Myocardial Infarction and Atrial Arrhythmias

By THOMAS N. JAMES, M.D.

ATRIAL ARRHYTHMIAS occur in about

10 per cent of acute myocardial infaretions and the commonest of these arrhythmias
is atrial fibrillation.' When atrial fibrillation
is sustained after beginning during myocardial infarction, it has been reported to be
associated with an 89 per cent mortality.2
Although there have been a number of studies on the clinical aspects of the association
of such rhythm disturbances with myocardial
infarction,3-9 little is known regarding their
pathogenesis.
This is a report of findings from 11 selected
cases of patients with myocardial infarction
who developed atrial arrhythmias. All were
necropsied. Each heart was carefully dissected to determine the manner of blood supply to the atria as well as the ventricles, and
special attention was given to the blood supply to the sinus node and AV (atrioventricular) node.10 11 Note was made whether
occlusions in the main coronary artery were
proximal or distal to the origin of the nodal
arteries. For histologic study the sinus and
AV nodes were cut serially at 2 mm. intervals
in all 11 cases.
Because atrial fibrillation both clinically
and experimentally is so closely related to
other atrial arrhythmias (atrial flutter, atrial
tachycardia, etc.), the terms "atrial fibrillation" and "atrial arrhythmias " in general
are used interchangeably.

Case Reports
Case 1

R.C., a 53-year-old man, died of subacute

bacterial endocarditis with rupture of the aortic
valve, and lamellar myoeardial infarction of both
ventricles. His final illness was associated with
multiple atrial arrhythmias (fig. 1). At necropsy
there was marked compromise of the lumen of the
left circumflex artery by old sclerosis, and this
artery crossed the crux to supply the AV node;
in addition there was a recent occlusion of the
small right coronary artery proximal to the origin
of the sinus node artery (fig. 2). Ecehymoses were
present in the epicardium of the sulcus terminalis
over the sinus node, and these corresponded to
infarction of the node seen microscopically (figs.
3 and 4). No pathology was found in the AV node.
Case 2
M.K., a 68-year-old woman, died during an
acute anterolateral myocardial infarction with
atrial fibrillation. At necropsy most of the left
ventricle was infareted and a fresh thrombus
occluded the main left coronary artery; the sinus
node artery arose from the left circumflex branch.
There was an old occlusion of the right coronary
artery just beyond the margo acutus and proximal
to the AV node, which it supplied. There was
infarction of the sinus node (fig. 5), but no
pathology was found in the AV node.
Case 3
J.D.H., a 78-year-old man, died of an acute
myocardial infarction of the left ventricular free
wall and septum. His final illness included the
onset of atrial fibrillation. At necropsy there was
a recent occlusion of the main left coronary artery,
plus an old occlusion of the right coronary artery
proximal to the origins of the arteries supplying
both the sinus node and AV node. In the sulcus
terminalis there were gross epicardial henorrhages over the sinus node (fig. 6), which corresponded to a hemorrhagic infarction seen histologically (fig. 7). There was no infarction in the
AV node.
Case 4
H.L., a 72-year-old man, died of an acute posterior myocardial infarction. Initially his electrocardiogram showed incomplete AV block but later

From the Division of Cardiovascular Diseases,

Henry Ford Hospital, Detroit, Michigan.
Supported in part by grants from the U. S. Public
Health Service (H-5197) and the Michigan Heart
Association.
Partially presented at the Scientific Sessions of the
American Heart Association, St. Louis, Missouri,
Ostober 21, 1960.

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7JAMES

762

Figure 1
Electrocardiogram of case 1, showing intermittent simis node activ ity.
he developed atrial fibrillation (fig. 8). At necropsy there were two recent occlusions, one in
the right coronary artery at the Iaar-o acutus and
the other at the origin of the left anterior descending. artery, eomiipIromising the lumen of the main
left coronary artery also. The sinus node artery
a.riose from the left circumflex branch, adjaent
to the main left coronary artery, and was partially
involved by the recent occlusion. The right coronary arterv crossed the crux of the heart and
supplied the AV node. Histologically, old and
new infaretion involved most of the sinus node
exit junctions (fig. 9); in the AV node there was
lesser damage.
Case 5
T.S., a 64-year-old man, died of congestive
failure due to intractable atrial fibrillation with
ralpid ventricular response. At necropsy there
was old occlusion of the left anterior descending,
the left circumflex, and right coronary arteries.
The right coronary occlusion was proximal to the
origin of both nodal arteries (fig. 10). Except
for some small new foci the ventricular infarction
in most of the left ventricle was old. In the epicardiuma of the sulcus termninalis there were ecehymoses over the sinus node (fig. 11), corresponding
to infarction present microscopically (figs. 12 and
13). No pathology was found in the AV node.

Case 6
L.V., al 61-vear-old maan, died of an acute posterolateral myocardial inflrction durinig which he
developed atrial fibrillation. At neciopsy there
was ain old occlusion of the riglht coronary artelrv
at the miiaro acutus, with that artery suupplying,
aln unusually large area of the posterior and lateral
left ventricle, as well as the AY node. There was
also a, recent occlusion of the smaller main left
corona my artery proximal to the origin of the
sinus node artery, which arose from the even
smaller left circumflex artery. There was infaretion
at, the exit junctions of the sinus node, and marked
sclerosis of the AY node artery (fig. 14) ; no
other pathology was found in the AkV node.
Case 7
C.C.B., a 66-vear-old miman, died of posterior
vlloca
oIrdiall inifaretion(during. which he developed
an atrial tachvcardia of 176 per minute. At mnccropsy there was a recent occlusion of the right
coronari artery proximaal to the ori-in of the
sinus node artery, the right coronary continuing
to supply the posterior wall and AV mmode. Ecehymoses were presemmt imm the epicardiuma over the
sinus node (fig. 15) and inmfarctiomm was present
in the sinus mnod(e. No pathology-\ was found inl the
\T node.
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-MYOCARDIAL INFARCTION AND ATRIAli ARRIHYTHAIAS

Figure 2

Photograph of the heart,

e((se 1. -Right arrow

indicates the cut edge of a receut occlusion of the
right (co'0arYa1( tirteriy; left arrow) in(lic(ltes the
sinus node artery, which (trose distal to the occll(sion. Jo, is the aorta; Ap, the right (trial a))pendage; SVC, the superior
(a; (lcid RV, the
right rentricle.
rena

763

Figure 4
Higher power photo micrograph of the siuus no(de,
case 1, showing hems0orrhage anid degeneration (at
the junction of the node and atrium.

Figure 3
photonm icrograph, o'( the sinus node,
c(a.se 1. In this tind subsequent photomicrographs
N refesrs to the sin as nlode aud A to the right
atriulm. There is hemorrhage and in(ar(tion at the
/un('tion of the n1ode a(d atr
l Miu

loiu'-p)o

ncr

Case

Figure 5

V.HI.
lateral

t,

62-vealr-old

llyaocardial

man,

(lied

infairction,

lhge anterodurilng which hte

at'

developed atrial fibrillation. At necropsy there was

old occlusion of the right coronary artery
plroximlal to where it crossed the crux, supplying
the AV node. The left circumflex artery was occluded by an old lesion at the origin of the sinus
node artery, and the left anterior descending
artery was oecluded by a, fresh thronibus 2 eimi.
froai its origin. Infaretion was found in both the
sinus node anid AV node.
all

Two photomicrographs of the sinas node, ('ase 2,

showing (on gestion and hemorrhage (it the junt'tion of the ncode and (tri((n( w(nder low. po(e('r (tap)

and high(

power

(bottom).

Case 9

V.G., a 64-year.-old mani, died of acute posterior

myocardial infarction. In his final illness he had
a variety of atrial arrhythmias, including atrial
fibrillation. At necropsy there was a recent occlusion of the left circumflex coronary artery near

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JAMES

764

Figure 7
A low-power photomicrograph of the sinus node
of case 3, showing hemorrhages in the epicardiam
and at the junctions of the node and atrium.

Figure 6
Photograph of the sinoatrial junction of the heart
of case 3. Arrow points to the ecchymoses in the
sulcus terminalis directly overlying the sinus node;
RA is right atrium.

the niargo obtusus, with the circumflex artery continuing to the crux of the heart and posterior left
ventricle, supplying the AV node. There was an
old occlusion of the relatively small right coronary
artery proximal to the origin of the sinus node
artery. Gross ecchymoses were present in the
epicardium of the sulcus terininalis over the sinus
node; these corresponded to an infaretion of the
sinus node seen microscopically (fig. 16). No
pathology was found in the AV node.
Case 10

W.S., a 48-year-old man, had a posterior myocardial infaretion 1 year previously and then died
during a lateral infarction. During both of these
he had intermittent cessation of sinus node activity
(fig. 17). At necropsy there was infarction of
most of the left ventricle, with old occlusions of
both the left anterior descending artery and the
left circumflex artery. The latter vessel supplied
the AV node and the entire left ventricle except
the anteroseptal portion, the right coronary artery
being diminutive. There was a fresh occlusion in
the first centimeter of the left circumflex artery,
the sinus node artery arising distal to this, at a
point of old occlusion near the margo obtusus.
Infaretion was present in both the sinus node
and AV node.
Case 11
T.L.D., a 66-year-old man, died of myocardial
insufficiency during intractable atrial flutter and
fibrillation with a rapid ventricular response; he

also had hemachromatosis. At necropsy there was

old occlusion of the left anterior descending artery
and of the right coronary artery proximal to the
origin of the sinus node artery; the right coronary
continued to the crux of the heart to supply the
posterior wall and AV node. Ventricular infaretion
was streaky and both old and new. There were
edema and hemorrhage at the exit junctions of the
sinus node. Degenerative changes were present in
the AV node about iron deposits (fig. 18); despite
careful searching, no iron could be demonstrated
in the sinus node.

Comment on the Eleven Cases

In all 11 cases a coronary occlusion was
present proximal to the origins of both the
sinus node artery and AV node artery. In
six of the hearts gross eechymoses were found
in the sulcus terminalis directly over the sinus
node. Data relating the nodal histopathology
to the arrhythmias are presented in table 1.
Microscopically, infaretion of the sinus
node was found in all 11 cases. Lesser changes
were apparent in the AV node in five eases.
These changes were acute and consisted primarily of hemorrhage and edema; however,
collagen deposition and fatty infiltration
were present in scattered foci of all the sinus
nodes, suggesting that previous focal damage
had occurred.
The sites of damage in the sinus node were
characteristic in every case, occurring at the
junctions of the node with the right atrium
and sinus intereavarum. Hemorrhages (at
these locations involved Purkinje tracts leaving the node and may be presumed to be asso-

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Figure 8
4 showing inceomp)lete AlVIblc(1 (P-R time 0.26
fd'rom
Two
second) at the onset of anl (IaUcf )sfterior mqocar(lwl in fare/ion (top), and atrial
fibrillationk 2 days later (bottom).
case

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JAMES

766

Figure 10

Figure 9
Low-powver (top) and high-power (bottoni) photomicrograpvhs of the sinns node, case 4, showing
fibrosis, fatty replacenient, and recent hem orrhage
ait the junction of the sinus node and atrium.

Photograph of the heart of case ), (lemost rating

the sinus node arterql (left arrow.) a risinl from
the rig7ht coronary artery (right (arrow'7); in the
nuclue ~of right coronary artery inlica ted hq the
('crled arrow there iCaS a complete occlusioni. -1 O,
the aorta; Ap, the right atrial appendage; SVC,
the superior rena cara. The sinus node (1itery'i
courses into the sinus node at the junctioi oJ the
atrial appendage and rena cora.

(iated with impairment of normal transmnissioni of the sinus impulse to the rest of the
heart. Pathologic(changes were less often seen
in the central portion of the node or in the
more distal atrial muscle, suggesting that the
exit junctions of the node may be peculiarly
vulnerable to acute hypoxia.
Ilistopathology of the AV node was less
eonsistent and less striking. Presenee of an
oeelusion in the main coronary artery proximal to the origin of the AV liode artery in
all 11 eases certainly suggests that those AV'
nodes must have been rendered hypoxie. The
possible contribution of this AY nodal hypoxia to the pathogenesis of atrial arrhythmias is discussed later; however, at present

this remains a speculative probability.

Discussion

Although it has long been thought that

atrial arrhythmias ini acute iinyocardial infarction probably represent concomitant

Figure 11
Another ciew a]f the heart in figure It (case .3),
denionistra(tingl the ecchymoses in the su/l(c.s ternira bet eewn
nalis o e thesicnas node, bueing the are
the two )iii he('ads. SiT, the spelr)ior r(en(a (c0 C;
and RBA, the right atrium.

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MYOCARDIAL INFARCTION AND ATRIAL ARRHYTHMTIAS

767

Figure 1J2A
Lo u'-po Iwer ph otom icrograph of the sin us node
froin case 5. Hemeiorr)-hagic infarction is present
between the bodq of the ncode and the atrium.

Figure 13
Mlediin m -powieer (top) and high-pu wer (bottom)
photomicrographs o!7 the hemnorrhagfic inifar(tioni at
(case 5).
thle juncl(tioni of the no(de (ln t

Figure 14

Figure 12B
Low-power pwhotonticrograph through the tail of
the node, 10 mm. from figure 12A. Hemorrhage
and old fibrosis hare virtuallib replaced the node.

Photomicrograph of the two branches of the AIncode artery, both sclerosed for more thaw 75 per
cent of their laminai and surrounded 1)1/ marV ode (case 6).
phologicalli normal AT'

atrial dliinage, evidence to support this clinical impression has been meager. A notable
exception was the demionstration by Cushing
et al.12 that the commonest elinically recognizable manifestation of atrial infarction was

the presence of an atrial arrhythmliia, hut they

did iiot specifically relate these observations
to the pacemaker of the heart. Atrial infarction in experimental animals is not, however,
associated with regular production of atrial

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JAMES

768

Figure 16
Photomicrograph of the sinus node of ease 9.
There is hemorrhage ant the junction of the node
and atrium, with degeneration of the node.

Figure 15
Photograph of the heart from case 7, showing the
ecchymoses in the sulcus terminalis over the sinius
node, indicated between the two arrows. RA, the
right atrium; RV, the right ventricle.

6. Atrial distention.
7. Hyperealeemia.
8. Increased circulating cateeholamines.
9. latrogenic factors.
Usually more than one of these factors is
present in any Riven case, but each is dis-

a.rrhythmlias,13' 14 and ligation of the primary

cussed separately.

blood supply to the sinus node of the dog

only rarely disturbs the sinus rhythnm.15 It
must be concluded that atrial arrhythmias
occurring during acute myocardial infarction
have a more complex pathogenesis.
There are few studies on the pathology of
the sinus node, exceptions being the recent
reports of Lev16' 1 and Hudson.18 Lev observed that increasing fibrosis in the sinus
node is a normal consequence of aging, making evaluation of old focal lesions there difficult. Hudson has noted that various pathologic changes in the sinus node are by no
means uncommon.
Based on a study of the 11 cases reported
here, and a review of the. published observations on this subject, the following factors
may be considered as influencing the onset of
atrial fibrillation (or other atrial arrhvthmias) during acute myoeardia~l infarction:
1. Depressed sinus node "dominance.'"
2. Impaired sinus impulse transmission.
3. Vagal and vagomimetic reflexes.
4. AV node injury.
5. Extranodal atrial injury.

Depressed Sinus Node "Dominance"

Since the cardiac pacemaker is naturally so

located that its regular stimulation of the
heart is distributed with maximal efficiency,
any condition producing sustained replacement of sinus rhythm by some other rhythm
must either destroy or weaken the sinus impulse, block this impulse, or be of such strong
potential itself as to supersede this impulse.
Experimental application of aconitine to canine atria is an example of the latter, but it
is significant that atrial fibrillation so induced
is self limniting. and aconitine must be reapplied if the arrhythmia is to be sustained;
as the extranodal impulse weakens, the undamaged sinus node resumes dominance.
Whether transmission of the sinus impulse
from the node to the atria can be suppressed
without damage to the sinus node and atrium
is problematical. That the impulse can be
blocked in its passage from the atria to the
ventricles without damaging the AV node is
well substantiated both experimentally and
clinically, .and the role of such block is dis('missed later.
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MYOCARDIAL INFARCTION AND ATRIAL ARRHYTHMIAS

769

Figure 18
High-power photomicrograph from the AV node
of case 11, demonstrating iron deposits and degeneration of the nodal fibers in this patient with
hemachromatosis.

Figure 17
Electrocardiogram (case 10) showing intermittent
cessation of sinus node activity during an acute
posterior myocardial infarction.

The present observations suggest that ischemia or injury of the human sinus node
influences the onset of atrial fibrillation in
myoeardial infaretion. That this alone is inadequate to produce such arrhythmia was
long ago suggested by the persistence of regular rhythm following destruction of the
region of the sinus node,19' 20 and further
suggested by the persistence of sinus rhythm
following ligation of the sinus node artery
of the dog.15 It must nevertheless be presumed
that ischemia or injury of the sinus node, by
weakening normal sinus node dominance of
the heart, is an important factor in this problem, and particularly a factor in prolongation
or sustaining of such arrhythmias.
Another important factor depressing sinus
node "dominance" is vagotonia. That some
vagotonia occurs in most acute myocardial
infaretions can little be doubted. It has even
been stated that increased vagal tone is the
universal mechanism of sudden death in myoeardial infaretion.21 The effect on the sinus
node of increasing vagal tone (especially the

right vagus) is well known22' 23 and consists

of increasing bradyeardia to ultimate cessation of all sinus node activity. When this occurs in a patient with other factors favoring
the onset of atrial fibrillation, it must be presumed to contribute to the onset of the arrhythmia. In addition there are other effects
of vagal stimulation that favor the onset of
fibrillation, such as increasing the normal
disparity of repolarization speed in atrial
fibers.24
Sinus arrest observed during acute myocardial infarction may be the result of either
vagotonia or sinus node ischemia or both, and
the clinical differentiation of the two factors
may be difficult. Atropine counteracts vagotonia, but its effect on sinus bradyeardia or
sinus arrest due to ischemic weakening of
sinus impulse formation is unknown. In man,
vagotonia encountered clinically is unlikely
to be unilateral, and bilateral vagotonia
should result not only in sinus bradyeardia
but also prolongation of AV conduction time;
in myocardial infarction, however, not only is
there likely to be bilateral vagotonia, but both
sinus and AV nodes may be rendered isehemic
at the same time by a coronary occlusion
proximal to both their nutrient arteries. In
every case in this study the main coronary
arteries were occluded proximal to the origin
of the blood supply of both nodes.

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Table 1
Summary of the Arrhythmias and Nodal Pathology in 11 Cases of Myocardial Infarction
Atrial arrhythmias

Case

Sinus node

1
2
3
4

Infareted
Infareted
Infareted
Infareted

Infarcted

5
6

Infarcted
Infarcted
Infarcted
Infareted
Infarcted
Infarcted
Infareted

No pathology found
Sclerotic AV node artery
No pathology found
Infarcted
No pathology found
Infarcted
Degeneration

7
8
9
10
11

AV node

No pathology found
No pathology found
No pathology found

Impaired Sinus Impulse Transmission

In all 11 of the cases, infarction occurred

at the junctions of the sinus node with the
right atrium and sinus intercavarum, regions
through which the normal sinus impulse must
pass to the heart. Although hemorrhages at
these points were impressive, in none of the
hearts were all the junctions damaged, so that
potential points of exit still existed.
Since potential points of exit still were
present, and since in experimental animals
virtually all the connections to the sinus node
can be severed without the occurrence of
atrial fibrillation,20 it must be concluded that
impaired sinus impulse transmission, like suppressed sinus node "dominance," may be a
contributing factor to the onset of atrial fibrillation during myocardial infarction, but
that it is rarely capable of producing this

effect by itself.
Other factors that may impair sinus impulse transmission during acute myocardial
infarction are atrial distention and cellular
anoxia. In the presence of congestive heart
failure atrial pressure rises and the atrium
distends as the ventricle fails to empty; in
addition to the reflex effects of atrial distention,25 the stretching of the atrial fibers
lengthens the distance the normal impulse
must travel, as well as probably further increasing the normal disparity of atrial fiber
repolarization. Hypoxia of the atrial fibers
during acute myocardial infarction also contributes to atrial dilatation, impaired atrial

Multiple atrial arrhythmias

Atrial fibrillation
Atrial fibrillation
Incomplete AV block, then
atrial fibrillation
Atrial fibrillation
Atrial fibrillation
Atrial tachycardia (176/minute)
Atrial fibrillation
Multiple atrial arrhythmias
Intermittent sinus arrest
Atrial flutter then fibrillation

conduction, and increase in normal disparity

of atrial fiber repolarization.
Vagal and Vagomimetic Reflexes

The effects of these very important reflexes

that contribute to the onset of atrial fibrillation during acute myocardial infarction are
discussed in detail under the other headings.
Both the origin and specific pathways of these
reflexes in acute myocardial infarction are
poorly understood. For possible mechanisms
and routes, considering the pathophysiology
of acute myocardial infarction, one may consult the comprehensive reviews of cardiovascular reflexes.25-29
AV Node Injury

The AV node is an efficient alternate cardiac pacemaker. Persistence of an efficient

regular cardiac rhythm in experiments in
which the sinus node is destroyed is most
likely due to assumption of pacemaking by
the AV node or juxtanodal centers. It seems
most reasonable, therefore, to believe that
main coronary artery occlusions that compromise the blood supply to both the sinus node
and AV node are more likely to evoke a disorganized rhythm than occlusions that compromise the blood supply of only the sinus
node. This proved to be the case in the present

study.
Since the right coronary artery supplies
the AV node in about 90 per cent of human
hearts, and the sinus node in about 55 per
cent,10' 11, 30 it is occlusion proximal to the
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MYOCARDIAL INFARCTION AND ATRIAL ARRHYTHMIAS

origin of the sinus node artery in the right
coronary artery that is most likely to be associated with atrial fibrillation.
Klainer and Altschule31, 32 observed that
patients who developed atrial arrhythmias
during myocardial infarction often had prolongation of the P-R interval in their electrocardiograms prior to the onset of the arrhythmia, and further that this AV block could be
reduced by the administration of atropine.
Although this is strong evidence that a vagomimetic influence on the AV node was present
in their cases, the possibility that the AV
block was due to ischemia or damage to the
AV node rather than to vagotonia was not
discussed, and the histology of the node was
not reported.
Injury to the AV node may impair AV
conduction sufficiently to reduce cardiac output and coronary flow. The importance of reduced coronary flow in the pathogenesis of
arrhythmias during acute myocardial infarction has recently been stressed by Corday
and others.33 3
Extranodal Atrial Injury

Cushing et al.'2 emphasized the clinical importance of atrial arrhythmias in atrial infarction. Although damage to the sinus node
is probably the most important atrial injury,
damage to the "working" muscle of the atria
may also contribute to the onset of atrial
arrhythmias during acute myocardial infarction. For example, irritable atrial muscle at
the periphery of such injury may establish
a competing ectopic pacemaker, eager to take
over if the sinus node should fail. Such a
pacemaker may remain regular, but would
more likely deteriorate to fibrillation, especially under the influence of other factors.
Additionally extranodal atrial injury may
impair normal sinus impulse transmission, a
factor already discussed, and increase further
the normal disparity of repolarization speed
in atrial fibers.24 A weakened area of atrial
muscle may also contribute to atrial dilatation
from any other cause.
Since the sinus node artery is the largest
and most constant atrial artery in man,30 one

771

might expect an occlusion proximal to its origin to produce a large atrial infarct. This
did not prove to be the case in the 11 cases
studied, only four of the 11 having a grossly
recognizable atrial infarct, and the largest of
these was less than 1 cm.2 in size; all four
were in the right atrium. Thus extranodal
atrial injury does not seem to be a regular
accompaniment of sinus node infarction, but
is an associated factor contributing to the onset of atrial arrhythmias in less than half of
the cases.
Atrial Distention

Although listed separately as a contributing

factor to atrial arrhythmias during myocardial infarction, which it is, atrial distention's
specific effects and causes have been discussed
under other headings.
Hypercalcemia and Increased Circulating Catecholamines

Both these factors influence the onset of

atrial fibrillation during acute myocardial
infarction through their effect on repolarization speed and are discussed together, although their pathogenesis differs. They
further increase the normal disparity of repolarization speed in atrial fibers,22-24 thus
favoring both onset and perpetuation of fibrillation. They may also enhance any potential
ectopic pacemaker.
Kleitman has shown that in man hypercalcemia normally occurs within a very short
time after assuming the supine positions
Furthermore, this increase in circulating calcium was in the ionizable, or biologically
active, form. Although it is well known that
prolonged inactivity, as in poliomyelitis, is
associated with increased calcium mobilization,36 it is unlikely that these observations
are applicable to patients placed at bed rest
because of acute myocardial infarction. Kleitman 's observations, however, are certainly
pertinent and need to be studied further.
An increase in circulating catecholamines
during acute myocardial infarction has been
observed.37 When of sufficient quantity these
would not only have a chronotropic effect, but
might raise the arterial blood pressure and

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SINUS NODE ARTERY LIGATION

EPINEPHRINE

CALCIUM or

DISTENTION

or RT. ATRIUM

or

NOREPINEPH RI NE

VAGAL STIMULATION

ATRIAL FIBRILLATION
Figure 19
A summary of some experimental observations on atrial arrhythmias in myocairdial
infarction.

thereby produce a vagomimetic reflex (Marey's reflex).25 Acute hypertension does sometimes occur during acute myocardial infarction.38
Iatrogenic Factors

A number of therapeutic measures commonly employed in patients with acute myocardial infarction may contribute to the onset
of atrial arrhythmias. Prominent among these
is quinidine. Because it suppresses all myocardial excitability, quinidine may suppress
an already weakened sinus node or AV node
still further and thereby facilitate atrial
arrhythmias. Although this possibility is not
a strong contraindication to the use of quinidine otherwise indicated, its effect on the
nodal centers should be kept in mind.
The effects of digitalis on the sinus node
and AV node depend on the dosage administered. In therapeutic levels it mildly suppresses AV conduction, while in toxic doses
it completely blocks it. In therapeutic doses
its effect on the sinus node is not clinically
significant, but in toxic doses it sometimes
produces sinus arrest. In addition to nodal
effects, digitalis accelerates repolarization of
atrial myocardium,22' 23 thus increasing the
normal disparity of repolarization speed in
atrial fibers and favoring the onset of atrial

fibrillation. As with quinidine, digitalis should

still be employed when indicated in myocardial infarction, but in determining its indication it is well to remember its effects on the
conduction centers.
Pressor amines are being employed with

increasing frequency in the therapy of acute

myocardial infarction with hypotension, and

have undoubtedly been responsible for the
saving of many lives. However, they too may
contribute to the onset of atrial arrhythmias.
The two ways in which this may occur are by
a chronotropic effect on myoeardium (already
discussed) and by overshooting the therapeutic mark and producing acute hypertension.
A remarkable example of the latter problem
was recently reported by Smith and Logue ;39
their emphasis on the vagomimetic reflexes
brought into play by their therapy is most
important.
Other therapeutic measures may also play
a role in iatrogenic facilitation of the onset
of atrial arrhythmias, but the ones presented
serve to orient thought to these factors.
General Comment

In a recent experimental study on the pathogenesis of atrial arrhythmias in myocardial

infarction the validity of most of these clinical considerations was confirmed in the laboratory,40 and a schematic summary is presented
in figure 19. Not one of the factors listed
was capable alone of producing atrial fibrillation except in rare circumstances; additionally, any two of the factors also usually failed
to induce atrial fibrillation. When the sinus
node was made ischemic, and calcium, catecholamines, or atrial distention was added,
then vagal stimulation regularly produced
atrial fibrillation. It was concluded that this
complex combination, employing only factors
that are known to occur in the course of
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773

MYOCARDIAL INFARCTION AND ATRIAL ARRHYTHMIAS

HIGH LATERAL

POSTERIOR INFARCT
Q in Il1 and aVF
but not in 1, aVL, HV3-6

INFARCT
A.

(Q inI1.aVL, HV
3-6

ATRIAL
FIBRILLATION

ATR IAL
FI1B RI1LLATIO0N

/<
l-F

L.Y.

Figure 21
Figure 20
A combination of acute posterior myocardial infarction and atrial fibrillation indicates an occlusion of the first 2 cm. of the right coronary artery.

acute myocardial infarction in man, was a

valid demonstration of the true complexity
of pathogenesis of atrial arrhythmias in myo-

cardial infarction.
The consistent demonstration of morphologic changes in the sinus node at necropsy
of patients dying of acute myocardial infarction with atrial arrhythmias requires special
study of the region that is somewhat more
detailed than technics conventionally employed in the routine necropsy. Numerous
descriptions of the anatomy of the sinus node
are available.4' 46 To determine whether a
main coronary occlusion is proximal to the
origin of the sinus node artery only requires
knowledge of the anatomy of the latter vessel.
10, 30 which may arise from the proximal
portion of either the right or left circumflex
coronary artery.
The frequency of serial sectioning in the
region of the sinus node need not be every
5 micra. Sections obtained approximately 2
mm. apart are satisfactory to assure incorporation of significant focal lesions of the node.
For the average node this produces about 10
slides, a number that one can conveniently
study carefully. Hudson has recently reported
a similar experience in "serial " sectioning
of the sinus node.'8
Using the normal anatomy of the coronary
arteries in conjunction with the behavior of

A combination of acute high lateral myocardial

infarction and atrial fibrillation indicates an occlusion of the first centimeter of the left circumflex
coronary artery and is associated with a grave
prognosis.

the ischemic sinus node and AV node, one

can determine in vivo the exact location of
some acute coronary occlusions. Just as a
neurologist is able to determine the location
of a cerebral artery occlusion by the abnormal
neurologic manifestations, a cardiologist can
determine the location of some coronary occlusions from the abnormal behavior of the
cardiac conduction centers.
It is well known that most myocardial
infarctions occur in hearts with pathology
in more than one coronary artery, but some
infarctions occur by the occlusion of a single
artery. If the atrial arrhythmias of an acute
myocardial infarct are due to recent occlusion
of one artery with blood supply to the sinus
node originating beyond an old occlusion in
another artery, finding of infarction in the
sinus node (as in every case of this study)
suggests that collateral circulation to the node
was dependent on patency of the recently occluded artery. Thus atrial arrhythmias during myocardial infarction imply ischemia of
the sinus node plus coronary occlusion proximal to the origin of its blood supply, but the
occlusion may be either recent or remote. In
this regard such reasoning tells neither more
nor less than coronary angiography.
The complex problem of multiple coronary
occlusions may be more rationally approached
if we understand the behavior of myocardial

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774

JAMES

infarction that follows a single coronary occlusion. The concept of this type of analysis
may be introduced by considering right coronary artery occlusion. Since the right coronary supplies the AV node in 90 per cent of
human hearts, a patient with acute myocardial infarction who develops any degree of
heart block almost certainly has a right coronary occlusion.4749 Vagotonia associated
with acute infarction may contribute to this
block, but this factor is usually more transient.
Determination that the right coronary is
occluded still leaves a long segment of vessel
in which to localize the occlusion. Of some
help is the fact that most clinically recognizable myocardial infarctions are associated
with an occlusion in the first 4 or 5 cm. of
the artery. Of much greater localizing value,
however, is the onset of atrial arrhythmias.
This can be detected on clinical auscultation,
and confirmed electrocardiographically in all
except the most transient cases.
If an atrial arrhythmia occurs in a patient
with a posterior myocardial infarction, the
coronary occlusion is most likely to be proximal to the origin of the sinus node artery.
Since true posterior infarctions are in 90 per
cent of cases due to right coronary occlusion,
anrd since the sinus node artery from the right
(55 per cent of humans) arises most frequently within 2 or 3 cm. from the aorta, the
coronary occlusion in a posterior myocardial
infarction with an atrial arrhythmia is most
likely in the first 2 or 3 cm. of the right coronary artery (fig. 20).
In the 10 per cent of patients who supply
the crux of the heart from the left circumflex
artery, a clinically recognizable myocardial
infarction is most likely to follow occlusion
in the proximal left circumflex artery, which
produces not only a true posterior but also a
high lateral ventricular infarction. In such a
case the electrocardiographic evidence of infarction is not limited to leads III, aVF, and
V8, but is also seen in aVL, lead I, and high
leads HV3 to HV6. Thus posterior infarction
when due to left circumflex occlusion may be
diagnosed with the use of conventional supplementary electrocardiographic leads. In

such cases the added occurrence of atrial

arrhythmias serves to localize the occlusion to
the very first centimeter of the left circumflex
artery, for the sinus node artery from the left
(45 per cent of humans) only rarely arises
any greater distance from the bifurcation
than this (fig. 21). Proximity of such occlusions to the main left coronary artery, and
the increased likelihood of eventual occlusion
of this main trunk, serves to explain why such
a high mortality rate has been described in
lateral myocardial infarctions associated with
atrial fibrillation,50 an observation which has
previously been unexplained.
From these two basic considerations of occlusions of the right and left circumflex coronary arteries, it is simple to extend the same
reasoning to other combinations in the heart.
Since the sinus node artery virtually always
arises from either the right or left side, not
from both, location of an occlusion proximal
to this vessel becomes a very useful tool.
It is unusual (less than 10 per cent) for
the right coronary artery not to reach the
crux of the heart and AV node, and conversely it is unusual for the left circumflex
to reach this point; the lengths of these two
arteries are reciprocal.51 Lateral infarctions
not associated with atrial arrhythmias suggest
that the sinus node artery arose proximal to
the point of occlusion in the left circumflex
artery, or that the sinus node artery in that
case arose from the right side; the latter explanation is the usual one in clinically recognizable infarctions. On the right side, a posterior infarction not associated with atrial
arrhythmias suggests that the sinus node artery either arose proximal to the point of
occlusion in the right coronary artery or
arose from the left side; either of these is
equally possible, since the right coronary is
usually longer than the left circumflex. It is
apparent that the absence of atrial arrhythmias is much less helpful than their presence
in localizing a coronary occlusion.
Anteroseptal myocardial infaretions, which
in single coronary occlusions are almost invariably due to left anterior descending coronary occlusion, are rarely associated with
either atrial arrhythmias or heart block. If
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1961

MYOCARDIAL INFARCTION AND ATRIAL ARRHYTHMIAS

AV block occurs, it is usually due to a vagomimetic reflex rather than damage of the AV
node. If an atrial arrhythmia occurs there is
virtually always an associated second coronary
occlusion (old or new) involving the left circumflex or right coronary artery.
Finally, comment is offered regarding the
significant differences in canine and human
coronary anatomy'0' 30 relative to interpretation of changes in cardiac rhythm in canine
experiments on myocardial infarction. The
sinus node artery of the dog is nearly always
a terminal branch of the right coronary artery, whereas the sinus node artery in man
arises with about equal frequency from the
right and left sides, and from the anterior
third rather than the distal third. The arterial supply of the AV node in the dog is more
complex than in man and cannot be so simply
analyzed as determining which artery crosses
the crux. The left coronary artery of the dog
supplies almost the entire left ventricle and
interventricular septum, whereas the posterior
wall of the left ventricle in man is most often
supplied by the right coronary artery. It is
unnecessary to go into more detail regarding
these differences here. The careful planner of
canine experiments on myocardial infarction
should be more familiar with them than is
commonly the case, however.
Summary
In each of 11 necropsied patients with myocardial infarction and atrial arrhythmias, a
coronary occlusion was found proximal to the
origin of the sinus node artery and there was
infarction of the sinus node.
The multiple factors influencing the onset
of atrial arrhythmias during acute myocardial infarction are discussed. Infarction of
the sinus node is only one of these factors.
Other important ones are ischemia of the AV
node, vagal and vagomimetic reflexes, atrial
distention, and circulating chronotropic substances.
By combination of a knowledge of the anatomy and pathology of the human coronary

arteries with the observation of atrial arrhythnias during acute myoeardial infarction, an
accurate diagnosis of the point of coronary
occlusion can often be made.

775
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Myocardial Infarction and Atrial Arrhythmias

THOMAS N. JAMES
Circulation. 1961;24:761-776
doi: 10.1161/01.CIR.24.4.761
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