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the thinned trabeculae in the proximal ends of the
ribs.'"
The tumor-simulating intrathoracic masses of heterotopic marrow occur characteristically either unilaterally
or bilaterally in the posterior mediastinum, often below
the seventh thoracic vertebra and sometimes with a
segmental arrangement.ll Radiologically, they present
as rounded, soft tissue opacities paravertebrally with a
clear-cut outline, sometimes lobulated due to the superimposition of several densities. No calcification has been
reported in these masses, nor has there been any report
of bone erosion. Intrathoracic EMH appears to follow a
constant pattern resulting in this uniform radiologic picture, the findings of which have been correlated with
pathologic studies.s.5*15 Other diagnostic features in
EMH include a history of chronic anemia, splenomegaly
(or history of splenectomy) and possible radiologic bone
changes characteristic of the hemopoietic disorder
( eg thalassemia)
In the differential diagnosis, the following lesions
should be considered:
( 1) Neurogenic tumor should be considered first, as it
is the most common posterior mediastind tumor. However, in 50 percent of the cases there is evidence of
sclerosis or erosion in the adjacent bone;20 lobulation is
absent and there is no predilection for involvement of
the lower thoracic region.
(2) Hodglun's disease with mediastinal involvement
usually affects the anterior and superior mediastinal regions, and pain is often a prominent symptom.
(3) An abscess arising from the thoracic spine may
have systemic symptoms, has no lobulation and may
reveal involvement of bone structures.
( 4 ) Primary or secondary malignancies are not usually lobulated and may show bone involvement and systemic signs, with a rapidly progressive course.
(5) An extrapleural cyst is single, producing a curved
margin anteriorly and laterally.
(6) An intrathoracic meningocele may present radiologically as a single or occasionally as bilateral circular
opacities. Vertebral deformities are usually present with
or without associated neurofibromatosis.
Posterior mediastinal masses are commonly neoplastic
and thoracotomy is invariably considered under these
circumstances. A diagnosis of EMH before operation is
therefore vital, as it would avoid unnecessary surgery.
An awareness of the condition and a careful consideration of the diagnostic features mentioned will lead to a
confident diagnosis before operation.
.
1 Brannan D: Extramedullary hematopoiesis in anemias.
John Hopkins Med J 41 :104, 1927
2 Gleave HH: Paravertebral heterotopia of bone marrow in
case of acholuric jaundice. J Pathol42:538, 1936
3 Dawson BE: Hume Lectures on haemolytic icterus. Br
Med J 1:963, 1931
4 Wintrobe MW: Clinical Hematology (ed 4). Philadelphia, Lea & Febiger, 1956, p 48
5 Hartfall SJ, Stewart MJ: Massive paravertebral heterotopia of bone marrow in a case of acholuric jaundice. J
Pathol37:455, 1933
212 JOE R WISE
6 Hanford RB, Schneider GF, MacCarthy JD: Massive
thoracic extramedullary hemopoiesis. N Engl J Med
203: 120, 1960
7 Ross P, Logan W: Roentgen findings in extramedullary
hematopoiesis. Am J Roentgen01 Radium Ther Nucl Med
106:604,1969
8 Marinozzi V: Aspetti insoliti dell'iperplasia midollare
nelle anemie emolitiche. Haematologica 43:737, 1958
9 Knoblich R: Extramedullary hematopoiesis presenting as
intrathoracic tumour: report of case in patient with
thalassaemia minor. Cancer 13:462, 1960
10 Malamos B, Papavasiliou C, Avramidis A: Tumour simulating intrathoracic extramedullary hemopoiesis: report of
case. Acta Radio1 57227, 1962
11 Papavasiliou C, S6kakis P: Tumour-simulating intrathoracic marrow heterotopia in thalassaemia major.
Thorax 19:121, 1964
12 Sorsdahl OS, Taylor PE, Noyes WD: Extramedullary
hematopoiesis: Mediastinal masses and spinal cord compression. JAMA 109:343, 1964
13 Seidler RC, Becker JA: Intrathoracic extramedullary
hematopoiesis. Radiology 83: 1057, 1964
14 Hanam E: Massive thoracic extramedullary haemopoiesis
in a case of haemoglobin E-thalassaemia. Singapore Med
J 5: 122, 1904
15 Plonskier M: Uber tumorformige (extramedullare, heterotype) subpleurale Knockenmarksherde. Virchows
Arch [Pathol Anat] 277:804, 1930
16 Saleeby ER: Heterotopia of bone marrow without apparent cause. Am J Pathol 139, 1925
17 Lyall A: Massive extramedullary bone formation in case
of pernicious anemia. J Pathol 41:469, 1935
18 Gray H: Anatomy of the Human Body (Lewis WH, ed),
( ed 24). Philadelphia, Lea, 1942, p 1428
19 Case records of Massachusetts General Hospital, Case 14,
1968. N Engl J Med 278:782, 1968
20 Good CA: Roentgenologic diagnosis of surgical lesions of
mediastinum. Chicago Med Soc Bull 53:51, 1950
Patient-Activated Atrial Pacing. in
the Treatment of Recurrent
Supraventricular ~ a c h ~ c a r d i a *
Joe R. Wise, Jr., M.D.
A specially designed pacemaker was implanted in a patient witb recnrrent supraventricular tachycardia complicated by pulmonary edema. The unit is designed to
pace the right atrium temporarily when activated by the
patient, wing a hand-held magnet. All subsequent episodes of snpraventricular tachycardia have been terminated within a few seconds.
R
ecurrent supraventricular tachycardia can usually
be prevented by suppressive antiarrhythmic drug
*From the Cardiology Section, Medical Services Eastern
Maine Medical Center, Bangor, Me.
Reprint requests: Dr. Wise, One Fern Street, Bangor, Maine
04401
CHEST, 65: 2, FEBRUARY, 1974
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therapy. In some patients, however, drugs alone are
ineffective and other methods of control have been recommended including combinations of drugs and ventricular p a ~ i n g , ~and
. ~ the use of implanted carotid
sinus stim~lators.~
Recently, temporary atrial pacing has
been used successfully to terminate episodes of supraventricular tachycardia.4~7In some cases, the tachycardia recurs so frequently that temporary atrial pacing is
impractical and a more permanent method of control is
required.sJ0 The purpose of this report is to describe
the use of a specially designed permanent pacemaker
which can be activated on demand by the patient to
pace the right atrium and interrupt paroxysms of supraventricular tachycardia, which could not be controlled
by more conventional means.
The patient, a 36-year-old man, first noticed intermittent
palpitation at age 19. Medical evaluation at that time disclosed no associated cardiovascular abnormality. Episodes of
rapid heart action were brief, terminated spontaneously and
occurred several times each year. At age 36, after two years
of progressive dyspnea on exertion, he developed cardiac
failure which responded promptly to treatment with digitalis
and diuretics, but left ventricular hypertrophy and third and
fourth heart sounds persisted. The episodes of rapid heart
action, subsequently found to be supraventricular tachycardia, occurred much more frequently and often precipitated
acute pulmonary edema. Electrical cardioversion was required
For termination of the supraventricular tachycardia on 13
occasions in one year. Combinations of antiarrhythmic drugs
including digoxin (0.25 mg, twice a day), and quinidine
gluconate (450 mg every eight hours), propranolol ( U) mg
four times daily), diphenylhydantoin ( 100 mg four times per
day) and procainamide (250 mg every four hours) failed to
reduce the frequency or duration of the attacks. There was
no evidence of ventricular pre-excitation and thyroid function
studies ,showed no abnormalities. Blood pressure was never
elevated. On two occasions intra-atrial electrograms showed
what appeared to be a reciprocating tachycardia which could
be terminated by atrial stimulation at rates of 70 per minute
and 100 per minute (Fig 1). Ventricular stimulation was
ineff ective ( Fig 2 ) . In view of the dilliculty in c o n b b g the
arrhythmia, a trial of longterm atrial pacing was elected.
Attempts to position a pacing catheter within the coronary
sinus were unsuccessful. On March 18, 1972, an epicardial
electrode was attached to the right atrium, low near the
junction of the atrium and the inferior vena cava in a region
where endocardial pacing had been effective previously. The
pulse generator (General Electric dual rate A207OAA) implanted in the right axilla was designed to operate at a fixed
rate of 110 beats per minute only when activated by handheld magnet. Since implantation of this unit, the episodes of
rapid heart action have continued to occur several times a
week, but are terminated quickly, usually within 10 to U)
seconds, after activation of the pacemaker.
Re-entrant or reciprocal rhythm rather than a rapidly
discharging ectopic focus may be the basis for the majority of supraventricular tachycardias.~Jl~l~
According
to this view, an atrial premature beat occurring during
the relatively refractory period of the atrioventricular
node is conducted to the ventricle more slowly than
normally timed sinus beats. This slowed conduction allows time for some of the fibers of the A-V node to recover so that the wave of excitation may be conducted, not
RCURE
1( A ) . Intra-atrial electrogram. Continuous recording from catheter advanced
slowly into right atrium from superior vena
cava. Note that atrial depolarization appears
within (toward end of top strip) but after onset of QRS complex.
FIGURE
1( B ) . Surface electrocardiomam dur-
ing atrial ;acing. Random atrial st&ation at
100 per minute. ( .) restores sinus rhythm (t)
CHEST, 65: 2, FEBRUARY, 1974
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PATIENT-ACTIVATED ATRIAL PACIN6 213
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FIGURE2. Surface electrocardiogram. Ventricular pacing (.) produces ventricular depolarizations which fail to terminate the tachycardia.
only to the ventricles, but also retrograde to the atrium
there producing an atrial depolarization, which is in turn
conducted to the ventricles, and a reciprocal cycle is
established. For at least some of the arrhythmias, the reentry cycle seems to be entirely confined within the A-V
junctional tissue.13 A single, critically timed electrical
stimulus can intenupt a re-entry cycle by prematurely
depolarizing a portion of the pathway. Using this principal, lowenergy direct endocardial stimulation using
pacemaker devices has been used to terminate a variety
of supraventricular tachycardias.4-9*14,15
In our patient, on two occasions, atrial stimulation
with a standard external pacemaker (Medtronic 5880)
at rates of 70 per minute and 100 per minute terminated
the tachycardia. Termination of the arrhythrma by random atrial stimuli in thls manner suggests that the
rhythm was a re-entrant or reciprocal type. During the
temporary pacing, rates of 70 per minute and 100 per
minute and stimulus strengths of less than 10 ma were
selected since they were within the capability of standard available pacemaker pulse generators. No attempt
was made to initiate the tachycardia. It is of interest that
ventricular pacing in this case produced ventricular contractions, which did not tenninate the tachycardia (Fig
2 ) . This suggests that retrograde conduction to the reentry pathway was blocked and that ventricular pacing
would have been ineffective in terminating the tachycardia. After the effectiveness of atrial pacing was established, a permanent pacing system was implanted. The
pulse generator, used previously by Preston and Kirsha
in a patient with Wolff-Parkinson-White pre-excitation,
is capable of pacing at either of two pre-selected rates.
The basic or primary pre-set rate is zero so that the pulse
generator remains off until activated. A magnet held over
the pulse generator activates a reed-switch which converts the unit to the second pre-set rate, in this case 110
beats per minute, and the pulse generator paces at this
rate until the magnet is withdrawn and the unit reverts
to the primary rate of zero. Our patient has no d&culty
in recognizing the onset and termination of his episodes
of tachycardia. At the onset of the tachycardia, the magnet is held over the pulse generator for a few seconds
until the tachycardia is terminated. The magnet is then
returned to a small case attached to the patient's belt.
Battery life should be prolonged since the unit remains
inactive most of the time and no sensing circuit is
involved. Pacing from the atrium rather than competitive ventricular pacing avoids the danger of ventricular
fibrillation. Thoracotomy can be avoided by pacing from
the coronary sinus but this,too, is not without r i ~ k . l ~ - ~ s
ACKNOWLEDGMENT: We thank David M. Sensenig,
M.D., Eastern Maine Medical Center, for performing the
thoracotomy.
1 Cheng TO: Transvenous ventricular pacing in the treat-
ment of paroxysmal atrial tachyarrhythmias alternating
with sinus bradycardia and standstill. Am J Cardiol 22:
874-879,1968
2 Cohen HE, Kahn M, Donoso E: Treatment of supraventricular tachycardias with catheter and permanent pacemakers. Am J Cardiol20:735-738, 1967
3 Cantwell JO, Weaver WT, Fletcher GF: Paroxysmal
atrioventricular junctional tachycardia. Treatment with
carotid sinus stimulation. JAMA 216: 1860-1862, 1971
4 Haft JI, Kosowsky BO, Lau SH, et al: Termination of
atrial flutter by rapid electrical pacing of the atrium. Am J
Cardiol20:239-244, 1967
5 Massumi RA, Kistin AD, Tawakkol AA: Termination of
reciprocating tachycardia by atrial stimulation. Circulation 36:637-643, 1967
6 Hunt NC, Cobb FR, Waxman MB, et al: Conversion of
supraventricular tachycardias with atrial stimulation:
Evidence for re-entry mechanism. Circulation 38:10601065, 1968
7 Cohen HE, Meltzer LE, Latimer G, et al: The treatment
of refractory supraventricular arrhythmias with induced
permanent atrial fibrillation ( abstr ) . Circulation ( Suppl
3 ) 42:III-144, 1970
8 Zipes DP, Wdace AG, Sealy WC, et al: Artificial atrial
and ventricular pacing in the treatment of arrhythmias.
Ann Intern Med 70:885-896, 1969
9 Preston TA, Kirsh NM: Permanent pacing of the left
atrium for treatment of WPW tachycardia. Circulation
42: 1073-1077,1970
10 Davidson RM, Wallace AG, Sealy WC, et al: Electrically
induced atrial tachycardia with block. Circulation 44:
1014-1021, 1971
11 Moe GK, Preston JB, Burlington H: Physiologic evidence
for a dual A-V transmission system. Circulation Res 4:357375, 1956
12 Bigger JT Jr, Goldreyer BN: The mechanism of supraventricular tachycardia. Circulation 42373-688, 1970
13 Coldreyer BN, Bigger JT Jr: Site of re-entry in paroxysmal supraventricular tachycardia in man. Circulation 43:
15-26, 1972
14 Barold SS, Linhart JW, Samet P, et al: Supraventricular
214 JOE R. WISE
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CHEST, 65: 2, FEBRUARY, 1974
tachycardia initiated and terminated by a single electrical
stimulus. Am J Cardio124:37-48, 1969
15 Kitchen JC, Goldre~erBN: Demand pacemaker for refractory supraventricular tachycardia. N Engl J Med
287:596-599,1972
16 h e r DH, Moss AJ: Permanent percutaneous atrial
pacing from the coronary vein. Circulation 42427-436,
1970
17 Moss AJ, Rivers RJ, Cooper M: Long-term pervenous
atrial pacing from the proximal portion of the coronary
vein. JAMA 209:543-545, 1969
18 Nepodono RJ, Cannon E, Zaroff L: Two observations
regarding pervenous atrial pacing from the coronary sinus. J Electrocardiol4:275-278,1971
Mycotic Aneurysm of the Ascending
Aorta Secondary to Serratia
Infection: Differentiation from
Prosthetic Valve ~ndocarditis*
Burt R. Meyers, M.D., Rashmikant Shah, M.D., and Martin
Lefkowitz, M.D.
Twenty-one months after prosthetic aortic and mltral
valve replacement, a 64-year-oM man developed bacteremia secondary to a Serratia infection. intensive investigation failed to reveal the origin of infection and gentamicin therapy did not eradicate the organisms from the
bloodstream. 'Ihe patient died. Postmortem examination
revealed a large mycotic aneurysm arising from the aortotomy site but no evidence of prosthetic valve endocarditis. Late occurring bacteremia following valve replacement is discussed. Aortography may be necessary to delineate this problem.
B
acterial and fungal endocarditis in patients with
prosthetic cardiac valves may respond to antibiotic
therapy alone but generally requires surgery with valve
Sande et all recently reported
replacement for
22 patients with prosthetic cardiac valves who had
sustained bacteremia and suggested a way of differentiating valvular involvement from other causes. We
recently treated a patient with prosthetic aortic and
mitral valves who developed sustained Serratia bacteremia. This was secondary to a mycotic aneurysm of
the ascending aorta, which could not be clinically differentiated from bacterial endocarditis. Mycotic aneurysms
in this area are uncommon and involvement with the
'From the Division of Infectious Diseases Department of
e the City
Medicine, The Mount Sinai School of ~ d c i n of
University of New York, New York, N.Y., and the Department of Pathology, Grasslands Hospital, Valhalla, N.Y.
Reprint requests: Dr. Meyers, Mount S i ~ Hospital,
i
100th
Street and Fifth Avenue, New York City 10029
species of the genus Serratia has not been previously
reported.
A 64-year-old man underwent aortic and mitral valve
replacement on June 19, 1970. After operation he developed
a wound infection at the lower end of the sternum which was
treated by debridement, cauterization and local measures.
Drainage persisted and in June, 1971, after culture revealed
Enterobacter organisms, doxycycline was given orally for ten
days, with some clinical improvement.
In September, 1971, Enterobacter organisms were cultured
again, and doxycyche therapy was reinstituted. Drainage
persisted and two days prior to admission, the patient complained of cough, fever and weakness, and 1 ml of serosanguinous fluid was aspirated from the wound but was not
cultured. Administration of tetracycline was resumed but the
fever and symptoms persisted and the patient was readmitted
on March 31, 1972. Physical examination on admission revealed an irregular pulse rate of 88/min; respirations,
16/min; blood pressure 110/60 m m Hg; and temperature,
39.4444 CO.The conjunctivae were free of petechiae. The
neck veins were distended and showed a positive hepatojugular rdlex. There were rilles and rhonchi at the lung bases.
Examination of the heart revealed cardiomegaly with the
point of maximum intensity (PMI) in the sixth intercostal
space at the anterior arillary line. There was a blowing
systolic murmur heard at the apex (grade 3/6) and a short
harsh systolic murmur (grade 4/6) heard over the aortic
area. The liver was palpable 2 cm below the costal margin;
the spleen was not enlarged. There was 2+ clubbing of the
fingers.
Administration of antibiotics was discontinued and blood
cultures were obtained. Roentgenograms of the chest revealed an enlarged heart with prosthetic aortic and mitral
valves and prominence of the pulmonary vasculature. An
intravenous pyelogram showed an intrarenal mass suggestive
of a cyst. Laboratory studies disclosed the following values:
hematocrit, 32 percent; white blood cell count 7,50O/rnms,
with 74 percent polymorphonuclear leukocytes, 20 percent
lymphocytes and 6 percent monocytes; blood urea nitrogen
( BUN),16 mg/100 ml; serum protein, 6.9 gm/ml; albumin,
3.1 gm/100 ml; alkaline phosphatase, 110 international units
( IU ) ; serum glutamic oxaloacetic transaminase ( SCOT ) , 65
IU; and the urinalysis was normal. The latex-fixation test was
positive in a dilution of 1/160. Daily temperature spikes to
38.8889 COoccurred, and blood cultures drawn on the sixth
hospital day revealed the presence of Serratia. Intramuscular
administration of gentamicin was begun and blood cultures
drawn on April 13 and 14 again revealed this micro-organism.
Twenty days after gentamicin therapy was begun, he became
lethargic and less responsive. Blood cultures obtained on the
36th hospital day were again positive for Serratia. Repeated
chest films showed cardiomegaly and congestive heart failure, without evidence of sternal osteomyelitis. On the 46th
hospital day he became unresponsive, passed a tarry stool,
developed hypotension and died.
Autopsy findings revealed a healed midsternal incision
with no evidence of infection, abscess formation, or
osteomyelitis.
A fibrous walled saccular false aneurysm 8 cm in its
greatest diameter, was noted between ;he sternum and
the anterior wall of the aorta. The inner wall had a
granular fibrinous, shaggy and cobblestone appearance
CHEST, 65: 2, FEBRUARY, 1974
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MYCOTIC ANEURYSM 215