial-LV diastolic pressure gradient is less during simultaneous atrioventricular pacing than during atria1 pacing at a similar rate (Table I). Second, in these 6 patients, the effective mitral valve areas during sinus rhythm were 1.0 to 2.1 cm2 (average 1.3 f 0.4) (Table I], and only 1 had fluoroscopic evidence of valvular calcification. Thus, most of these subjects had mild or moderate MS without calcification; as a result, they were likely to have relatively pliable valves capable of allowing an atria1 augmentation of LV filling. We do not know if similar events would occur in patients with heavily calcified and severely stenosed valves. Third, the formula of Gorlin and Gorlin17 uses the mean transmitral pressure gradient during diastole and the mean diastolic flow across the valve. Although this formula ideally should use instantaneous rather than average pressure-flow relations, it is not clinically feasible to measure instantaneous mitral valve flow. Therefore, alterations in the instantaneous pressureflow relation during simultaneous atrioventricular
140 beats/minute
FIGURE 4. Representative left atrial (LA) and left ventricular (LV) pressure recordings during atrial pacing and simultaneous atrioventricular pacing at 110 and 140 beats/min from patient 5. Note that the LA-LV diastolic pressure gradient is greater during atrial than during simultaneous atrioventricular pacing.
I
/ 0 1 Second
I
II
I
I ” I Second-
I
February 15, 1986
pacing (in contrast to atria1 pacing] may, in part, explain the difference in the calculated mitral valve orifice areas. Clinical implications: The loss of atria1 kick during atria1 fibrillation may be accompanied by a decrease in the effective mitral valve orifice area. Such changes in calculated valve area have been described during exercise in patients with aortic stenosis.lg Our observations are supported by those of Nakhjavan et a1,2who noted that the effective mitral valve area may vary with different hemodynamic conditions in patients with MS. Thus, the hemodynamic deterioration sometimes seen in patients with MS when atria1 fibrillation develops may be a result of 3 factors: a reduction in the diastolic filling period, a loss of atria1 kick, and a diminution in the effective mitral valve orifice area. Our findings await confirmation by a hemodynamic study in patients with MS who are evaluated in atria1 fibrillation and sinus rhythm with a short intervening time interval. Acknowledgment: The technical assistance of Randy Christian, Sara Hawkins, Nancy Smith and R. Scott Lyons is gratefully acknowledged. The expert secretarial assistance of Belinda Lambert and Rose Ruiz is greatly appreciated.
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JOURNAL
OF CARDIOLOGY
Volume 57
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1969;23359-666.
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