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Sudden increase in left ventricular mass secondary to acute myocarditis
200
Brief Communications
American
July 1988 Heart Journal
Fig. 3. Parasternal long-axis view after a Nissen fundoplication was performed, with no left atria1 mass effect and no mitral valve obstruction. Ao = aorta; LV = left ventricle; RV = right ventricle.
The patient is a 3I-year-old, previously normotensive mimickingleft atria1 myxomas: clinical and two-dimensional echecardioeranhic features.J Am Co11 Cardiol 1985:6:1422. healthy male, who presented to the hospital with a 2-hour 4. KronsonI,-RosenzweigB, Dack S. Diagnosisof a largeleft history of fever, chills, pleuritic chest pain, and a greenish atrial myxoma: the role of two-dimensionalechocardiograproductive cough. On physical examination his pulse was phy. J Clin Ultrasound1982;10:39. 90 beats/min, temperature was 103.4” F, and blood pres5. Nishimura RA, Tajk AJ, SchattenbergTT, Seward JB. sure was IlO/ mm Hg. He had rales and decreased Diaphragmatichernia mimicking an atria1 mass:a twodimensional echocardiographic pitfall. J Am Co11 Cardiol breath soundsat the mid left lung field. Cardiac examina1985;5:992. tion and the remainder of the physical examination were essentially negative. The initial white blood count was 1000/mms,with a marked shift to the left. A chest x-ray film revealed a left perihilar infiltrate consistent with Sudden increase in left ventricular mass pneumonia. Although the sputum smear and routine culture were unrevealing, a direct fluorescent antibody secondary to acute myocarditis test for Legionella pneumophila was positive. The ECG showednonspecific ST and T wave changes. Stephen Arvan, MD, and Elmer Manalo, MD. On the first hospital day, the patient had a witnessed Pittsburgh, Pa. cardiac arrest as a result of ventricular fibrillation. His blood pressureand rhythm were restored to normal within 5 to 10 minutes of the event. Although the chest x-ray film The echocardiographic findings of acute myocarditis conshowed pulmonary edema, blood gases on 60% Fio, sist of regional or diffuse wall motion abnormalities that showed a PO, of 140 mm Hg, PcoZ of 20 mm Hg, percent may disappear within a few days or evolve to a chronic saturation of 99 %, and a pH of 7.47 U. The pulmonary dilated cardiomyopathy.‘-4 Uncommonly, transient inartery pressure was 40/24 mm Hg and the mean wedge creasesin left ventricular (LV) wall thickness have been pressure was 24 mm Hg. The cardiac index was 2.4 observed following acute myocarditis.5*6 In the present L/min/mz. He was started on furosemide and intravenous case, a sudden and persistent increase in LV wall dimenerythromycin with a good symptomatic responseover the sions developed as a result of acute Legionella myocardinext 3 days. A lung perfusion scan and aerial creatine tis, a complication that has yet to be recognized in adults. phosphokinase (CPK) isoenzymeswere negative for pulIt is most likely that these changes are secondary to monary emboli and acute myocardial infarction, respeccompensatory LV hypertrophy. tively. A Iwo-ciimensionalechocardiogramtaken 24 hours after the cardiac arrest showed diffuse wall motion abnormaliFrom the Department of Medicine, University of Pittsburgh, School of ties of the left ventricle and hypokinesia of the free right Medicine; and Montefiore Hospital. ventricular wall. A biplane LV ejection fraction (LVEF) Reprint requests: Stephen Arvan, MD, Dept. of Cardiology, Montefiore taken with the area-length method was 27%. Septal and Hospital, 3459 Fifth Ave., Pittsburgh, PA 15213.
Volum* Number
116 1, Part 1
Brief
Communications
201
Fig. 1. A, The first echocardiogram taken on July 2, 1987 showed diffuse hopokinesia of the left ventricular segments and normal septal and posterior wall dimensions. B, An echocardiogram taken 8 days later shows better wall motion and systolic thickening, but there is now a marked increase in the wall dimensions.
posterior wall thickness were normal (LV mass = 374 gm),6 as shown in Fig. 1, A. The LV diastolic diameter was 5.2 cm. A repeat study taken 8 days later showed better wall motion of the myocardium. The LVEF was 34%. However, there was now concentric ventricular wall thickening (septum = 2.0 cm and posterior ventricular wall (PVW) = 1.9 cm) with an LV mass of 744 gm. The diastolic LV diameter was 4.5 cm (Fig. 1, B). Almost 4 months later (Fig. 2), LV function was restored to normal (LVEF = 55%) but wall thickness and mass were still significantly increased (septum = 1.4 cm, PVW = 1.5 cm, and LV mass = 499 gm). The diastolic diameter of the left ventricle was 4.8 cm. The patient has remained normotensive (110/75 mm Hg) and is not receiving any medication. The supporting evidence for acute myocarditis is this patient is the presence of a bacterial infection, a malignant ventricular arrhythmia in the absence of ischemia or severe hypoxia, and significant LV dysfunction that persisted for more than 2 weeks after the patient’s cardiac arrest. An increase in myocardial wall thickness has been noted on both pathologic examination and noninvasive studies after the onset of acute myocarditis. Histologically, both interstitial edema and myocardial hypertrophy have been seen!,? Most noninvasive studies have shown that wall thickness abnormalities are transient and last only several days to a few weeks. 2,*-10This suggests that the increase in myocardial mass is due to myocardial edema and inflammatory cellular infiltrates that tend to resolve as the underlying process improves. The LV myocardium has remained abnormally thick in our patient over a prolonged period of time despite full recovery of contractility. Although slow resolution of myocardial edema may still account for these changes, the presence of LV hypertrophy is more likely. Interstitial changes in the myocardium, as occurs for example in amyloidosis, is associated with
,
,
,
,.
(
)
,)
,
,
I
,“‘,.“.),
‘)‘,I,.
,‘(‘,
,
Fig. 2. There was concentric “hypertrophy” of the left ventricle 8 days after admission. There is still significant, “hypertrophy” of the left ventricle almost 4 months after admission. LV function at this time was normal.
some degree of L’v‘ dysfunction.” This is particularly true when there is significant enlargement of ventricular wall dimensions. On the other hand, early LV hypertrophy is associated with normal or even hyperdynamic LV systolic contractility.12 Several months after the patient’s admission, LV function was completely normal in the presence of significant symmetric LV wall thickening. LV hypertrophy may occur in response to impaired pump function as a result of a compensatory increase in the unaffected con-
202
Brief
Communications
American
tractile elements.13 The persistence of LV hypertrophy after resolution of acute myocarditis is harder to explain. Perhaps there is slowly reversible or irreversible depression of contractility involving a significant number of units of the myocardium. Cardiac compensation could only be maintained by an increase in muscle mass. Chronic compensatory myocardial hypertrophy resulting in improved systolic function has been reported in experimental animals with cardiac dysfunction.14-16 The clinical significance of persistent LV wall thickness following acute myocarditis is unknown. However, LV hypertrophy in general has been shown to increase ventricular ectopic impulses and to increase the risk of sudden death.13 Further long-term follow-up and the accumulation of similar cases may help to determine the significance of chronic increases in LV wall dimensions. REFERENCES
1.
2. 3. 4.
5. 6.
7.
lkaheimo MJ, Takkunen JT. Echocardiography in acute infectious myocarditis. Chest 1986;89:106. Nieminen MS, Heikkila J, Karjalainen J. Echocardiography in acute infectious myocarditis: relation to clinical and electrocardiographic findings. Am J Cardiol 1984;53:1331. Pasquini JA, Gottdiener JS, Cutler DJ, Fletcher RD. Myocarditis with transient left ventricular apical dyskinesis. AM HEART J 1985;109:371. Chandraratna PAN, Nimalasuriya A, Reid CL, Cohn S, Rahimtoola SH. Left ventricular asynergy in acute myocarditis. Simulation of acute myocardial infarction. JAMA 1983;250:1428. Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man. Circulation 1977:66:613. Tanimura A, Nakashima N, Komatau Y, Arakawa M, Ookita Y, Senoo T, Toshima H, Koike S. Clinicopathologic study of Coxsackie B viral myocarditis. Acta Path01 Jpn 1980; 30~161. Wookruff JF. Viral myocarditis, a review. Am J Path01 1980;101:427.
8. Hauser AM, Gordon S, Cieszkowski J, Timmis GC. Severe transient left ventricular “hypertrophy” occuring during acute myocarditis. Chest 1983;83:275. 9. Gerhring J, Rudroff W. Reversible asymmetric septal thickening in the echocardiogram in a case with suspected perimyocarditis (author’s translation) A Kardiol 1981; 76~389. 10. Oda T, Hamamoto K. Morinaaa H. Left ventricular hvuertro11.
phy in non-rheumatic 1982;46:1235. Cueto-Garcia L, Reeder
myo&ditis
in children.
GS, Kyle
RA,
Wood
Jpn-Circ
J
Dl, Seward
JB,
Naissens J, Offord KP, Greipp PR, Edwards WD, Tajak AJ.
12.
13.
Echocardiographic findings in systemic trum of cardiac involvement and relation Co11 Cardiol 1985;6:737. Lundin S, Friberg P, Hallback-Norlander hypertrophy improves cardiac function hypertensive rats. Clin Sci 1981;61(Suppl
Messerli FH. Clinical determinants ventricular
14.
hypertrophy.
dium
in cardiomegaly.
Circ
specJ Am
M. Left ventricular in spontaneously 7):109s.
and consequences of left
Am J Med
Grimm AF, Kubota R, Whitehorn
amyloidosis: to survival.
1983;74:51.
Res 1963;12:118.
Bing OHL, Matsushita S, Fanburg BL, Levine HJ. Mechanical properties of rat cardiac muscle during experimental
16.
Spann
Ciy-
Jf,
Buccino
Reversibility of prolonged chronotropic dysfunction with theophylline following orthytopic cardiac transplantation Kenneth A. Ellenbogen, MD, Szabolcs Szentpetery, and Marc R. Katz, MD. Richmond, Va.
A relatively high incidence of sinus node dysfunction after orthotopic heart transplantation has been reported by several groups. Is2 Impairment of sinus node automaticity as well as sinoatrial conduction has been documented.3 Sinus node dysfunction has been observed in the early postoperative period of follow-up for orthotopic heart transplantation as well as in asymptomatic long-term survivors. The incidence of sudden death observed in transplant patients may be associated with sinus node dysfunction of the donor atria. Little is known about the mechanism or natural history of sinus node dysfunction in heart transplant patients. The treatment of sinus node dysfunction with permanent pacemakers is problematic in this population, since infection remains a significant cause of morbidity and mortality in transplant patients. One recent report5 describes some complications of pacing unique to heart transplant patients. In this report we describe two cases of symptomatic sinus node dysfunction associated with cardiac allograft rejection that were reversed by theophylline treatment. Case No. 1. A 21-year-old man developed a flu-like syndrome followed by progressive shortness of breath and orthopnea. An echocardiogram showed severe four-chamber enlargement and an estimated ejection fraction of 10% to 20%. Further work-up confirmed a diagnosis of idiopathic dilated cardiomyopathy and the patient underwent othotopic cardiac transplantation.‘j The donor heart ischemic time was 2 hours and 24 minutes. Immunosuppression was achieved with cyclosporine, axathioprine, and perioperative antithymocyte globulin (ATG). Fortyeight hours following heart transplantation, the donor heart rate was noted to vary between 60 and 85 beats/min. Two weeks after transplantation, a transvenous endomyocardial biopsy showed moderate allograft rejection. The donor heart rate decreased to 40 to 45 beatslmin, with multiple episodes of junctional rhythm at a rate of 35 to 40 beats/min (Fig. 1). A 24-hour Holter recording revealed heart rates varying between 34 to 59 beats/min and averaging 44 beats/min (Fig. 2). Rejection was treated with pulsed methylprednisolone therapy and an increased maintenance dose of cyclosporine.
‘071.~8:234. _-. A,_ RA, Sonnenblick
F.ec
EH,
Braunwald
E.
From the Division of Cardiology Veterans Administration Medical ia. Supported
Contractile state of cardiac muscle obtained from cats with experimentally produced ventricular hypertrophy and heart
Reprint McGuire
failure.
23249.
Circ
Res 1967;21:341.
MD,
WV. Properties of myocar-
15.
hvpertmyh>r
July 1988 Heart Journal
by funds
from
and Cardiothoracic Center, and Medical
the Veterans
Surgery, College
McGuire of Virgin-
Administration.
requests: Kenneth A. Ellenbogen, MD, Cardiology VA Medical Center, 1201 Broad Rock Blvd.,
Division (lllJ), Richmond, VA
Brief Communications
American
July 1988 Heart Journal
Fig. 3. Parasternal long-axis view after a Nissen fundoplication was performed, with no left atria1 mass effect and no mitral valve obstruction. Ao = aorta; LV = left ventricle; RV = right ventricle.
The patient is a 3I-year-old, previously normotensive mimickingleft atria1 myxomas: clinical and two-dimensional echecardioeranhic features.J Am Co11 Cardiol 1985:6:1422. healthy male, who presented to the hospital with a 2-hour 4. KronsonI,-RosenzweigB, Dack S. Diagnosisof a largeleft history of fever, chills, pleuritic chest pain, and a greenish atrial myxoma: the role of two-dimensionalechocardiograproductive cough. On physical examination his pulse was phy. J Clin Ultrasound1982;10:39. 90 beats/min, temperature was 103.4” F, and blood pres5. Nishimura RA, Tajk AJ, SchattenbergTT, Seward JB. sure was IlO/ mm Hg. He had rales and decreased Diaphragmatichernia mimicking an atria1 mass:a twodimensional echocardiographic pitfall. J Am Co11 Cardiol breath soundsat the mid left lung field. Cardiac examina1985;5:992. tion and the remainder of the physical examination were essentially negative. The initial white blood count was 1000/mms,with a marked shift to the left. A chest x-ray film revealed a left perihilar infiltrate consistent with Sudden increase in left ventricular mass pneumonia. Although the sputum smear and routine culture were unrevealing, a direct fluorescent antibody secondary to acute myocarditis test for Legionella pneumophila was positive. The ECG showednonspecific ST and T wave changes. Stephen Arvan, MD, and Elmer Manalo, MD. On the first hospital day, the patient had a witnessed Pittsburgh, Pa. cardiac arrest as a result of ventricular fibrillation. His blood pressureand rhythm were restored to normal within 5 to 10 minutes of the event. Although the chest x-ray film The echocardiographic findings of acute myocarditis conshowed pulmonary edema, blood gases on 60% Fio, sist of regional or diffuse wall motion abnormalities that showed a PO, of 140 mm Hg, PcoZ of 20 mm Hg, percent may disappear within a few days or evolve to a chronic saturation of 99 %, and a pH of 7.47 U. The pulmonary dilated cardiomyopathy.‘-4 Uncommonly, transient inartery pressure was 40/24 mm Hg and the mean wedge creasesin left ventricular (LV) wall thickness have been pressure was 24 mm Hg. The cardiac index was 2.4 observed following acute myocarditis.5*6 In the present L/min/mz. He was started on furosemide and intravenous case, a sudden and persistent increase in LV wall dimenerythromycin with a good symptomatic responseover the sions developed as a result of acute Legionella myocardinext 3 days. A lung perfusion scan and aerial creatine tis, a complication that has yet to be recognized in adults. phosphokinase (CPK) isoenzymeswere negative for pulIt is most likely that these changes are secondary to monary emboli and acute myocardial infarction, respeccompensatory LV hypertrophy. tively. A Iwo-ciimensionalechocardiogramtaken 24 hours after the cardiac arrest showed diffuse wall motion abnormaliFrom the Department of Medicine, University of Pittsburgh, School of ties of the left ventricle and hypokinesia of the free right Medicine; and Montefiore Hospital. ventricular wall. A biplane LV ejection fraction (LVEF) Reprint requests: Stephen Arvan, MD, Dept. of Cardiology, Montefiore taken with the area-length method was 27%. Septal and Hospital, 3459 Fifth Ave., Pittsburgh, PA 15213.
Volum* Number
116 1, Part 1
Brief
Communications
201
Fig. 1. A, The first echocardiogram taken on July 2, 1987 showed diffuse hopokinesia of the left ventricular segments and normal septal and posterior wall dimensions. B, An echocardiogram taken 8 days later shows better wall motion and systolic thickening, but there is now a marked increase in the wall dimensions.
posterior wall thickness were normal (LV mass = 374 gm),6 as shown in Fig. 1, A. The LV diastolic diameter was 5.2 cm. A repeat study taken 8 days later showed better wall motion of the myocardium. The LVEF was 34%. However, there was now concentric ventricular wall thickening (septum = 2.0 cm and posterior ventricular wall (PVW) = 1.9 cm) with an LV mass of 744 gm. The diastolic LV diameter was 4.5 cm (Fig. 1, B). Almost 4 months later (Fig. 2), LV function was restored to normal (LVEF = 55%) but wall thickness and mass were still significantly increased (septum = 1.4 cm, PVW = 1.5 cm, and LV mass = 499 gm). The diastolic diameter of the left ventricle was 4.8 cm. The patient has remained normotensive (110/75 mm Hg) and is not receiving any medication. The supporting evidence for acute myocarditis is this patient is the presence of a bacterial infection, a malignant ventricular arrhythmia in the absence of ischemia or severe hypoxia, and significant LV dysfunction that persisted for more than 2 weeks after the patient’s cardiac arrest. An increase in myocardial wall thickness has been noted on both pathologic examination and noninvasive studies after the onset of acute myocarditis. Histologically, both interstitial edema and myocardial hypertrophy have been seen!,? Most noninvasive studies have shown that wall thickness abnormalities are transient and last only several days to a few weeks. 2,*-10This suggests that the increase in myocardial mass is due to myocardial edema and inflammatory cellular infiltrates that tend to resolve as the underlying process improves. The LV myocardium has remained abnormally thick in our patient over a prolonged period of time despite full recovery of contractility. Although slow resolution of myocardial edema may still account for these changes, the presence of LV hypertrophy is more likely. Interstitial changes in the myocardium, as occurs for example in amyloidosis, is associated with
,
,
,
,.
(
)
,)
,
,
I
,“‘,.“.),
‘)‘,I,.
,‘(‘,
,
Fig. 2. There was concentric “hypertrophy” of the left ventricle 8 days after admission. There is still significant, “hypertrophy” of the left ventricle almost 4 months after admission. LV function at this time was normal.
some degree of L’v‘ dysfunction.” This is particularly true when there is significant enlargement of ventricular wall dimensions. On the other hand, early LV hypertrophy is associated with normal or even hyperdynamic LV systolic contractility.12 Several months after the patient’s admission, LV function was completely normal in the presence of significant symmetric LV wall thickening. LV hypertrophy may occur in response to impaired pump function as a result of a compensatory increase in the unaffected con-
202
Brief
Communications
American
tractile elements.13 The persistence of LV hypertrophy after resolution of acute myocarditis is harder to explain. Perhaps there is slowly reversible or irreversible depression of contractility involving a significant number of units of the myocardium. Cardiac compensation could only be maintained by an increase in muscle mass. Chronic compensatory myocardial hypertrophy resulting in improved systolic function has been reported in experimental animals with cardiac dysfunction.14-16 The clinical significance of persistent LV wall thickness following acute myocarditis is unknown. However, LV hypertrophy in general has been shown to increase ventricular ectopic impulses and to increase the risk of sudden death.13 Further long-term follow-up and the accumulation of similar cases may help to determine the significance of chronic increases in LV wall dimensions. REFERENCES
1.
2. 3. 4.
5. 6.
7.
lkaheimo MJ, Takkunen JT. Echocardiography in acute infectious myocarditis. Chest 1986;89:106. Nieminen MS, Heikkila J, Karjalainen J. Echocardiography in acute infectious myocarditis: relation to clinical and electrocardiographic findings. Am J Cardiol 1984;53:1331. Pasquini JA, Gottdiener JS, Cutler DJ, Fletcher RD. Myocarditis with transient left ventricular apical dyskinesis. AM HEART J 1985;109:371. Chandraratna PAN, Nimalasuriya A, Reid CL, Cohn S, Rahimtoola SH. Left ventricular asynergy in acute myocarditis. Simulation of acute myocardial infarction. JAMA 1983;250:1428. Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man. Circulation 1977:66:613. Tanimura A, Nakashima N, Komatau Y, Arakawa M, Ookita Y, Senoo T, Toshima H, Koike S. Clinicopathologic study of Coxsackie B viral myocarditis. Acta Path01 Jpn 1980; 30~161. Wookruff JF. Viral myocarditis, a review. Am J Path01 1980;101:427.
8. Hauser AM, Gordon S, Cieszkowski J, Timmis GC. Severe transient left ventricular “hypertrophy” occuring during acute myocarditis. Chest 1983;83:275. 9. Gerhring J, Rudroff W. Reversible asymmetric septal thickening in the echocardiogram in a case with suspected perimyocarditis (author’s translation) A Kardiol 1981; 76~389. 10. Oda T, Hamamoto K. Morinaaa H. Left ventricular hvuertro11.
phy in non-rheumatic 1982;46:1235. Cueto-Garcia L, Reeder
myo&ditis
in children.
GS, Kyle
RA,
Wood
Jpn-Circ
J
Dl, Seward
JB,
Naissens J, Offord KP, Greipp PR, Edwards WD, Tajak AJ.
12.
13.
Echocardiographic findings in systemic trum of cardiac involvement and relation Co11 Cardiol 1985;6:737. Lundin S, Friberg P, Hallback-Norlander hypertrophy improves cardiac function hypertensive rats. Clin Sci 1981;61(Suppl
Messerli FH. Clinical determinants ventricular
14.
hypertrophy.
dium
in cardiomegaly.
Circ
specJ Am
M. Left ventricular in spontaneously 7):109s.
and consequences of left
Am J Med
Grimm AF, Kubota R, Whitehorn
amyloidosis: to survival.
1983;74:51.
Res 1963;12:118.
Bing OHL, Matsushita S, Fanburg BL, Levine HJ. Mechanical properties of rat cardiac muscle during experimental
16.
Spann
Ciy-
Jf,
Buccino
Reversibility of prolonged chronotropic dysfunction with theophylline following orthytopic cardiac transplantation Kenneth A. Ellenbogen, MD, Szabolcs Szentpetery, and Marc R. Katz, MD. Richmond, Va.
A relatively high incidence of sinus node dysfunction after orthotopic heart transplantation has been reported by several groups. Is2 Impairment of sinus node automaticity as well as sinoatrial conduction has been documented.3 Sinus node dysfunction has been observed in the early postoperative period of follow-up for orthotopic heart transplantation as well as in asymptomatic long-term survivors. The incidence of sudden death observed in transplant patients may be associated with sinus node dysfunction of the donor atria. Little is known about the mechanism or natural history of sinus node dysfunction in heart transplant patients. The treatment of sinus node dysfunction with permanent pacemakers is problematic in this population, since infection remains a significant cause of morbidity and mortality in transplant patients. One recent report5 describes some complications of pacing unique to heart transplant patients. In this report we describe two cases of symptomatic sinus node dysfunction associated with cardiac allograft rejection that were reversed by theophylline treatment. Case No. 1. A 21-year-old man developed a flu-like syndrome followed by progressive shortness of breath and orthopnea. An echocardiogram showed severe four-chamber enlargement and an estimated ejection fraction of 10% to 20%. Further work-up confirmed a diagnosis of idiopathic dilated cardiomyopathy and the patient underwent othotopic cardiac transplantation.‘j The donor heart ischemic time was 2 hours and 24 minutes. Immunosuppression was achieved with cyclosporine, axathioprine, and perioperative antithymocyte globulin (ATG). Fortyeight hours following heart transplantation, the donor heart rate was noted to vary between 60 and 85 beats/min. Two weeks after transplantation, a transvenous endomyocardial biopsy showed moderate allograft rejection. The donor heart rate decreased to 40 to 45 beatslmin, with multiple episodes of junctional rhythm at a rate of 35 to 40 beats/min (Fig. 1). A 24-hour Holter recording revealed heart rates varying between 34 to 59 beats/min and averaging 44 beats/min (Fig. 2). Rejection was treated with pulsed methylprednisolone therapy and an increased maintenance dose of cyclosporine.
‘071.~8:234. _-. A,_ RA, Sonnenblick
F.ec
EH,
Braunwald
E.
From the Division of Cardiology Veterans Administration Medical ia. Supported
Contractile state of cardiac muscle obtained from cats with experimentally produced ventricular hypertrophy and heart
Reprint McGuire
failure.
23249.
Circ
Res 1967;21:341.
MD,
WV. Properties of myocar-
15.
hvpertmyh>r
July 1988 Heart Journal
by funds
from
and Cardiothoracic Center, and Medical
the Veterans
Surgery, College
McGuire of Virgin-
Administration.
requests: Kenneth A. Ellenbogen, MD, Cardiology VA Medical Center, 1201 Broad Rock Blvd.,
Division (lllJ), Richmond, VA