- Email: [email protected]
Skeletal Muscle Atrophy and Peak Oxygen Consumption in Heart Failure
Skeletal Muscle Atrophy and Peak Oxygen Consumption in Heart Failure Michael J. Toth,
PhD,
Stephen S. Gottlieb,
MD,
Michael L. Fisher,
educed peak oxygen consumption (peak VO ) is a hallmark of chronic heart failure. Skeletal musR cle atrophy may contribute to reduced peak VO . 2
1
2
Examination of skeletal muscle atrophy and its contribution to reduced exercise capacity in patients with heart failure has been limited by the lack of reliable techniques to measure skeletal muscle mass. Dual energy x-ray absorptiometry is a promising technique for the in vivo assessment of skeletal muscle mass in healthy and diseased humans.2 Thus, we used dual-energy x-ray absorptiometry to examine skeletal muscle mass in patients with heart failure and its relation to peak VO2. We hypothesized that skeletal muscle mass would be lower in cachectic heart failure patients compared with noncachectic patients and healthy controls. Moreover, skeletal muscle atrophy would be related to low peak VO2 in heart failure patients. jjj Twenty-seven patients (26 men and 1 woman) with heart failure were selected from the Heart Failure Services of the Baltimore Veterans Affairs and University of Maryland Medical Centers. Inclusion criteria included: (1) hemodynamically stable, (2) free of signs or symptoms of edema, (3) ambulatory; and (4) no peripheral arterial disease or other exercise-limiting noncardiac disease. We recruited both weight-stable patients and patients with marked weight loss. Patients had mean resting left ventricular ejection fraction of 23 { 9% by radionuclide ventriculography. Symptoms were categorized as New York Heart Association class II (n Å 10), class III (n Å 12), or class IV (n Å 5). Thirteen patients were classified as cachectic (loss of ú10% of their reported premorbid body weight, weight loss 15 { 6 kg) and 14 as noncachectic (weight loss 2 { 4 kg). Data from this cohort regarding the effect of heart failure on energy expenditure has been reported elsewhere.3,4 Data from 52 healthy elderly subjects (50 men and 2 women) were used as a control group. Healthy subjects were recruited by newspaper advertisements From the Divisions of Gerontology and Cardiology, Department of Medicine, University of Maryland, Baltimore, and the Gerontology Research Education and Clinical Center, Baltimore VA Medical Center, Baltimore, Maryland. This work was supported by Grants AG00219, AG-00608, AG-07857, and AG-00564 from the National Institutes of Health, Bethesda, Maryland, and the Geriatrics and Gerontology Education and Research Program of the University of Maryland, Baltimore, Maryland. Michael J. Toth was the recipient of a Scholarship for Research in the Biology of Aging from the AFAR/ Glenn Foundation. Dr. Poehlman’s address is: Division of Clinical Pharmacology and Metabolic Research, Department of Medicine, Given Building C-247, Burlington, Vermont 05405. Manuscript received September 5, 1996; revised manuscript received and accepted January 2, 1997.
MD,
and Eric T. Poehlman,
and community organizations and had (1) no symptoms or signs of heart disease or diabetes, (2) normal resting electrocardiogram, (3) normal electrocardiographic response to an exercise stress test, (4) absence of medication that could affect cardiovascular or metabolic function, and (5) weight stability ({2 kg) within 6 months of testing. Fat mass, fat-free tissue mass, and appendicular (arms and legs) skeletal muscle mass were measured by dual-energy x-ray absorptiometry using a Lunar DPX-L densitometer (Madison, Wisconsin). Fat-free tissue mass of the arms and legs represented appendicular skeletal muscle mass assuming that bone marrow, skin, and associated subcutaneous tissues contribute a negligible amount to the total mass of each extremity.5 Total skeletal muscle mass was calculated by dividing appendicular skeletal muscle mass by 0.75.2 Total skeletal muscle mass estimated with this model has shown excellent agreement with total skeletal muscle mass determined by computed tomography in healthy subjects and in diseased persons with varying degrees of weight loss.2 Peak VO2 was assessed using an open circuit gas analysis system during a maximal treadmill exercise test to exhaustion. Peak VO2 measurements were obtained on 16 patients with congestive heart failure (8 cachectic, 8 noncachectic). Patients who had poor clinical status, physical frailty, or were currently taking b-blocker medication were not tested. Analysis of variance was used to identify differences in skeletal muscle mass among groups. If a significant group effect was found, a Student-Neuman-Keuls test was used to identify the location of significant differences. Analysis of covariance was TABLE I Physical Characteristics of Cachectic (n Å 13) and Noncachectic (n Å 14) Heart Failure and Healthy Controls (n Å 52) Variable
Cachectic Patients
Age (yr) 72 { 8 Height (cm) 170 { 9 Body mass (kg) 65 { 15 Fat mass (kg) 13 { 9 Fat-free tissue mass (kg) 48 { 7 Arm skeletal muscle mass (kg) 4.8 { 1.2 Leg skeletal muscle mass (kg) 14 { 3 Total skeletal muscle mass (kg) 26 { 5 Peak VO2 (L/min) 0.8 { 0.3
67 173 83 23 55
{6 {6 { 13 { 10 {6
6.4 { 0.8 18 { 3 32 { 4 1.4 { 0.2
Healthy Controls 69 173 80 20 54
Wednesday Apr 09 07:45 PM
{7 {8 { 14* { 8* { 8*
6.4 { 1.5* 18 { 3* 33 { 6* 1.9 { 0.6†
0002-9149/97/$17.00 PII S0002-9149(97)00098-2
All rights reserved.
1267
Noncachectic Patients
*p õ 0.05 cachectic patients less than noncachectic patients and healthy controls; †p õ 0.05 all groups different. Values are expressed as mean { SD. VO2 Å oxygen consumption (n Å 16 heart failure patient; n Å 52 controls).
Q1997 by Excerpta Medica, Inc.
/ 2w21 0970 Mp
PhD
EL–AJC (v. 79, no. 9 ’97)
0970
1267
were divided into cachectic (n Å 8, r Å 0.90, põ0.01) and noncachectic groups (n Å 8, r Å 0.82, p õ0.01). jjj Recent studies suggest that skeletal muscle atrophy contributes to reduced peak VO2 in heart failure patients.1 The absence of reliable techniques to measure skeletal muscle mass in humans has limited the examination of skeletal muscle atrophy and its relation to peak VO2. Using dual energy x-ray absorptiometry, we found lower skeletal muscle mass in cachectic heart failure patients than in noncachectic patients and healthy controls. These differences persisted after statistical control for standing height to adjust skeletal muscle mass for body size. A similar degree of reduced skeletal muscle mass was found in the arms and legs of cachectic versu noncachectic patients and healthy controls, suggesting that muscle atrophy was not specific to weight-bearing muscles. Collectively, these findings suggest that skeletal muscle atrophy in heart failure patients is associated with prior weight loss. Skeletal muscle atrophy may contribute to reduced peak VO2 by reducing the quantity of tissue available to utilize oxygen during exercise. We found a strong correlation between peak VO2 and skeletal muscle mass in FIGURE 1. Relation between peak oxygen consumption (VO2) and total skeletal muscle mass in heart failure patients (A) and healthy controls (B). The correlation heart failure patients, suggesting that between peak VO2 and total skeletal muscle mass was significantly stronger (p skeletal muscle atrophy contributes to õ0.01) in heart failure patients than in controls, as assessed by Fisher’s z test. low peak VO2. Our findings agree with those of Miyagi et al6 who found used to test for differences in total skeletal muscle lower leg muscle mass and peak VO2 in symptomatic mass after statistical control for standing height. Lin- heart failure patientscompared with asymptomatic ear regression analysis was used to examine relations patients and healthy controls. In contrast, Mancini between variables. et al1 found a marginal correlation between calf Groups did not differ in age or standing height muscle volume and peak VO2 in heart failure pa(Table I). Body mass, fat mass, fat-free tissue mass, tients. However, their analysis used peak VO2 exarm muscle mass, leg muscle mass, and total skeletal pressed relative to body weight, which may have muscle mass were lower (all p õ0.05) in cachectic diminished the relation between muscle mass and patients than in noncachectic patients and healthy peak VO2 given the covariance between body controls. Differences in total skeletal muscle mass weight and skeletal muscle mass (r Å 0.86, p among groups persisted after statistical control for õ0.01, n Å 27 heart failure patients). standing height (adjusted skeletal muscle mass: caAlthough a strong relation between peak VO2 and chectic, 27 { 5; noncachectic, 32 { 5; healthy con- skeletal muscle mass may seem intuitive, we found trols, 33 { 5 kg [p õ0.05]). Peak VO2 differed only a marginal correlation between peak VO2 and among all groups (p õ0.05), with healthy controls skeletal muscle mass in healthy subjects. Thus, it having the highest values and cachectic patients hav- seems that peak VO2 is more dependent on variation ing the lowest. in skeletal muscle mass in heart failure patients than The relation of peak VO2 with total skeletal mus- in healthy persons. Reduced skeletal muscle blood cle mass in heart failure patients (r Å 0.91; p õ0.01; flow during exercise7 may explain the strong depenslope 0.059 L/min/kg) and healthy controls (r Å dence of peak VO2 on skeletal muscle mass in heart 0.34; p õ0.05; slope 0.030 L/min/kg) is shown in failure patients. Reduced oxygen delivery to exercisFigure 1. The relation of peak VO2 to total skeletal ing skeletal muscles necessitates an increase in oxymuscle mass persisted when heart failure patients gen extraction by skeletal muscle to sustain exercise 1268
THE AMERICAN JOURNAL OF CARDIOLOGYT
/ 2w21 0970 Mp
1268
VOL. 79
Wednesday Apr 09 07:45 PM
MAY 1, 1997
EL–AJC (v. 79, no. 9 ’97)
0970
at a given workload. Increased oxygen extraction depends on both the quantity and oxidative capacity of skeletal muscle. Thus, a reduction in skeletal muscle mass or oxidative capacity would decrease peak VO2 in heart failure patients. However, the degree of cardiac dysfunction and reduced oxidative capacity of skeletal muscle8 are also likely contributors. Studies that examine changes in skeletal muscle mass and peak VO2 over time or in response to interventions designed to increase skeletal muscle mass (i.e., resistance training) are needed to further clarify the relative contribution of skeletal muscle mass to variation in peak VO2 in heart failure patients. Our results show that skeletal muscle atrophy in heart failure patients is associated with prior weight loss and contributes to variation in peak VO2 in heart failure patients.
1. Mancini DM, Walter G, Reichek N, Lenkinski R, McCully KK, Mullen JL, Wilson JR. Contribution of skeletal muscle atrophy to exercise intolerance and altered muscle metabolism in heart failure. Circulation 1992; 85:1364 – 1373. 2. Wang Z, Visser M, Ma R, Baumgartner RN, Kotler D, Gallagher D, Heymsfield SB. Skeletal muscle mass: evaluation of neutron activation and dual-energy x-ray absorptiometry methods. J Appl Physiol 1996;80:824–831. 3. Toth MJ, Gottlieb SS, Goran MI, Fisher ML, Poehlman ET. Daily energy expenditure in free-living heart failure patients. Am J Physiol. In Press. 4. Toth MJ, Gottlieb SS, Fisher ML, Ryan AS, Nicklas BJ, Poehlman ET. Plasma leptin concentrations and energy expenditure in heart failure patients. Metabolism. In Press. 5. Heymsfield SB, Smith R, Aulet M, Bensen B, Lichtman S, Wang J, Pierson RN. Appendicular skeletal muscle mass: measurement by dual-photon absorptiometry. Am J Clin Nutr 1990;52:214–218. 6. Miyagi K, Asanoi H, Ishizaka S, Kameyama T, Wada O, Seto H, Sasayama S. Importance of total leg muscle mass for exercise intolerance in chronic heart failure. Jpn Heart J 1994;35:15–26. 7. Wilson JR, Martin JL, Schwartz D, Ferraro N. Exercise intolerance in patients with chronic heart failure: role of impaired nutritive flow to skeletal muscle. Am J Cardiol 1984;69:1079–1087. 8. Minotti JR, Christoph I, Oka R, Weiner MW, Wells L, Massie BM. Impaired skeletal muscle function in patients with congestive heart failure: relationship to systemic exercise performance. J Clin Invest 1991;88: 2077 – 2082.
Mitral and Tricuspid Valve Aneurysms Evaluated by Transesophageal Echocardiography Michael Mollod,
MD,
Kevin J. Felner, and Joel M. Felner,
MD
TABLE I Clinical and Echocardiographic Findings in Four Patients With Atrioventricular Valve Aneurysms
Case
Age (yr) & Sex
Predisposition
Presentation
Echocardiography Findings
Organism Isolated
Valve Replacement
Alive
MR 2/ TR 2/
MV
2 mo
AR 3/ MR 3/
(MV / AV)
3 mo
TR 2/
0
2 mo
TR 3/
0
0
TTE
TEE
Doppler
MV veg. AML aneur. Healed TV veg. Bicuspid AV AV veg. AML aneur.
Mitral Valve 1
49M
IVDA
Syncope
S. Aureus
MV mass
2
26M
Bicuspid AV
Flu-like illness
Alpha-strep. (group D)
AV veg MV mass
Tricuspid Valve 3
45M
Pneumonia; epidural abscess
Fever
S. pneumoniae
TV veg
4
40F
IVDA
Flu-like illness
S. Aureus
Probable TV veg
TV veg. ATL aneur. IAS aneur. TV veg. STL aneur.
AML Å anterior mitral leaflet; aneur Å aneurysm; AR Å aortic regurgitation; ATL Å anterior tricuspid leaflet; AV Å aortic valve; IAS Å interatrial septum; IVDA Å intravenous drug abuse; MR Å mitral regurgitation; MV Å mitral valve; S./strep. Å streptococcus; TEE Å transesophageal echocardiogram; TTE Å transthoracic echocardiogram; TR Å tricuspid regurgitation; TV Å tricuspid valve; veg. Å vegetation.
omplications of endocarditis may have devastating consequences. Formation of abscesses, fisC tulous tracts, and valve aneurysms can now be detected early and followed serially by noninvasive techniques. The awareness of the clinical significance of mitral and tricuspid valve aneurysms is a direct consequence of the use of 2-dimensional echoFrom the Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia. Dr. Felner’s address is: Emory University School of Medicine; Division of Cardiology, 69 Butler Street; Atlanta, Georgia 30303. Manuscript received December 5, 1996; revised manuscript received and accepted January 14, 1997.
cardiography. Before 2-dimensional echocardiography, the diagnosis was generally made either at autopsy1,2 or surgery.3 Recently, there have been several reported cases diagnosed by transthoracic echocardiography (TTE),3 – 12 and a few diagnosed by transesophageal echocardiography (TEE).13 – 18 In the past 6 months, we have seen 4 patients with clinically unsuspected atrioventricular valve aneurysms diagnosed by transesophageal echocardiography. A brief description of our cases and a review of previous echo-diagnosed published reports is the purpose of this report.
Q1997 by Excerpta Medica, Inc.
0002-9149/97/$17.00 PII S0002-9149(97)00099-4
All rights reserved.
/ 2w21 0970 Mp
1269
Wednesday Apr 09 07:45 PM
EL–AJC (v. 79, no. 9 ’97)
0971
1269
PhD,
Stephen S. Gottlieb,
MD,
Michael L. Fisher,
educed peak oxygen consumption (peak VO ) is a hallmark of chronic heart failure. Skeletal musR cle atrophy may contribute to reduced peak VO . 2
1
2
Examination of skeletal muscle atrophy and its contribution to reduced exercise capacity in patients with heart failure has been limited by the lack of reliable techniques to measure skeletal muscle mass. Dual energy x-ray absorptiometry is a promising technique for the in vivo assessment of skeletal muscle mass in healthy and diseased humans.2 Thus, we used dual-energy x-ray absorptiometry to examine skeletal muscle mass in patients with heart failure and its relation to peak VO2. We hypothesized that skeletal muscle mass would be lower in cachectic heart failure patients compared with noncachectic patients and healthy controls. Moreover, skeletal muscle atrophy would be related to low peak VO2 in heart failure patients. jjj Twenty-seven patients (26 men and 1 woman) with heart failure were selected from the Heart Failure Services of the Baltimore Veterans Affairs and University of Maryland Medical Centers. Inclusion criteria included: (1) hemodynamically stable, (2) free of signs or symptoms of edema, (3) ambulatory; and (4) no peripheral arterial disease or other exercise-limiting noncardiac disease. We recruited both weight-stable patients and patients with marked weight loss. Patients had mean resting left ventricular ejection fraction of 23 { 9% by radionuclide ventriculography. Symptoms were categorized as New York Heart Association class II (n Å 10), class III (n Å 12), or class IV (n Å 5). Thirteen patients were classified as cachectic (loss of ú10% of their reported premorbid body weight, weight loss 15 { 6 kg) and 14 as noncachectic (weight loss 2 { 4 kg). Data from this cohort regarding the effect of heart failure on energy expenditure has been reported elsewhere.3,4 Data from 52 healthy elderly subjects (50 men and 2 women) were used as a control group. Healthy subjects were recruited by newspaper advertisements From the Divisions of Gerontology and Cardiology, Department of Medicine, University of Maryland, Baltimore, and the Gerontology Research Education and Clinical Center, Baltimore VA Medical Center, Baltimore, Maryland. This work was supported by Grants AG00219, AG-00608, AG-07857, and AG-00564 from the National Institutes of Health, Bethesda, Maryland, and the Geriatrics and Gerontology Education and Research Program of the University of Maryland, Baltimore, Maryland. Michael J. Toth was the recipient of a Scholarship for Research in the Biology of Aging from the AFAR/ Glenn Foundation. Dr. Poehlman’s address is: Division of Clinical Pharmacology and Metabolic Research, Department of Medicine, Given Building C-247, Burlington, Vermont 05405. Manuscript received September 5, 1996; revised manuscript received and accepted January 2, 1997.
MD,
and Eric T. Poehlman,
and community organizations and had (1) no symptoms or signs of heart disease or diabetes, (2) normal resting electrocardiogram, (3) normal electrocardiographic response to an exercise stress test, (4) absence of medication that could affect cardiovascular or metabolic function, and (5) weight stability ({2 kg) within 6 months of testing. Fat mass, fat-free tissue mass, and appendicular (arms and legs) skeletal muscle mass were measured by dual-energy x-ray absorptiometry using a Lunar DPX-L densitometer (Madison, Wisconsin). Fat-free tissue mass of the arms and legs represented appendicular skeletal muscle mass assuming that bone marrow, skin, and associated subcutaneous tissues contribute a negligible amount to the total mass of each extremity.5 Total skeletal muscle mass was calculated by dividing appendicular skeletal muscle mass by 0.75.2 Total skeletal muscle mass estimated with this model has shown excellent agreement with total skeletal muscle mass determined by computed tomography in healthy subjects and in diseased persons with varying degrees of weight loss.2 Peak VO2 was assessed using an open circuit gas analysis system during a maximal treadmill exercise test to exhaustion. Peak VO2 measurements were obtained on 16 patients with congestive heart failure (8 cachectic, 8 noncachectic). Patients who had poor clinical status, physical frailty, or were currently taking b-blocker medication were not tested. Analysis of variance was used to identify differences in skeletal muscle mass among groups. If a significant group effect was found, a Student-Neuman-Keuls test was used to identify the location of significant differences. Analysis of covariance was TABLE I Physical Characteristics of Cachectic (n Å 13) and Noncachectic (n Å 14) Heart Failure and Healthy Controls (n Å 52) Variable
Cachectic Patients
Age (yr) 72 { 8 Height (cm) 170 { 9 Body mass (kg) 65 { 15 Fat mass (kg) 13 { 9 Fat-free tissue mass (kg) 48 { 7 Arm skeletal muscle mass (kg) 4.8 { 1.2 Leg skeletal muscle mass (kg) 14 { 3 Total skeletal muscle mass (kg) 26 { 5 Peak VO2 (L/min) 0.8 { 0.3
67 173 83 23 55
{6 {6 { 13 { 10 {6
6.4 { 0.8 18 { 3 32 { 4 1.4 { 0.2
Healthy Controls 69 173 80 20 54
Wednesday Apr 09 07:45 PM
{7 {8 { 14* { 8* { 8*
6.4 { 1.5* 18 { 3* 33 { 6* 1.9 { 0.6†
0002-9149/97/$17.00 PII S0002-9149(97)00098-2
All rights reserved.
1267
Noncachectic Patients
*p õ 0.05 cachectic patients less than noncachectic patients and healthy controls; †p õ 0.05 all groups different. Values are expressed as mean { SD. VO2 Å oxygen consumption (n Å 16 heart failure patient; n Å 52 controls).
Q1997 by Excerpta Medica, Inc.
/ 2w21 0970 Mp
PhD
EL–AJC (v. 79, no. 9 ’97)
0970
1267
were divided into cachectic (n Å 8, r Å 0.90, põ0.01) and noncachectic groups (n Å 8, r Å 0.82, p õ0.01). jjj Recent studies suggest that skeletal muscle atrophy contributes to reduced peak VO2 in heart failure patients.1 The absence of reliable techniques to measure skeletal muscle mass in humans has limited the examination of skeletal muscle atrophy and its relation to peak VO2. Using dual energy x-ray absorptiometry, we found lower skeletal muscle mass in cachectic heart failure patients than in noncachectic patients and healthy controls. These differences persisted after statistical control for standing height to adjust skeletal muscle mass for body size. A similar degree of reduced skeletal muscle mass was found in the arms and legs of cachectic versu noncachectic patients and healthy controls, suggesting that muscle atrophy was not specific to weight-bearing muscles. Collectively, these findings suggest that skeletal muscle atrophy in heart failure patients is associated with prior weight loss. Skeletal muscle atrophy may contribute to reduced peak VO2 by reducing the quantity of tissue available to utilize oxygen during exercise. We found a strong correlation between peak VO2 and skeletal muscle mass in FIGURE 1. Relation between peak oxygen consumption (VO2) and total skeletal muscle mass in heart failure patients (A) and healthy controls (B). The correlation heart failure patients, suggesting that between peak VO2 and total skeletal muscle mass was significantly stronger (p skeletal muscle atrophy contributes to õ0.01) in heart failure patients than in controls, as assessed by Fisher’s z test. low peak VO2. Our findings agree with those of Miyagi et al6 who found used to test for differences in total skeletal muscle lower leg muscle mass and peak VO2 in symptomatic mass after statistical control for standing height. Lin- heart failure patientscompared with asymptomatic ear regression analysis was used to examine relations patients and healthy controls. In contrast, Mancini between variables. et al1 found a marginal correlation between calf Groups did not differ in age or standing height muscle volume and peak VO2 in heart failure pa(Table I). Body mass, fat mass, fat-free tissue mass, tients. However, their analysis used peak VO2 exarm muscle mass, leg muscle mass, and total skeletal pressed relative to body weight, which may have muscle mass were lower (all p õ0.05) in cachectic diminished the relation between muscle mass and patients than in noncachectic patients and healthy peak VO2 given the covariance between body controls. Differences in total skeletal muscle mass weight and skeletal muscle mass (r Å 0.86, p among groups persisted after statistical control for õ0.01, n Å 27 heart failure patients). standing height (adjusted skeletal muscle mass: caAlthough a strong relation between peak VO2 and chectic, 27 { 5; noncachectic, 32 { 5; healthy con- skeletal muscle mass may seem intuitive, we found trols, 33 { 5 kg [p õ0.05]). Peak VO2 differed only a marginal correlation between peak VO2 and among all groups (p õ0.05), with healthy controls skeletal muscle mass in healthy subjects. Thus, it having the highest values and cachectic patients hav- seems that peak VO2 is more dependent on variation ing the lowest. in skeletal muscle mass in heart failure patients than The relation of peak VO2 with total skeletal mus- in healthy persons. Reduced skeletal muscle blood cle mass in heart failure patients (r Å 0.91; p õ0.01; flow during exercise7 may explain the strong depenslope 0.059 L/min/kg) and healthy controls (r Å dence of peak VO2 on skeletal muscle mass in heart 0.34; p õ0.05; slope 0.030 L/min/kg) is shown in failure patients. Reduced oxygen delivery to exercisFigure 1. The relation of peak VO2 to total skeletal ing skeletal muscles necessitates an increase in oxymuscle mass persisted when heart failure patients gen extraction by skeletal muscle to sustain exercise 1268
THE AMERICAN JOURNAL OF CARDIOLOGYT
/ 2w21 0970 Mp
1268
VOL. 79
Wednesday Apr 09 07:45 PM
MAY 1, 1997
EL–AJC (v. 79, no. 9 ’97)
0970
at a given workload. Increased oxygen extraction depends on both the quantity and oxidative capacity of skeletal muscle. Thus, a reduction in skeletal muscle mass or oxidative capacity would decrease peak VO2 in heart failure patients. However, the degree of cardiac dysfunction and reduced oxidative capacity of skeletal muscle8 are also likely contributors. Studies that examine changes in skeletal muscle mass and peak VO2 over time or in response to interventions designed to increase skeletal muscle mass (i.e., resistance training) are needed to further clarify the relative contribution of skeletal muscle mass to variation in peak VO2 in heart failure patients. Our results show that skeletal muscle atrophy in heart failure patients is associated with prior weight loss and contributes to variation in peak VO2 in heart failure patients.
1. Mancini DM, Walter G, Reichek N, Lenkinski R, McCully KK, Mullen JL, Wilson JR. Contribution of skeletal muscle atrophy to exercise intolerance and altered muscle metabolism in heart failure. Circulation 1992; 85:1364 – 1373. 2. Wang Z, Visser M, Ma R, Baumgartner RN, Kotler D, Gallagher D, Heymsfield SB. Skeletal muscle mass: evaluation of neutron activation and dual-energy x-ray absorptiometry methods. J Appl Physiol 1996;80:824–831. 3. Toth MJ, Gottlieb SS, Goran MI, Fisher ML, Poehlman ET. Daily energy expenditure in free-living heart failure patients. Am J Physiol. In Press. 4. Toth MJ, Gottlieb SS, Fisher ML, Ryan AS, Nicklas BJ, Poehlman ET. Plasma leptin concentrations and energy expenditure in heart failure patients. Metabolism. In Press. 5. Heymsfield SB, Smith R, Aulet M, Bensen B, Lichtman S, Wang J, Pierson RN. Appendicular skeletal muscle mass: measurement by dual-photon absorptiometry. Am J Clin Nutr 1990;52:214–218. 6. Miyagi K, Asanoi H, Ishizaka S, Kameyama T, Wada O, Seto H, Sasayama S. Importance of total leg muscle mass for exercise intolerance in chronic heart failure. Jpn Heart J 1994;35:15–26. 7. Wilson JR, Martin JL, Schwartz D, Ferraro N. Exercise intolerance in patients with chronic heart failure: role of impaired nutritive flow to skeletal muscle. Am J Cardiol 1984;69:1079–1087. 8. Minotti JR, Christoph I, Oka R, Weiner MW, Wells L, Massie BM. Impaired skeletal muscle function in patients with congestive heart failure: relationship to systemic exercise performance. J Clin Invest 1991;88: 2077 – 2082.
Mitral and Tricuspid Valve Aneurysms Evaluated by Transesophageal Echocardiography Michael Mollod,
MD,
Kevin J. Felner, and Joel M. Felner,
MD
TABLE I Clinical and Echocardiographic Findings in Four Patients With Atrioventricular Valve Aneurysms
Case
Age (yr) & Sex
Predisposition
Presentation
Echocardiography Findings
Organism Isolated
Valve Replacement
Alive
MR 2/ TR 2/
MV
2 mo
AR 3/ MR 3/
(MV / AV)
3 mo
TR 2/
0
2 mo
TR 3/
0
0
TTE
TEE
Doppler
MV veg. AML aneur. Healed TV veg. Bicuspid AV AV veg. AML aneur.
Mitral Valve 1
49M
IVDA
Syncope
S. Aureus
MV mass
2
26M
Bicuspid AV
Flu-like illness
Alpha-strep. (group D)
AV veg MV mass
Tricuspid Valve 3
45M
Pneumonia; epidural abscess
Fever
S. pneumoniae
TV veg
4
40F
IVDA
Flu-like illness
S. Aureus
Probable TV veg
TV veg. ATL aneur. IAS aneur. TV veg. STL aneur.
AML Å anterior mitral leaflet; aneur Å aneurysm; AR Å aortic regurgitation; ATL Å anterior tricuspid leaflet; AV Å aortic valve; IAS Å interatrial septum; IVDA Å intravenous drug abuse; MR Å mitral regurgitation; MV Å mitral valve; S./strep. Å streptococcus; TEE Å transesophageal echocardiogram; TTE Å transthoracic echocardiogram; TR Å tricuspid regurgitation; TV Å tricuspid valve; veg. Å vegetation.
omplications of endocarditis may have devastating consequences. Formation of abscesses, fisC tulous tracts, and valve aneurysms can now be detected early and followed serially by noninvasive techniques. The awareness of the clinical significance of mitral and tricuspid valve aneurysms is a direct consequence of the use of 2-dimensional echoFrom the Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia. Dr. Felner’s address is: Emory University School of Medicine; Division of Cardiology, 69 Butler Street; Atlanta, Georgia 30303. Manuscript received December 5, 1996; revised manuscript received and accepted January 14, 1997.
cardiography. Before 2-dimensional echocardiography, the diagnosis was generally made either at autopsy1,2 or surgery.3 Recently, there have been several reported cases diagnosed by transthoracic echocardiography (TTE),3 – 12 and a few diagnosed by transesophageal echocardiography (TEE).13 – 18 In the past 6 months, we have seen 4 patients with clinically unsuspected atrioventricular valve aneurysms diagnosed by transesophageal echocardiography. A brief description of our cases and a review of previous echo-diagnosed published reports is the purpose of this report.
Q1997 by Excerpta Medica, Inc.
0002-9149/97/$17.00 PII S0002-9149(97)00099-4
All rights reserved.
/ 2w21 0970 Mp
1269
Wednesday Apr 09 07:45 PM
EL–AJC (v. 79, no. 9 ’97)
0971
1269