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Skeletal muscle hypoperfusion during recovery from maximal supine bicycle exercise in patients with heart failure
Skeletal Muscle Hypoperfusion During Recovery from Maximal Supine Bicycle Exercise in Patients With Heart Failure Tsutomu
Sumimoto, MD, Mutsuhito Kaida, MD, Fumio Yuasa, MD, Toshimitsu Jikuhara, MD, Makoto Hikosaka, MD, Masayuki Tetsuro Sugiura, MD, and Toshiji iwasaka,
n patients with heart failure, skeletal muscle hyduring exercise is known to be the Imajorpoperfusion factor causing early skeletal muscle anaeroand limiting exercise perforbic metabolism’-3 mance. 4-‘2 Recent studies of heart failure5,6.13J4 have demonstrated that impaired skeletal muscle vasodilation has an important role in reducing skeletal muscle perfusion during exercise, which functions to maintain blood flow to the nonexercising vital regions under condition of low cardiac output. During recovery from dynamic exercise, peripheral hypoperfusion is also responsible for the prolonged rate of exercise recovery with profound or sustained skeletal muscle fatigue in heart failure, I5916but its specific mechanism has not been completely elucidated. Thus, the present study examined leg blood flow (LBF) in relation to central hemodynamic responses during recovery following maximal supine bicycle exercise in heart failure. . . . We evaluated 57 consecutive male patients with recent myocardial infarction, who had patent infarctrelated coronary arteries with negative exercise test results. None of the patients had obstructive lung disease, mitral regurgitation, or intermittent claudication. Of these, 11 patients with heart failure were selected on the basis of both left ventricular dysfunction (ejection fraction ~35%) and exercise impairment (peak oxygen consumption < 18 ml/min/ kg) 4. Twenty patients with normal exercise capacity (peak oxygen consumption 220 ml/min/kg) were also selected.’ Informed consent was obtained and all medications were discontinued for 48 hours before the study. Supine bicycle exercise was performed with expired gas analysis (Oxycon-4, Mijnhardt Company, Bunnik, Holland) and the insertions of a 7Fr SwanGanz catheter into the pulmonary artery, a short polyethylene catheter into the radial artery, and a 5Fr thermodilution catheter into the iliac vein. Exercise began at a workload of 15 W and increased by 15 W every 3 minutes until exhaustion. Measurements of expired gases, hemodynamics, and arterial plasma norepinephrine were obtained at rest, at peak exercise, and at 2 and 5 minutes of recovery. Femoral venous flow (LBF) was determined by from the Second Department of Internal Medicine, Kansai Medical University, Osaka, Japan. Dr. Sumimoto’s address is. CCU, Kansoi Medical University, lo-15 F umizono-cho, Moriguchi City, Osaka 570, Japan. Manuscript received January 29, 1996; revised manuscript received and accepted April 19, 1996.
0 1996 by Excerpta All rights reserved.
Medico,
Inc.
Toshihiko Motohiro,
Hat-tori,
MD,
MD,
MD
thermodilution technique.17-19 Cardiac output was determined by the Fick principle. From these data, nonleg blood flow (nonLBF), the percentage of cardiac output distributed to the legs, and leg vascular resistance were calculated using previously described formulas.’ All data are presented as mean t SD. Intergroup comparisons of variables were made using the Wilcoxon rank sum test. The least-squares regression was used to assess the relationship between the 2 variables. Probability values <0.05 were considered to be significant. Table I demonstrates clinical characteristics and ergometric data at peak exercise in heart failure and normal capacity. The bicycle exercise was primarily limited by muscle fatigue in all patients. None of the patients developed angina or ischemic ST segment changes during exercise and recovery. There were no significant differences in central and peripheral hemodynamics at rest between the 2 groups (Figures 1 and 2). At peak exercise and recovery, cardiac output was significantly lower and systemic vascular resistance significantly higher in heart failure than those with normal capacity. Mean arterial blood pressure was significantly lower at peak exercise, reflecting the reduced cardiac output response in heart failure, but was not different be-
TABLE I Clinical
Characteristics
and
Ergometric
Data
at Peak
Exercise Heart
Failure*
[n=
Age (~4 Body weight
Normal
11)
Capacity’ p Value
(n = 20)
52? 11 62 2 9
50 63
24 22 6 522 13
482 80?
NS
2 8 ? 8
NS
kl
LVEF (%) Exercise
workload (W) Exercise time
565
+- 153
w Oxygen
14.5
i
consumption (ml/min/kg] Minutes
43+-
1.8
913 22.0
10
56
CO.01 CO.01
14 17 ? 197
f
co.01
1.9
2 11
-Co.01
ventilation
(l/min) Respiratory exchange
gas
1.07
2 0.08
1.08
t
0.06
NS
ratio * Heart failure = peak oxygen consumption < 18 ml/min/kg. ’ Normal capacity = peak oxygen consumption 220 ml/min/kg. LVEF = left ventricular ejection fraction.
0002.9 PII SOOO2-9
149/96/S 149(96)0042
15.00 1-3
84 1
A
A
II
/?---?I
l
_ “O”l
nest
D
P.rk Rxorcis.
Rest
R~COVwy
R8CW.ry
2 min
5 nin
*
~0.01,
corgarm.3
with
no-l.
**
wo.05.
colparul
with
norrul,
L
J
FIGURE 1. Comparison of /A) cardiac norepinephrine between heart failure recovery-period.
output, [open
(tl) systemic vascular resistance, (Cl mean arterial blood pressure, and (D] plasma circles) and normal capacity (closed circlesj at rest, at peak exercise, and in the
B
A
ti:‘I;;II
il’.’A 500-c PIs .: a 8400. ‘,> .-I . ~,,,I 3
80 L
f 2 k,:_
t
z 40 2 m
c
200
: z
60
z
loo-
cn 3
0
,
0
*
p
**
p
ca&mr.d cwrsd
with with
norm&m normals
FIGURE 2. Comparison of (A) leg blood flow, (6) nonleg blood Row, [Cl leg vascular resistance, and the percentage ot cardiac output distributed to the legs ID) between heart failure (open circles) and normal capacity (closed cirdesj at rest, at peak exercise, and in the recovery period.
tween the 2 groups at 2 and 5 minutes of recovery. At peak exercise and recovery, LBF was markedly reduced in heart failure, whereas nonLBF was maintained identically in both groups. Leg vascular resistance was significantly higher and the percentage of 842
THE AMERICAN
JOURNAL
OF
CARDIOLOGY@
VOL.
78
cardiac output distributed to cantly lower at peak exercise failure than those with normal epinephrine was significantly failure, but was not different OCTOBER
1, 1996
the legs was signifiand recovery in heart capacity. Plasma norhigher at rest in heart between the 2 groups
extraction after exercise was speculated to be primarily caused by en0.6 hanced peripheral vasoconstriction * that maintained arterial blood pressure under condition of low cardiac output.15 This observation supports the concept of Zelis et a1,1.1,14emr=O 86 phasizing that enhanced skeletal n
goI:O, rl
.
,NS
61 B
I
,I[
:--
BRIEF REPORTS
843
5. Sullivan MI, Knight D, Higginbotham MB, Cobb FR. Relation between central and peripheral hemodynamics during exercise in patients with chronic heart failure: muscle blood flow is reduced with maintenance of arterial perfusion pressure. Circulation 1989;80:769-781, 6. Zelis R, Longhurst J, Capone RJ, Mason DT. A comparison of regional blood flow and oxygen utilization during dynamic forearm exercise in normal subjects and patients with congestive heart failure. Circularion 1974; 50:137-143. 7. Longhurst J, Gifford W, Zelis R. Impaired forearm oxygen consumption during static exercise in patients with congestive heart failure. Circulation 1976;54:477-480. 8. Franciosa JA, Ziesche S, Wilen M. Functional capacity of patients with chronic left ventricular failure: relationship of bicycle exercise performance to clinical and hemodynamic characterization. Am J Med 1979;67:460-466. 9. Weber KT, Kinasewitz GT, Janicki JS, Fishman AP. Oxygen utilization and ventilation during exercise in patients with chronic cardiac failure. Circulation 1982;65:1218-1223. 10. Wilson JR, Ferraro N. Exercise intolerance in patients with chronic left heart failure: relationship to oxygen transport and ventilatory abnormalities. Am J Cardiol 1983;51:1358-1363. 11. Wilson JR, Martin JL, Ferraro N. Impaired skeletal muscle nutritive Row during exercise in patients with congestive heart failure: mie of cardiac pump dysfunction as determined by the effect of dobutamine. Am J Cardiol 1984;53:1308-1315, 12. Lejemtel TH, Maskin CS, Lucido D, Chadwick BL. Failure to augment
maximal limb blood flow in response to one-leg versus two-leg exercise in patients with severe heart failure. Circulation 1986;74:245-251. 13. Zelis R, Flaim SF. Alteration in vasomotor tone in congestive heart failure. Prog Cardiovasc Dis 1982;24:437-459. 14. Zelis R, Longhurst J, Capone RJ, Lee G. Peripheral circulatory control mechanisms in congestive heart failure. Am J Cardiol 1973;32:481-490. 15. Sumimoto T, Sugiura T, Takeuchi M, Yuasa F, Iwasaka T, Inada M. Overshoot in mixed venous oxygen saturation during recovery from supine bicycle exercise in patients with recent myocardial infarction. Chesr 1993; 103:514520. 16. Blair DA, Glover WE, Roddie IC. The abolition of reactive and post-exercise hyperemia in the forearm by temporaly restriction of arterial inflow. J Physiol 1959; 148:648-658. 17. Wilson JR, Martin JL, Ferraro N, Weber KT. Effect of hydralazine on perfusion and metabolism in the leg during upright bicycle exercise in patients with heart failure. Circularion 1983;68:425-432. 18. Jorfeldt L, Jublin-Dannfelt A, Pemow B, Wassen E. Determination of human leg blood flow: a thermodilution technique based on femoral venous bolus injection. Clin Sci Mel Med 1968;54:517-523. 19. Jorfeldt L, Wahren J. Leg blood flow during exercise in men. Clin Sci 1971;41:459-473. 20. Sumimoto T, Sugiura T, Takeuchi M, Yuasa F, Hasegawa T, Nakamura S, Iwasaka T, Inada M. Oxygen utilization, carbon dioxide elimination and ventilation during recovery from supine bicycle exercise six to eight weeks after acute myocardial infarction. Am J Cardiol 1991;67:1170-1174.
e Function as a Risk importance of Left Atria1 Appenda ?ism in Patients With Factor for Systemic Thromboembo Rheumatic Mitral Valve Disease Yi-Heng
Li, MD, Juey-Jen Hwang, MD, Jiunn-Lee Lin, MD, Yung-Zu Tseng, MD, and Wen-Pin Lien, MD
eripheral arterial embolization is a serious comP plication of rheumatic mitral valve disease. There was a 17-fold increase in the rate of embolic stroke in patients with mitral stenosis and atria1 fibrillation.’ Previous reports 2-4 have demonstrated that left atria1 (LA) spontaneous echo contrast is an independent predictor of systemic embolism in patients with rheumatic mitral valve disease. Because of the predilection of both spontaneous echo contrast and thrombus to form in the LA appendage, the size and contractile function of the appendage may also be important determinants of thromboembolic risk. For many years, however, direct evidence has been limited and controversia15-’ with regard to the incidence of embolization and LA appendage size and contractile function. We therefore undertook an investigation to assess the clinical and echocardiographic characteristics, particularly LA appendage size and function, in a series of patients with rheumatic mitral valve disease and examined the relation between these characteristics and risk of systemic thromboembolism in these patients. . . . In a 3-year period, 156 consecutive patients with rheumatic mitral valve disease, including native miFrom the Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan, and Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan. This study was supported by Grant NTUH-85 196-A38 from the National Taiwan Universi Hospital, Taipei, Taiwan. Dr. Hwang’s address is: Department o “i Internal Medicine, National Taiwan University Hospital, 7 Chung-Shan South Road, Taipei, Taiwan.
844
THE
AMERICAN
JOURNAL
OF
CARDIOLOGY@
VOL.
78
tral valve and mitral valve replacement with a xenograft, were studied with echocardiography. In all patients, rheumatic mitral valve disease was mainly diagnosed by clinical, electrocardiographic, radiologic, and echocardiographic examinations. There were 55 men and 101 women, aged 22 to 85 years (mean + SD 50 2 14). Twenty-one patients had xenografts at the mitral position and developed xenograft dysfunction. At the time of echocardiographic study, 50 patients had sinus rhythm and the other 106 had atria1 fibrillation. Only 26 patients were receiving anticoagulation treatment with warfarin during the echocardiographic examinations, and all were associated with previous embolism. The histories and hospital records of all studied patients were reviewed in detail, and any event of arterial embolization was carefully searched. All embolic events should be documented by computed tomography of the head and angiographic or surgical findings of the peripheral artery in addition to typical clinical symptomatology. All patients underwent transthoracic M-mode, 2-dimensional, and Doppler echocardiography before transesophageal study with a 2.5-MHz transducer connected to the Aloka SSD 870 ultrasound system (Aloka Corp. Ltd., Tokyo, Japan). Left ventricular end-diastolic and end-systolic and LA dimensions were determined according to the standard M-mode criteria of the American Society of Echocardiography.’ Left ventricular ejection fraction was calculated by the method developed by Teichholz et al.” Mitral valve area was determined OCTOBER
1,
1996
Sumimoto, MD, Mutsuhito Kaida, MD, Fumio Yuasa, MD, Toshimitsu Jikuhara, MD, Makoto Hikosaka, MD, Masayuki Tetsuro Sugiura, MD, and Toshiji iwasaka,
n patients with heart failure, skeletal muscle hyduring exercise is known to be the Imajorpoperfusion factor causing early skeletal muscle anaeroand limiting exercise perforbic metabolism’-3 mance. 4-‘2 Recent studies of heart failure5,6.13J4 have demonstrated that impaired skeletal muscle vasodilation has an important role in reducing skeletal muscle perfusion during exercise, which functions to maintain blood flow to the nonexercising vital regions under condition of low cardiac output. During recovery from dynamic exercise, peripheral hypoperfusion is also responsible for the prolonged rate of exercise recovery with profound or sustained skeletal muscle fatigue in heart failure, I5916but its specific mechanism has not been completely elucidated. Thus, the present study examined leg blood flow (LBF) in relation to central hemodynamic responses during recovery following maximal supine bicycle exercise in heart failure. . . . We evaluated 57 consecutive male patients with recent myocardial infarction, who had patent infarctrelated coronary arteries with negative exercise test results. None of the patients had obstructive lung disease, mitral regurgitation, or intermittent claudication. Of these, 11 patients with heart failure were selected on the basis of both left ventricular dysfunction (ejection fraction ~35%) and exercise impairment (peak oxygen consumption < 18 ml/min/ kg) 4. Twenty patients with normal exercise capacity (peak oxygen consumption 220 ml/min/kg) were also selected.’ Informed consent was obtained and all medications were discontinued for 48 hours before the study. Supine bicycle exercise was performed with expired gas analysis (Oxycon-4, Mijnhardt Company, Bunnik, Holland) and the insertions of a 7Fr SwanGanz catheter into the pulmonary artery, a short polyethylene catheter into the radial artery, and a 5Fr thermodilution catheter into the iliac vein. Exercise began at a workload of 15 W and increased by 15 W every 3 minutes until exhaustion. Measurements of expired gases, hemodynamics, and arterial plasma norepinephrine were obtained at rest, at peak exercise, and at 2 and 5 minutes of recovery. Femoral venous flow (LBF) was determined by from the Second Department of Internal Medicine, Kansai Medical University, Osaka, Japan. Dr. Sumimoto’s address is. CCU, Kansoi Medical University, lo-15 F umizono-cho, Moriguchi City, Osaka 570, Japan. Manuscript received January 29, 1996; revised manuscript received and accepted April 19, 1996.
0 1996 by Excerpta All rights reserved.
Medico,
Inc.
Toshihiko Motohiro,
Hat-tori,
MD,
MD,
MD
thermodilution technique.17-19 Cardiac output was determined by the Fick principle. From these data, nonleg blood flow (nonLBF), the percentage of cardiac output distributed to the legs, and leg vascular resistance were calculated using previously described formulas.’ All data are presented as mean t SD. Intergroup comparisons of variables were made using the Wilcoxon rank sum test. The least-squares regression was used to assess the relationship between the 2 variables. Probability values <0.05 were considered to be significant. Table I demonstrates clinical characteristics and ergometric data at peak exercise in heart failure and normal capacity. The bicycle exercise was primarily limited by muscle fatigue in all patients. None of the patients developed angina or ischemic ST segment changes during exercise and recovery. There were no significant differences in central and peripheral hemodynamics at rest between the 2 groups (Figures 1 and 2). At peak exercise and recovery, cardiac output was significantly lower and systemic vascular resistance significantly higher in heart failure than those with normal capacity. Mean arterial blood pressure was significantly lower at peak exercise, reflecting the reduced cardiac output response in heart failure, but was not different be-
TABLE I Clinical
Characteristics
and
Ergometric
Data
at Peak
Exercise Heart
Failure*
[n=
Age (~4 Body weight
Normal
11)
Capacity’ p Value
(n = 20)
52? 11 62 2 9
50 63
24 22 6 522 13
482 80?
NS
2 8 ? 8
NS
kl
LVEF (%) Exercise
workload (W) Exercise time
565
+- 153
w Oxygen
14.5
i
consumption (ml/min/kg] Minutes
43+-
1.8
913 22.0
10
56
CO.01 CO.01
14 17 ? 197
f
co.01
1.9
2 11
-Co.01
ventilation
(l/min) Respiratory exchange
gas
1.07
2 0.08
1.08
t
0.06
NS
ratio * Heart failure = peak oxygen consumption < 18 ml/min/kg. ’ Normal capacity = peak oxygen consumption 220 ml/min/kg. LVEF = left ventricular ejection fraction.
0002.9 PII SOOO2-9
149/96/S 149(96)0042
15.00 1-3
84 1
A
A
II
/?---?I
l
_ “O”l
nest
D
P.rk Rxorcis.
Rest
R~COVwy
R8CW.ry
2 min
5 nin
*
~0.01,
corgarm.3
with
no-l.
**
wo.05.
colparul
with
norrul,
L
J
FIGURE 1. Comparison of /A) cardiac norepinephrine between heart failure recovery-period.
output, [open
(tl) systemic vascular resistance, (Cl mean arterial blood pressure, and (D] plasma circles) and normal capacity (closed circlesj at rest, at peak exercise, and in the
B
A
ti:‘I;;II
il’.’A 500-c PIs .: a 8400. ‘,> .-I . ~,,,I 3
80 L
f 2 k,:_
t
z 40 2 m
c
200
: z
60
z
loo-
cn 3
0
,
0
*
p
**
p
ca&mr.d cwrsd
with with
norm&m normals
FIGURE 2. Comparison of (A) leg blood flow, (6) nonleg blood Row, [Cl leg vascular resistance, and the percentage ot cardiac output distributed to the legs ID) between heart failure (open circles) and normal capacity (closed cirdesj at rest, at peak exercise, and in the recovery period.
tween the 2 groups at 2 and 5 minutes of recovery. At peak exercise and recovery, LBF was markedly reduced in heart failure, whereas nonLBF was maintained identically in both groups. Leg vascular resistance was significantly higher and the percentage of 842
THE AMERICAN
JOURNAL
OF
CARDIOLOGY@
VOL.
78
cardiac output distributed to cantly lower at peak exercise failure than those with normal epinephrine was significantly failure, but was not different OCTOBER
1, 1996
the legs was signifiand recovery in heart capacity. Plasma norhigher at rest in heart between the 2 groups
extraction after exercise was speculated to be primarily caused by en0.6 hanced peripheral vasoconstriction * that maintained arterial blood pressure under condition of low cardiac output.15 This observation supports the concept of Zelis et a1,1.1,14emr=O 86 phasizing that enhanced skeletal n
goI:O, rl
.
,NS
61 B
I
,I[
:--
BRIEF REPORTS
843
5. Sullivan MI, Knight D, Higginbotham MB, Cobb FR. Relation between central and peripheral hemodynamics during exercise in patients with chronic heart failure: muscle blood flow is reduced with maintenance of arterial perfusion pressure. Circulation 1989;80:769-781, 6. Zelis R, Longhurst J, Capone RJ, Mason DT. A comparison of regional blood flow and oxygen utilization during dynamic forearm exercise in normal subjects and patients with congestive heart failure. Circularion 1974; 50:137-143. 7. Longhurst J, Gifford W, Zelis R. Impaired forearm oxygen consumption during static exercise in patients with congestive heart failure. Circulation 1976;54:477-480. 8. Franciosa JA, Ziesche S, Wilen M. Functional capacity of patients with chronic left ventricular failure: relationship of bicycle exercise performance to clinical and hemodynamic characterization. Am J Med 1979;67:460-466. 9. Weber KT, Kinasewitz GT, Janicki JS, Fishman AP. Oxygen utilization and ventilation during exercise in patients with chronic cardiac failure. Circulation 1982;65:1218-1223. 10. Wilson JR, Ferraro N. Exercise intolerance in patients with chronic left heart failure: relationship to oxygen transport and ventilatory abnormalities. Am J Cardiol 1983;51:1358-1363. 11. Wilson JR, Martin JL, Ferraro N. Impaired skeletal muscle nutritive Row during exercise in patients with congestive heart failure: mie of cardiac pump dysfunction as determined by the effect of dobutamine. Am J Cardiol 1984;53:1308-1315, 12. Lejemtel TH, Maskin CS, Lucido D, Chadwick BL. Failure to augment
maximal limb blood flow in response to one-leg versus two-leg exercise in patients with severe heart failure. Circulation 1986;74:245-251. 13. Zelis R, Flaim SF. Alteration in vasomotor tone in congestive heart failure. Prog Cardiovasc Dis 1982;24:437-459. 14. Zelis R, Longhurst J, Capone RJ, Lee G. Peripheral circulatory control mechanisms in congestive heart failure. Am J Cardiol 1973;32:481-490. 15. Sumimoto T, Sugiura T, Takeuchi M, Yuasa F, Iwasaka T, Inada M. Overshoot in mixed venous oxygen saturation during recovery from supine bicycle exercise in patients with recent myocardial infarction. Chesr 1993; 103:514520. 16. Blair DA, Glover WE, Roddie IC. The abolition of reactive and post-exercise hyperemia in the forearm by temporaly restriction of arterial inflow. J Physiol 1959; 148:648-658. 17. Wilson JR, Martin JL, Ferraro N, Weber KT. Effect of hydralazine on perfusion and metabolism in the leg during upright bicycle exercise in patients with heart failure. Circularion 1983;68:425-432. 18. Jorfeldt L, Jublin-Dannfelt A, Pemow B, Wassen E. Determination of human leg blood flow: a thermodilution technique based on femoral venous bolus injection. Clin Sci Mel Med 1968;54:517-523. 19. Jorfeldt L, Wahren J. Leg blood flow during exercise in men. Clin Sci 1971;41:459-473. 20. Sumimoto T, Sugiura T, Takeuchi M, Yuasa F, Hasegawa T, Nakamura S, Iwasaka T, Inada M. Oxygen utilization, carbon dioxide elimination and ventilation during recovery from supine bicycle exercise six to eight weeks after acute myocardial infarction. Am J Cardiol 1991;67:1170-1174.
e Function as a Risk importance of Left Atria1 Appenda ?ism in Patients With Factor for Systemic Thromboembo Rheumatic Mitral Valve Disease Yi-Heng
Li, MD, Juey-Jen Hwang, MD, Jiunn-Lee Lin, MD, Yung-Zu Tseng, MD, and Wen-Pin Lien, MD
eripheral arterial embolization is a serious comP plication of rheumatic mitral valve disease. There was a 17-fold increase in the rate of embolic stroke in patients with mitral stenosis and atria1 fibrillation.’ Previous reports 2-4 have demonstrated that left atria1 (LA) spontaneous echo contrast is an independent predictor of systemic embolism in patients with rheumatic mitral valve disease. Because of the predilection of both spontaneous echo contrast and thrombus to form in the LA appendage, the size and contractile function of the appendage may also be important determinants of thromboembolic risk. For many years, however, direct evidence has been limited and controversia15-’ with regard to the incidence of embolization and LA appendage size and contractile function. We therefore undertook an investigation to assess the clinical and echocardiographic characteristics, particularly LA appendage size and function, in a series of patients with rheumatic mitral valve disease and examined the relation between these characteristics and risk of systemic thromboembolism in these patients. . . . In a 3-year period, 156 consecutive patients with rheumatic mitral valve disease, including native miFrom the Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan, and Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan. This study was supported by Grant NTUH-85 196-A38 from the National Taiwan Universi Hospital, Taipei, Taiwan. Dr. Hwang’s address is: Department o “i Internal Medicine, National Taiwan University Hospital, 7 Chung-Shan South Road, Taipei, Taiwan.
844
THE
AMERICAN
JOURNAL
OF
CARDIOLOGY@
VOL.
78
tral valve and mitral valve replacement with a xenograft, were studied with echocardiography. In all patients, rheumatic mitral valve disease was mainly diagnosed by clinical, electrocardiographic, radiologic, and echocardiographic examinations. There were 55 men and 101 women, aged 22 to 85 years (mean + SD 50 2 14). Twenty-one patients had xenografts at the mitral position and developed xenograft dysfunction. At the time of echocardiographic study, 50 patients had sinus rhythm and the other 106 had atria1 fibrillation. Only 26 patients were receiving anticoagulation treatment with warfarin during the echocardiographic examinations, and all were associated with previous embolism. The histories and hospital records of all studied patients were reviewed in detail, and any event of arterial embolization was carefully searched. All embolic events should be documented by computed tomography of the head and angiographic or surgical findings of the peripheral artery in addition to typical clinical symptomatology. All patients underwent transthoracic M-mode, 2-dimensional, and Doppler echocardiography before transesophageal study with a 2.5-MHz transducer connected to the Aloka SSD 870 ultrasound system (Aloka Corp. Ltd., Tokyo, Japan). Left ventricular end-diastolic and end-systolic and LA dimensions were determined according to the standard M-mode criteria of the American Society of Echocardiography.’ Left ventricular ejection fraction was calculated by the method developed by Teichholz et al.” Mitral valve area was determined OCTOBER
1,
1996