401

U Clinical Progress Series

Inferior Myocardial Infarction
High-Risk Subgroups
Peter B. Berger, MD, and Thomas J. Ryan, MD

I nferior myocardial infarctions account for 4050% of all acute myocardial infarctions1l2 and
are generally viewed as having a more favorable
prognosis than anterior wall infarctions. Data from a
number of recent trials of thrombolytic therapy in
acute infarction appear to support this view, with
mortality rates of 2-9% reported among patients
with inferior infarctions assigned to the "standard
care" or control groups within these studies.1-3 It is,
thus, not surprising that many of these trials have
failed to demonstrate reduced mortality after thrombolytic therapy in the subset of patients with inferior
infarction.1"3'4 It is important to note, however, that
nearly 50% of patients suffering inferior infarction
will have complications or distinguishing features
associated with an increased mortality that will substantially alter an otherwise favorable prognosis. It is
the purpose of this review to identify the complications most likely to occur during acute inferior infarction as defined electrocardiographically by STsegment elevation in leads II, III, and aVF.
Specifically, heart block, concomitant precordial STsegment depression, and right ventricular infarction
are discussed, their pathogenesis is reviewed, and
their impact on prognosis is considered. Also, the
data that exist on the impact of thrombolytic therapy
on these high-risk subgroups are reviewed.
Heart Block
As summarized in Table 1, there is a 19% incidence of high-degree (second- or third-degree) heart
block complicating acute inferior infarction.5-20
Approximately one half of the patients who develop
heart block do so through a gradual progression of
their conduction delay, whereas the remainder
abruptly develop the highest degree of heart block
they will attain.89,12,15,2' The timing of the onset of
the heart block in acute inferior infarction is presented in Table 2.9,15,16,22,23 Roughly 8% of all
patients who have an inferior infarction have highdegree heart block on arrival at the emergency
From the Evans Memorial Department of Clinical Research and
the Department of Medicine, the University Hospital, Boston,

Massachusetts.
Supported in part by NHLBI grant NO1-HV-38031.
Address for correspondence: Thomas J. Ryan, MD, 88 E.
Newton Street, Boston, MA 02118.
Received August 1, 1989; revision accepted October 10, 1989.

department, and approximately two thirds of the

patients who are eventually going to develop highdegree heart block have done so within 24 hours of
admission. Virtually all the remaining patients who
develop heart block do so within 3 days of admission.
The overall experience with heart block occurring
in association with acute inferior infarction indicates
that the heart block is responsive to atropine or
isoproterenol in the majority of cases, usually does
not require placement of a temporary pacemaker,
and almost never requires implantation of a permanent pacemaker.22 Given the relative ease of treatment and rather short duration of the conduction
abnormality, it is surprising that the development of
heart block during inferior infarction is associated
with an in-hospital mortality rate of more than 20%.
Virtually every study on the subject has shown a
markedly increased in-hospital mortality in patients
whose inferior infarctions are complicated by the
development of second- or third-degree (highdegree) heart block. As shown in Table 3, the mean
in-hospital mortality for patients with high-degree
heart block is 23%.5,9,14,17,18,21,22,24-26 When thirddegree heart block is present, the average mortality is
29% (Table 4).12,13,23,27-33 All of the studies cited
were conducted in the, era of coronary care units, and
pacemakers were used when appropriate. It is of
interest that almost none of the patients was believed
to have died as a result of their heart block (although
many died with persistent heart block) or from the
treatment of the heart block.
It now appears that this increased mortality relates
to the observation that heart block developing during
inferior infarction is a marker for increased infarction size. Many studies have shown that patients with
inferior infarctions associated with heart block have
larger infarctions than those without heart block
based on estimation of infarct size by enzyme
levels,91334 left and right ventricular ejection fractions determined by gated blood pool scan,'1425 and
wall motion analyses of the left and right ventricles
determined by echocardiography.25 While these studies serve to confirm an association between larger
infarcts and atrioventricular (AV) block, they do not
explain the nature of the relation or the mechanism
of the heart block itself.
The two most common explanations that have
been offered to explain the etiology of the heart block

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402

Circulation Vol 81, No 2, February 1990

TABLE 1. Incidence of High-Degree Heart Block in Acute Inferior

Infarction

Study
Rotman5

Jewitt6

Julian7
Stock8

Tans9
Bassan1'

Gupta10
Brown12
Nicod13

Kaul14

Feigll9
Braat16
Dubois17
Norris18

Courter19
Katz20

Patients
(n)
181
128
44
130
843

51
80

160
749
82
288
67
447
96
35
167

Total

Secondthirddegree

Seconddegree

Thirddegree

(%)

(%)

(%)

7
16

18
12
16
8
11
8
15
8
13

25
28
25
13
17
18

?
1?

1?
1?

1?
1?

1?
1?

1?
1?

(101 of
1,377) 7

(283 Of
2,366) 12

34
13
28
20
27
26
14
(492 of
2,559) 19

9
5
6
10
?
?

or

1) interruption of blood flow to the AV node and

2) high vagal tone resulting from the Bezold-Jarisch
reaction.
Inferior infarctions are caused by occlusion of the
dominant artery in more than 70% of cases. Because
the AV nodal artery is derived from the dominant
artery, it was originally believed that necrosis of the
AV node caused the heart block. However, it has
been shown that even complete occlusion of the AV
nodal artery rarely causes necrosis of the AV node.35
There are three reasons for this. First, the rate of
oxygen consumption in conducting tissue is only one
fifth as great as in contractile musculature, making it
more resistant to prolonged hypoxia.36 Second, conducting tissue has a high concentration of glycogen,
allowing lesser dependence on oxidative metabolism.37 The third postulate is that collateral blood flow
to the AV node may be sufficient to prevent significant or irreversible ischemic damage. Ischemia without necrosis may still be an important contributing
factor, and likely is. However, the AV nodal artery is
a relatively distal branch of the dominant artery,
arising some distance from the ostium as it bends to
are

along the crux of the heart. Because most

infarctions are the result of occlusions of the artery
proximal to the origin of the AV nodal artery, nodal
ischemia would be anticipated to occur in the majority of inferior infarctions. The fact that only 20% of
infarctions result in high-degree AV block suggests
that factors other than ischemia must also play a role.
An alternate hypothesis invokes increased vagal
tone resulting from the stimulation of afferent nerves
adjacent to the AV node by ischemia. The resultant
outpouring of parasympathetic stimulation via the
vagus nerve produces sinus bradycardia, hypotension,
and in some patients heart block. This has been
called the Bezold-Jarisch reflex.38 This proposed
mechanism fails to explain the increased infarct size
seen in patients with heart block and does not
account for the cases of heart block that occur in the
absence of sinus slowing, as is frequently the case.
Recently, two additional explanations for the
mechanism of heart block in acute inferior infarction
have been proposed that might account for the
association between heart block and an increase in
infarct size. The first recognizes the role of intracellular electrolytes and metabolites, in particular,
potassium and adenosine, that are released from
ischemic cells. It has been postulated that these
chemical mediators cause the transient block seen in
inferior infarction.6 High levels of potassium are well
known to cause heart block. It has been shown by
collecting blood samples in the coronary sinus during
infarction that local potassium levels can be as high
as 12 meq/dl.39 Adenosine has been shown in animal
models to produce AV block40 and has been used in
several human studies for this effect in the treatment
of AV nodal microreentrant rhythms.41 Interestingly,
aminophylline, which blocks adenosine receptors in
the heart, has been demonstrated to reverse the AV
block in animals42 and in three patients with inferior
infarction whose heart block was resistant to
atropine.4344 If these chemical mediators play an
important role in the development of heart block,
this mechanism might serve to explain the association
with larger infarcts because larger infarcts would be
expected to release more intracellular potassium and
adenosine.
The second theory that might explain the association of heart block with larger infarct size and
increased mortality relates to the collateral blood flow
to the AV node. It has been theorized that patients
course

TABLE 2. Onset of High-Degree Atrioventricular Block in Acute Inferior Infarction

Study
Sclarovsky22
Feigl11
Tans9
Braat16
Kostuk23
Total

Patients (n)
76
34
144
19
20
293

Present on
admission (n) (%)
22 (29)
15 (44)
69 (48)
5 (26)
11 (55)
122 (42)

Present within
24 hours (n) (%)
36 (47)
22 (65)
99 (69)
14 (74)
15 (75)

186 (63)

Occurred after
24 hours (n) (%)
40 (53)
12 (35)
45 (31)
5 (26)
5 (25)
107 (37)

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Berger and Ryan Inferior Myocardial Infarction

403

TABLE 3. Hospital Mortality in Acute Inferior Infarction Complicated by High-Degree Heart Block

Study
Dubois17
Kaul04
Sclarovsky22
Strasberg25
Tans9
Rotman5
Beregovich21

Norris'8
Chatterjee24
Friedberg26
Total

Year
1986
1986
1984
1984
1980
1973
1969
1969
1969
1968

With
heart block (n)
88
28
76
26
144
45
13
26
65
16
527

with inferior infarctions who develop heart block may

be more likely to have concomitant stenosis of the left
anterior descending artery (LAD) proximal to the
origin of the septal perforators, which provide a rich
network of collateral vessels between the LAD and
the AV nodal arteries. This would predispose the AV
node to greater degrees of ischemia. To test this
hypothesis, Bassan et all' studied a consecutive series
of 51 survivors of inferior infarction who underwent
coronary angiography. Eleven of the 51 developed
heart block. Comparing patients with and without heart
block revealed a sixfold greater incidence of heart block
if the LAD had a 75% or greater stenosis before the
second septal perforator. The presence of heart block
had a sensitivity of 31%, a specificity of 95%, and a
predictive value of 91% for the presence of concomitant LAD obstruction. However, two subsequent studies produced opposite findings. An increased incidence
of LAD disease was not found in the Thombolysis in
Acute Myocardial Infarction (TAMI)45 or Thrombolysis In Myocardial Infarction (TIMI)46 populations.
Heart block during inferior infarction was not predictive of multivessel disease in either of these
studies.
No placebo-controlled thrombolytic trial has
reported specifically on the outcome of patients with
inferior infarction who have high-degree heart block

Mortality (%)
24
27
13
15
22
24
23
19
23
44
23

Without
heart block (n)
359
54
?
113
699
136
?
?
?
?
1,225

Mortality (%)
4
6
?
6
9
16
?
?
?
?
9

presentation to the hospital. Data from the TIMI

trial, in which all patients enrolled in the study
were treated with intravenous recombinant tissue-type
plasminogen activator (rt-PA), reveal an in-hospital
mortality of 9% (20 of 231) for patients who developed
second- or third-degree heart block.46 The TAMI
investigators report a mortality of 14% among patients
with third-degree heart block after thrombolytic
therapy.45 The mortality rate among patients with
heart block in these trials in which thrombolytic
therapy was used is less than the 23% mortality among
patients with high-degree heart block from pooled
data from before the thrombolytic era. However, the
relative risk of mortality associated with heart block
after thrombolytic therapy (3.8 in the TIMI II trial
compared with 2.6 in the prethrombolytic era)
remains high. Therefore, we have no direct evidence
at the present time that thrombolytic therapy is of
particular benefit in this group of patients.
on
II

Precordial ST-Segment Depression

Acute inferior infarction is accompanied by STsegment depression in the precordial chest leads in
approximately one half of patients suffering a first,
inferior infarction. However, the significance of the
precordial ST-segment depression is less than clear.
Initially, it was believed that the anterior ST-segment

TABLE 4. Hospital Mortality in Acute Inferior Infarction Complicated by Complete Heart Block
With
Without
Year
heart block (n)
heart block (n)
Study
Mortality (%)
24
Nicod'3
1988
95
654
111
1987
32
?
Rodrigues27
16
6
Gould28
1979
?
Leth3'
1974
36
22
?
19
Christiansen32
1973
16
?
Kostuk23
1970
20
45
?
Brown12
1969
16
25
?
32
27
Lassers29
1968
?
1968
15
33
?
Gregory33
41
Paulk30
1966
32
?
654
Total
389
29
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Mortality (%)
6
?
?
?
?
?
?
?
?
?
6

404

Circulation Vol 81, No 2, February 1990

depression was merely an electrocardiographic phenomenon resulting from the "reciprocal" reflection of
the interior current of injury, with no anatomic or
physiologic significance. It now appears that this is the
case in only a minority of patients. Most studies have
shown that, taken as a group, patients with precordial
ST-segment depression have larger infarcts as determined by creatine phosphokinase (CPK) levels,47-51
more severe regional wall motion abnormalities,48-52
and lower left ventricular ejection fractions.48-53 In
addition, they may be prone to more short- and
long-term complications than patients without STsegment depression.47,50,5153-55 The two leading explanations for anterior ST-segment depression in acute
inferior infarction that are believed to explain the
larger infarcts and more complicated courses observed
in these patients are anterior ischemia due to concomitant LAD disease or more extensive and severe
inferoposterior infarction, which produces "posterior
ST elevation" manifest as anterior ST-segment
depression on the surface electrocardiogram.
Antertior Ischemia
It is well established that the incidence of multivessel disease among patients surviving even uncomplicated inferior infarction is high. Miller et a156
catheterized 84 consecutive patients with a mean age
of 52.82.8 years surviving uncomplicated inferior
infarction and found multivessel disease in 80% of
patients. This was initially believed to support the
concept that anterior ST-segment depression might
be due to anterior ischemia from concomitant LAD
disease. Although two subsequent studies revealed
statistically significant associations between precordial
ST-segment depression and the presence of LAD
disease, both of these studies included only those
patients who underwent catheterization for clinical
complications following inferior infarction and, thus,
are considerably biased.5758 There have been seven
studies of consecutive series of patients undergoing
catheterization after inferior infarction,51-53,59-62 and
only one reported a statistically significant difference
in the prevalence of LAD disease between patients
with and without anterior ST-segment depression.53
Roubin et a153 studied 84 consecutive survivors of a
first inferior infarction with angiography and ventriculography. The prevalence of significant stenosis
(more than 70%) in the LAD was significantly higher
in the group with precordial ST-segment disease
(36% vs. 3%, p<0.05), as was the prevalence of
multivessel disease (53% vs. 6%,p<0.01). The peak
CPK level was significantly higher in the group with
ST-segment depression (1,879935 vs. 1,122+800,
p<0.01). These patients had a higher incidence of
complications in the early postinfarction course,
including congestive heart failure, malignant ventricular arrhythmia, and high-degree heart block, than
patients without precordial ST-segment depression.
The mean left ventricular ejection fraction was significantly lower in patients with ST-segment depression (48 .-13% vs. 56-+-11%,p<0.05). It is interesting

to note that a comparison of the group of patients

with precordial ST-segment depression and onevessel disease (25 of 53) with those patients without
precordial ST-segment depression (only two of whom
had multivessel disease) reveals a significantly lower
ejection fraction (5112% vs. 56+11%,p<0.05) and
a significantly higher CPK release (1,595833 vs.
1J122+800, p<0.01.) in the group with precordial
ST-segment depression and one-vessel disease. In
these patients, a branch of the right coronary artery
supplied the lateral wall more commonly (48% vs.
19%, p<0.05), and the distal right coronary artery
more often supplied the apex (57% vs. 22%,p<0.05)
than it did in patients without anterior ST-segment
depression. These data provide strong evidence that
precordial ST-segment depression during acute inferior infarction is a marker for larger infarction as a
result of either ischemia at a distance due to the
presence of multivessel disease or a greater amount
of myocardium supplied by the infarct-related artery.
Shah et a148 studied 44 patients after acute inferior
infarction without a history of a previous infarction.
These authors found that the 24 patients with anterior ST-segment depression were far more likely to
have abnormal wall motion in the anteroseptal and
apical segments on gated blood pool scanning than
the 20 patients without anterior ST-segment depression (50% vs. 15%, p<0.05). These patients had
larger infarcts as determined by CPK release, a
greater degree of wall motion abnormalities in
infarct-related segments, and lower left ventricular
ejection fractions.
The best modality for studying the significance of
anterior ST-segment depression during inferior
infarction may be positron emission tomography
because of its ability to detect myocardial ischemia
based on the depression of metabolic activity. Billadello et a163 studied 13 consecutive patients with
inferior infarction, nine of whom had anterior STsegment depression. Positron tomography revealed
three of the nine patients to have anterior ischemia.
All three were shown to have significant stenosis of
the LAD on catheterization associated with anterior
wall motion abnormalities on ventriculography. Two
additional patients developed "true posterior infarction" (R>S in lead VJ). Despite the small number of
patients in this study, it does provide compelling
evidence that at least some patients with inferior
infarction and anterior ST-segment depression are
undoubtedly experiencing anterior ischemia.
Posterior Transmural Infarction
Evidence supporting the concept that anterior
ST-segment depression represents "reciprocal"
expression of a large area of transmural infarction
encompassing the posterior wall is found in the study
by Gibson et al.51 These investigators studied 48
consecutive patients after inferior infarction with
coronary angiography, submaximal thallium stress
tests, and gated blood pool scans, all within 2 weeks
of the acute event. The 27 patients (56%) with

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Berger and Ryan Inferior Myocardial Infarction

precordial ST-segment depression had significantly

higher peak CPK levels, significantly more severe
regional wall motion abnormalities, and lower overall
left ventricular ejection fractions. More patients with
anterior ST-segment depression evolved electrocardiographic evidence of true posterior infarction than
did patients without precordial ST depression (26%
vs. 5%, p<0.05). Thallium scanning revealed more
frequent and severe inferior and inferoapical perfusion abnormalities in the group with anterior STsegment depression.
Goldberg et a149 studied 25 consecutive patients
after a first inferior infarction with gated blood pool
scans. Thirteen of the 14 patients (93%) with anterior ST-segment depression had posterolateral akinesis on ventriculography in contrast to the 11
patients without anterior ST-segment depression,
none of whom had posterior akinesis (p<0.001).
Ong et a150 analyzed 70 patients with gated blood
pool scans and thallium scans. The 47 patients with
precordial ST-segment depression had more severely
reduced inferoposterior regional ejection fractions
(40% vs. 52%, p<0.005), lower left ventricular ejection fractions (45% vs. 52%,p<0.05), and more than
50% greater peak CPK levels (1,856+1,133 vs.
1,135 +705 units, p<0.05). Although the mortality of
the patients with precordial ST-segment depression
was greater than the mortality of patients without
this finding (28% vs. 4%), precordial ST-segment
depression was not an independent predictor of
mortality when infarct size and ventricular function
were included in multivariate analysis.
In one of the largest studies examining this issue,
Hlatky et a154 used the Duke University Data Bank to
retrospectively examine 162 consecutive patients suffering a first inferior infarction. These authors
required only 0.5-mm ST-segment depression in
leads V1 through V3 for inclusion into the precordial
ST-segment depression group, a less-stringent inclusion criterion than other studies. The group with
precordial ST-segment depression had significantly
larger infarctions and a greater percentage of posterior infarctions as judged by a QRS scoring system.
They also had a higher in-hospital mortality (13% vs.
4%,p <0.001) and significantly increased incidence of
"urgent, nonfatal complications" (defined as reinfarction, persistent hypotension, Killip class III or IV
congestive heart failure, and ventricular tachycardia
or fibrillation) than those patients without precordial
ST-segment depression (46% vs. 29%, p=0.026).
This was one of few studies to reveal a statistically
significant increase in mortality in patients with inferior infarction associated with precordial ST-segment
depression. The size of the study and the method of
analyzing precordial ST depression as a continuous
variable rather than a dichotomous one were likely to
have increased the statistical power of the study.
Not all studies investigating the significance of
precordial ST-segment depression have reported it to
be of clinical significance. Several studies failed to
show evidence of larger infarction,59 greater impair-

405

ment of ventricular function,59,62,64 or radionuclide

evidence of posterior infarction65 in patients presenting with precordial ST-segment depression. However, many of these studies used less-stringent criteria for precordial ST-segment depression,62,64

included patients presenting with inferior STsegment depression,6265 or were limited by small
sample size.59
Nonetheless, the majority of studies have shown
that patients presenting with inferior infarction associated with precordial ST-segment depression have
larger myocardial infarctions than patients without
precordial ST-segment depression. Despite this
finding, few studies have examined the impact of
thrombolysis on this high-risk group.
The Netherlands Interuniversity Cardiology Institute reported the results of 533 patients randomly
assigned to either standard care (n=264) or thrombolytic therapy (n=269).66 These investigators found
a strong relation between the amount of summed
ST-segment deviation, defined for inferior infarction
as the amount of ST-segment elevation in leads I, II,
III, aVL, aVF, V5, and V6 combined with the amount
of ST-segment depression in leads V, through V4, and
enzymatic infarct size, ejection fraction and mortality. Multivariate regression analysis revealed that the
largest limitation of infarct size after thrombolytic
therapy was present in patients with the greatest
summed ST-segment deviation. A preliminary report
by the same group on the results of a recent trial in
which 721 patients were randomized to receive either
rt-PA or placebo supports the finding that among
those patients with inferior infarction, those with
precordial ST-segment depression benefit the most
from thrombolytic therapy.67
Berland et a152 reported on 38 consecutive patients
who underwent left ventriculography, coronary angiography, and treatment with intracoronary streptokinase within 6 hours of a first inferior myocardial
infarction.52 A second angiographic study was performed on all patients between the 12th and 15th
hospital days. Pretreatment ventriculography revealed a lower mean ejection fraction in the 23
patients (60%) with precordial ST-segment depression than in the 15 patients (40%) without STsegment depression (5110% vs. 59+7%,p<0.01).
Follow-up ventriculography revealed that patients
who had successful thrombolysis and a patent coronary artery on repeat angiography had a better mean
ejection fraction than those patients with an occluded
vessel (569% vs. 478%, p<0.01). However, the
benefit in ventricular function was confined to those
patients with precordial ST-segment depression on
admission electrocardiogram. There was improvement in segmental contraction in those patients who
presented with anterior ST-segment depression, in
whom successful recanalization resulted in a
decrease in the hypokinetic surface (from 11.36 to
8.54.5 cm2,p<0.05) and in the hypokinetic percentage of the ventricular perimeter (from 4814% to
40-t9%, p<0-05). In contrast, there was no signifi-

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Circulation Vol 81, No 2, February 1990

cant change in the hypokinetic zone after successful

thrombolysis in the patients without precordial STsegment depression (hypokinetic surface area from
4.7+2.4 to 6.5+3.1 cm2, p=NS; and hypokinetic
percentage of the ventricular perimeter from
2513% to 34+12%,p=NS).
Bates et a168 reported on the impact of thrombolytic therapy in the 159 patients with inferior
infarctions treated with rt-PA and randomized to
early angioplasty or deferred angioplasty in the
TAMI-I trial. These investigators found that the 74
patients (47%) with precordial ST-segment depression had lower left ventricular ejection fractions
before treatment with thrombolytic therapy than the
85 patients (53%) without precordial ST-segment
depression (54% vs. 58%,p<0.02). Repeat ventriculography at 7 days revealed that the group with
precordial ST-segment depression had a persistently
lower mean left ventricular ejection fraction (53% vs.
57%, p<0.02). However, the difference in ejection
fraction between the patients with and without precordial ST-segment depression in this study is less
than has been reported in prior studies, leading the
authors to suggest that the patients with precordial
ST-segment depression benefited from thrombolytic
therapy.
Little et a169 administered intracoronary streptokinase to 17 patients in the acute phase of inferior
infarction. Fourteen of these patients had precordial
ST-segment depression. Recanalization of the right
coronary artery was successful in 12 of these patients
and resulted in the prompt resolution of the precordial ST-segment depression, including those patients
with LAD disease.

Right Ventricular Infarction

Only recently has the occurrence and significance of
right ventricular (RV) infarction been appreciated.
Previously, RV infarction was not believed to be a
clinically significant entity. Starr et al, in 1943,70 demonstrated no adverse hemodynamic effects after cauterizing the RV free wall in open-chest dogs. Sawatani
et al71 replaced the RV free wall in dogs with a
prosthetic patch and frequently found no hemodynamic impairment. It was not until 1973 that Cohn et
a172 first described the now classic clinical syndrome
produced by acute ischemic RV dysfunction.
RV myocardial infarction is predominantly a complication of inferior infarction. Whether it is diagnosed by echocardiography,73,74 first pass,75,76 or
equilibrium radionuclide ventriculography,76-82 or
autopsy,83,84 RV infarction has been shown to occur
in approximately one third of patients suffering an
acute inferior infarction. In about one half of these
patients, it is of hemodynamic significance.74,77,82,85 In
contrast, RV infarction occurs in association with
anterior myocardial infarction in less than 10% of
cases.86,87 Isolated RV infarction is rare.83
It is generally believed that patients suffering inferior infarctions complicated by RV involvement have
more proximal occlusions of their right coronary

artery resulting in infarction of the anterolateral wall

of the RV, which is primarily perfused by acute
marginal branches.77,79,81 However, several pathologic
analyses have shown that it is the posterior RV wall
that is most frequently involved in RV infarction and
nearly always in association with left ventricular posterior and posteroseptal infarction.8487,88 The occasional development of RV infarction after occlusion of

the circumflex artery in left dominant patients77'84'88

and in patients with occlusions of the distal right

artery and posterior descending artery87 support the significance of the posterior circulation in RV
infarction. It appears that obstruction of blood flow to
both the posterior circulation and acute marginal
coronary

vessels increases the likelihood, and size, of RV

infarction.88 Because most inferior infarctions result
from occlusion of the right coronary artery at its
proximal or middle portion before the acute marginal
vessels and the posterior descending artery, it is not
intuitively clear why only a minority of inferior infarctions are complicated by RV involvement. Theories
postulated to explain the relative infrequency of RV
infarction include 1) lower oxygen requirements of the
RV due to its smaller muscle mass and work load; 2) a
greater total amount of blood flow available due to
greater coronary blood flow during systole; 3) more
extensive collateralization of the RV, primarily from
the left coronary system; and 4) diffusion of oxygen
from intracavitary blood through the thin wall of the
RV.82,89 Several studies have indicated that patients
with RV hypertrophy are more likely to have RV
infarction,90-92 whereas others have not found this
association.84'87,89 One study shows that patients with
RV involvement are more likely to have concomitant
LAD lesions, reducing possible collateralization to the
posterior right and left ventricles,89 but others have
not found an increased prevalence of multivessel
disease in patients with RV involvement.77818490
Therefore, it remains unclear what the predisposing
factors are for RV involvement in acute inferior
myocardial infarction.
The clinical sequelae of RV infarction vary widely,
ranging from no hemodynamic compromise to severe
hypotension and cardiogenic shock.72'74'77'85 The
hypotension and shock occur when there is enough
RV ischemia to decrease RV compliance, raising the
diastolic filling pressure in the RV. Filling of the RV
is reduced, and RV stroke volume decreases. As a
result, filling of the left ventricle is impaired, cardiac
output is reduced, and systemic blood pressure
decreases.72

Therefore, patients with hemodynamic compromise due to RV infarction will often have an elevated
jugular venous pressure, usually 10 mm or more, with
a positive Kussmaul's venous sign and clear lung
fields.85 In severe cases, systemic hypotension is
present.72 There may also be signs of tricuspid
regurgitation.93,94 Characteristic findings on physical
examination may be absent despite noninvasive evidence of RV involvement.74,77,82,85

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Berger and Ryan Inferior Myocardial Infarction

Hemodynamic findings on catheterization typically

reveal disproportionate elevation of right heart pressures, with a ratio of right atrial to pulmonary capillary
wedge pressure of 0.80 or more.73,76,85,95 Because these
findings may also be present in pericardial constriction
and less frequently in cardiac tamponade, an accurate
diagnosis may be difficult.84,96
The most reliable electrocardiographic evidence of
RV infarction is ST-segment elevation of 1 mm or
more in the right precordial leads and, in particular,
lead V4R, when there is associated ST elevation in
leads II, III, and aVF. Several studies have shown
this to have a sensitivity and specificity for RV
infarction of more than 90%, with a positive predictive value of more than 80%.16,79,97,98 Right precordial ST-segment elevation usually resolves early in
the course of inferior infarction and must be looked
for promptly.
Early recognition of RV infarction is clinically
important to ensure not only that appropriate treatment is instituted but also that treatments that are
contraindicated are avoided. Initial therapy for a
hemodynamically significant RV infarction requires
the administration of volume to increase filling of the
ischemic, noncomplicant RV. This is essential to
raise the cardiac output and increase the preload of
the underfilled left ventricle.7280'9599 It is critically
important to avoid drugs that result in venodilation
and a decrease in RV filling because these may
dramatically worsen systemic hypotension. In fact,
hypotension after administration of sublingual nitroglycerin in the setting of inferior infarction should
immediately raise the suspicion of RV involvement.
In those patients who fail to increase their cardiac
output despite volume loading, dobutamine'00 and
dopamine82 have been shown to be effective. When
treated correctly, the hypotension and shock are
readily reversed in the majority of patients. In the
absence of hemodynamic compromise, no specific
treatment for a RV infarction is required.
Controversy exists regarding the natural history of
RV wall motion abnormalities that develop in association with inferior infarction. A number of investigators have shown through the use of serial radionuclide
ventriculograms that RV dysfunction often improves
with time after acute inferior infarction.77,10' In contrast, others have shown that the RV wall motion
abnormalities generally persist.75 02 This discrepancy
may reflect the existence of two different populations
of patients. In some cases, RV wall motion abnormalities detected early in the course of inferior infarction
may represent stunned myocardium resulting from
ischemia that does not produce substantial necrosis.
Those patients in whom RV dysfunction persists presumably have had ischemia resulting in infarction.
The short-term consequences of RV infarction are
not limited to the characteristic hypotension and
right heart failure. Barrillon et al in 19741'3 were the
first to report that patients with right precordial
ST-segment elevation during inferior myocardial
infarction were at least threefold more likely to

407

develop second- or third-degree heart block than

patients without ST elevation. Others have found ST
elevation in V4R to be predictive of the subsequent
development of high-degree heart block in 48-75%
of patients during acute inferior infarction.16'104
The long-term clinical consequences of RV infarction are not well known. The available evidence
suggests that RV infarction is not only predictive of
major complications during the hospital course but
also a possible independent risk factor for long-term
mortality as well. Polak et al105 have shown in
patients with coronary artery disease and chronic
heart failure that RV dysfunction is a risk factor for
mortality independent of left ventricular dysfunction.
Pfisterer et al106 found that RV dysfunction is an
independent risk factor for complex ventricular
ectopy and sudden death in the year after a myocardial infarction. However, Gadsboll et al107 found no
independent association between RV dysfunction
and mortality during the year after acute myocardial
infarction. Unfortunately, each of these studies failed
to distinguish between true RV infarction associated
with inferior infarction and RV dysfunction that
occurs most commonly after anterior infarction as a
result of left ventricular infarction and the secondary
elevation of pulmonary pressures, increasing the RV
afterload. Patients suffering RV infarction may be
more susceptible to the future development of right
heart failure; further studies involving long-term
follow-up are needed.
There is little experimental or clinical evidence
about the impact of thrombolysis on patients with
RV involvement during inferior infarction. Schuler et
al108 retrospectively studied 19 patients with acute
inferior infarction due to proximal right coronary
artery occlusion from a larger series of patients with
acute inferior infarction to study the response of the
RV to successful thrombolysis. All patients underwent radionuclide ventriculography before administration of intravenous streptokinase that was followed by acute catheterization, intracoronary
streptokinase, and percutaneous transluminal coronary angioplasty, if needed. Patients were divided
into two groups based on whether recanalization was
successful (12 patients, 63%) or unsuccessful (seven
patients, 37%). Radionuclide imaging repeated 4
weeks after acute infarction revealed marked
improvement in RV function only in the patients in
whom thrombolysis was successful (29.7+8.7% to
43.25.0%, p<0.01); there was no improvement in
RV function in the patients without successful
thrombolysis (33.4+4.8% to 32.2+6.1%, p=NS).
These findings are in contrast to those of Verani et
al,77 who found that RV function improved even in
those patients without successful thrombolysis. However, both of these studies suffered from small sample size. Data from the TIMI II trial support the view
that successful thrombolysis reduces the incidence of
RV involvement during inferior infarction.109 In the
trial, 1,017 patients with acute inferior infarction
underwent radionuclide ventriculography before dis-

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Circulation Vol 81, No 2, February 1990

charge. RV wall motion abnormalities were present

in 62 patients (6%). Angiographic analysis of those
patients undergoing protocol catheterization 18-48
hours after treatment with rt-PA reveals that patients
with patency of the infarct-related artery had a much
lower incidence of RV infarction (15 of 387, 4%,
compared with 11 of 68, 16% incidence among
patients with occluded arteries; p<O.OO1). In addition, patients with RV infarction were significantly
more likely to have occlusion of the infarct-related
artery despite thrombolytic therapy (11 of 26, 42%)
than patients without RV involvement (57 of 429,
13%, p<O.OO1). The low incidence of RV infarction
among patients with patency and the greater incidence of occlusion in patients with RV infarction
provide evidence that successful thrombolysis
reduces the incidence of RV infarction.
Conclusion
Patients with inferior infarction complicated by
heart block, concomitant precordial ST-segment
depression, and RV involvement have larger infarctions and a worse prognosis than patients without
these features. The effect of thrombolysis on these
high-risk groups is not well known. At the present
time, there is conflicting evidence regarding the
efficacy of thrombolytic therapy in patients with
inferior infarction. In view of the increasing evidence
that patients with the largest infarctions benefit the
most from acute reperfusion, patients in these highrisk subgroups may be particularly good candidates
for thrombolytic therapy.

References
1. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI): Effectiveness of intravenous
thrombolytic treatment in acute myocardiac infarction. Lancet 1986;1:397-402
2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group: Randomized trial of intravenous streptokinase, oral aspirin, both or neither among 17,187 cases of
suspected acute myocardial infarction: ISIS-2. Lancet 1988;
2:349-360
3. Kennedy JW, Martin GV, Davis KB, Maynard C, Stadius M,
Sheehan FH, Ritchie JL: The Western Washington intravenous streptokinase in acute myocardial infarction randomized trial. Circulation 1988;77:345-352
4. Kennedy JW, Ritchie JL, Davis KB, Fritz JK: Western
Washington randomized trial of intracoronary streptokinase
in acute myocardial infarction. N Engl J Med 1983;
309:1477-1482
5. Rotman M, Wagner GS, Waugh RA: Significance of high
degree atrioventricular block in acute posterior myocardial
infarction. Circulation 1973;47:257-262
6. Jewitt D: The genesis of cardiac arrhythmias in acute myocardial infarction. Prog Cardiol 1972;1:61-94
7. Julian DJ, Valentine PA, Miller GG: Disturbances of rate,
rhythm and conduction in acute myocardial infarction. Am J
Med 1964;37:915-927
8. Stock RJ, Macken RJ: Observations on heart block during
continuous electrocardiographic monitoring in myocardial
infarction. Circulation 1968;38:993-1005
9. Tans, Lie KI, Durrer D: Clinical setting and prognostic
significance of high degree atrioventricular block in acute
inferior myocardial infarction: A study of 144 patients. Am
Heart J 1980;99:4-8

10. Gupta MC, Singh MM, Wahal PK, Mehrotra MP, Gupta SK:
Complete heart block complicating acute myocardial infarction. Angiology 1978;10:749-757
11. Bassan R, Maig IG, Bozza A, Amino JGC, Santos M:
Atrioventricular block in acute inferior wall myocardial
infarction: Harbinger of associated obstruction of the left
anterior descending coronary artery. J Am Coil Cardiol
1986;8:773-778
12. Brown RW, Hunt D, Slomon JG: The natural history of
atrioventricular conduction defects in acute myocardial
infarction. Am Heart J 1969;78:460-466
13. Nicod P, Gilpin E, Dittrich H, Polikar R, Henning H, Ross J:
Long-term outcome in patients with inferior myocardial
infarction and complete atrioventricular block. J Am Coll
Cardiol 1988;12:589-594
14. Kaul V, Haron H, Malhotra A, Bhatia ML: Significance of
advanced atrioventricular block in acute myocardial infarction-A study based on ventricular function and holter
monitoring. Int J Cardiol 1986;11:187-193
15. Feigl D, Ashkenasy J, Kishon Y: Early and late atrioventricular block in acute inferior myocardial infarction. JAm Coll
Cardiol 1984;4:35-38
16. Braat SH, deZwaan C, Brugada P, Coenegracht JM, Wellens
HJJ: Right ventricular involvement with acute inferior wall
myocardial infarction identifies high risk of developing atrioventricular nodal conduction disturbances. Am Heart J
1984;107:1183-1187
17. Dubois C, Pierard LA, Smeets JP, Demoulin JC, Kultertus
NE: Atrioventricular block in inferior acute myocardial
infarction (abstract). Circulation 1986;74(suppl II):II-272
18. Norris RM: Heart block in posterior and anterior myocardial
infarction. Br Heart J 1969;31:352-356
19. Courter SR, Moffat J, Fowler NO: Advanced atrioventricular
block in acute myocardial infarction. Circulation 1963;
27:1034-1042
20. Katz R, Conroy RM, Robinson K, Mulcahy R: The aetiology
and prognostic implications of reciprocal changes in acute
myocardial infarction. Br Heart J 1986;55:423-427
21. Beregovich J, Fenig S, Lasser J, Allen D: Management of
acute myocardial infarction complicated by advanced atrioventricular block. Am J Cardiol 1969;23:54-65
22. Sclarovsky S, Strasberg B, Hirshberg A, Arditi A, Lewin RF,
Agmon J: Advanced early and late atrioventricular block in
acute inferior wall myocardial infarction. Am Heart J 1984;
108:19-24
23. Kostuk WJ, Beanlands DS: Complete heart block associated
with acute myocardial infarction. Am J Cardiol 1970;
26:380-384
24. Chatterjee K, Leathem A, Harris A: The risk of pacing after
infarction and current recommendations. Lancet 1969;
2:1061-1063
25. Strasberg B, Pinchas A, Arditti A, Lewin RF, Sclarovsky S,
Hellman C, Zafrir N, Agmon J: Left and right ventricular
function in inferior acute myocardial infarction and significance of advanced atrioventricular block. Am J Cardiol
1984;54:985-987
26. Friedberg CK, Cohen H, Donoso E: Advanced heart block as
a complication of acute myocardial infarction: Role of pacemaker therapy. Prog Cardiovasc Dis 1968;10:466-481
27. Rodrigues RD, Vidaillet HJ, Hlatky MA: Long term prognosis of complete heart block during acute myocardial infarction (abstract). Circulation 1987;76(suppl IV):IV-283
28. Gould L, Reddy CVR, Kim SG, On KC: Bundle electrogram
in patients with acute myocardial infarction. PACE 1979;
2:428-434
29. Lassers BW, Julian DG: Artificial pacing in management of
complete heart block complicating acute myocardial infarction. Br Med J 1968;20:142-146
30. Paulk EA, Hurst JW: Complete heart block in acute myocardial infarction. Am J Cardiol 1966;17:695-706
31. Leth A, Hansen JF, Meibom J: Acute myocardial infarction
complicated by third degree atrioventricular block treated
with temporary pacemaker; hospital and long-term survival in
57 patients. Acta Med Scand 1974;195:391-395

Downloaded from http://circ.ahajournals.org/ by guest on December 28, 2015

Berger and Ryan Inferior Myocardial Infarction

32. Christiansen I, Haghelt T, Amtorp 0: Complete heart block
in acute myocardial infarction: Drug therapy. Am Heart J
1973;85:162-166
33. Gregory JJ, Grace WJ: The management of sinus bradycardia, nodal rhythm and heart block for the prevention of
cardiac arrest in acute myocardial infarction. Prog Cardiovasc
Dis 1968;10:505-517
34. Opolski G, Kraska T, Ostrzycki A, Zielinski T, Korewicki J:
The effect of the infarct size on atrioventricular and intraventricular conduction disturbances in acute myocardial
infarction. Int J Cardiol 1986;10:141-147
35. Bilbao FJ, Zabalza IE, Vilanova JR, Froufe J: Atrioventricular block in posterior acute myocardial infarction: A clinicopathologic correlation. Circulation 1987;75:733-736
36. Schiebler TH, Stark M, Caesar R: Die stoffwechselsituation
des reizleitungssystems. Klin Wochenschr 1956;34:181-183
37. Dehaan R: Differentiation of the atrioventricular conducting
system of the heart. Circulation 1961;24:458-469
38. Von Bezold A, Hirt L: Uber die physiologischen Wirkungen
des essigsauren veratrin's. Unter a d Physiol Lab Wurzburg

1867;1:73-96
39. Harris AS: Factors which determine prognosis in experimental coronary occlusion, in Surawicz B, Pellagrino ED (eds):
Sudden Cardiac Death. New York, Grune & Stratton, 1964,
pp 110-121
40. Belardinelli L, Mattos EC, Berne RM: Evidence for adenosine mediation of atrioventricular block in the ischemic
canine myocardium. J Clin Invest 1981;68:195-205
41. DiMarco JP, Sellers TD, Berne RM, West GA, Bellardinelli
L: Adenosine: Electrophysiologic effects and therapeutic use
for terminating paroxysmal supraventricular tachycardia. Circulation 1983;68:1254-1263
42. Belardinelli L, Fenton R, West A, Linden J, Althaus J, Berne
RM: Extracellular action of adenosine and the antagonism by
aminophylline on the atrioventricular conduction in isolated
perfused guinea pig and rat hearts. Circ Res 1982;51:569-579
43. Shah PK, Nalos P, Peter T: Atropine resistant post infarction
complete AV block: Possible role of adenosine and improvement with aminophylline. Am Heart J 1987;113:194-195
44. Wesley RC, Lerman BB, DiMarco JP, Berne RM, Belardinelli L: Mechanism of atropine-resistant atrioventricular
block during inferior myocardial infarction: Possible role of
adenosine. J Am Coll Cardiol 1986;8:1232-1234
45. Clemmensen P, Bates ER, Califf RM, Hlatky M, George BS,
Kereiakes DJ, Aronson L, Berrios E, Topol EL: Is complete
heart block in inferior infarction a benign phenomenon
following reperfusion therapy (abstract)? J Am CoIl Cardiol
1989;13(suppl II):26
46. Berger PB, Ruocco NA, Jacobs AK, Ryan TJ: Increased
mortality associated with heart block during inferior infarction: Results from TIMI II. Circulation 1989;80(suppl II):
II-347
47. Gelman JS, Saltups A: Precordial ST segment depression in
patients with inferior infarction; Clinical implications. Br
Heart J 1982;48:560-565
48. Shah PK, Pichler M, Berman DS, Maddahi J, Peter T, Singh
BN, Swan HJC: Noninvasive identification of a high risk
subset of patients with acute inferior myocardial infarction.
Am J Cardiol 1980;46:915-921
49. Goldberg HL, Borer JS, Jacobstein JG, Kluger J. Scheidt SS,
Alonso DR: Anterior S-T segment depression in acute
inferior myocardial infarction: Indicator of posterolateral
infarction. Am J Cardiol 1981;48:1009-1015
50. Ong L, Valdellon B, Coromilas J, Brody R, Reiser P,
Morrison J: Precordial S-T segment depression in inferior
myocardial infarction: Evaluation by quantitative thallium201 scintigraphy and technetium-99m ventriculography. Am J
Cardiol 1983;51:734-739
51. Gibson RS, Crampton RS, Watson DD, Taylor GJ, Carabello
BA, Holt ND, Beller GA: Precordial ST-segment depression
during acute inferior myocardial infarction: Clinical, scintigraphic and angiographic correlations. Circulation 1982;
66:732-741

409

52. Berland J, Criber A, Behar P, Letac B: Anterior ST depression in inferior myocardial infarction: Correlation with
results of intracoronary thrombolysis. Am Heart J 1986;
3:481-488
53. Roubin GS, Shen WF, Nicholson M, Dunn RF, Kelly DT,
Harris PJ: Anterolateral ST segment depression in acute
inferior myocardial infarction: Angiographic and clinical
implications. Am Heart J 1984;107:1177-1782
54. Hlatky MA, Calif RM, Lee KL, Piyor DB, Wagner GS,
Rosati RA: Prognostic significance of precordial ST-segment
depression during inferior acute myocardial infarction. Am J
Cardiol 1985;55:325-329
55. Nasmith J, Marpole D, Rahal D, Homan J, Stewart S,
Sniderman A: Clinical outcomes after inferior myocardial
infarction. Ann Int Med 1982;96:22-26
56. Miller RR, DeMaria AN, Vismara LA, Salel AF, Maxwell
KS, Amsterdam EA, Mason DT: Chronic stable inferior
infarction: Unsuspected harbinger of high risk proximal left
coronary arterial obstruction amenable to surgical revascularization. Am J Cardiol 1977;39:954-960
57. Salcedo JR, Baird MG, Chambers RJ, Beanlands DS: Significance of reciprocal S-T segment depression in anterior
precordial leads in acute inferior myocardial infarction:
Concomitant left anterior descending coronary artery disease? Am J Cardiol 1981;48:1003-1008
58. Haraphongse M, Jugdutt BI, Rossall RE: Significance of
precordial ST-segment depression in acute transmural inferior infarction: Coronary angiographic findings. Cathet Cardiovas Diagn 1983;9:143-151
59. Cohen M, Blanke H, Karsh KR, Holt J, Rentrop P: Implications of precordial ST segment depression during acute
inferior myocardial infarction: Arteriographic and ventriculographic correlations during the acute phase. Br Heart J
1984;52:497-501
60. DeWood MA, Heit J, Spores J, Eugster GS, Coulston D,
Reisig AH, Hinnen ML, Shields JP: Significance of precordial ST segment depression in acute inferior transmural
myocardial infarction: Assessment by coronary arteriography
and ventriculography during the early hours (abstract). Circulation 1982;66(suppl II):II-182
61. Oneill WM, Walton J, Colfer HT, Weiss R, Brymer J, Khaja
F, Goldstein S, Pitt B: Anterior ST segment depression in
inferior myocardial infarction: Angiographic and santographic findings (abstract). Circulation 1982;66(suppl II):
11-182
62. Feit F, Rey M, Sherman W, Cohen M, Stecy P, Cole W,
Nachamie M, Thornton, Rentrop P, and the Mt Sinai-NYU
Reperfusion Study Group: Does anterior ST-depression in
acute inferior wall MI (IWMI) have predictive value
(abstract)? Circulation 1988;78(suppl II):II-212
63. Billadello JJ, Smith JL, Ludbrooke PA, Tiefenbrunn AJ,
Jaffe AS, Sobel BE, Geltman EM: Implications of "reciprqcal" ST segment depression associated with ac4te myocardial
infarction identified by position tomography. J Am Coll
Cardiol 1983;2:616-624
64. Croft CH, Woodward W, Nicod P, Corbett JR, Vpwis SE,
Willerson JT, Rude RE: Clinical implications of anterior S-T
segment depression in patients with acute myocardial infarction. Am J Cardiol 1982;50:428-436
65. Mukharji J, Murray S, Lewis SE, Croft CH, Corbett JR,
Willerson JT, Rude RE: Is anterior ST depression with acute
transmural inferior infarction due to posterior infarction? A
vectorcardiographic and scintographic study. J Am Coll Cardiol 1984;4:28-34
66. Vermeer F, Simoons ML, Bar FW, Tijssen JGP, Domburg
RT van, Serruys PW, Verheugt FWA, Res JCJ, Zwann C de,
Loarse A van der, Krauss XH, Lubsen J, Hugenholtz PG:
Which patients benefit most from early thrombolytic therapy
with intracoronary streptokinase? Circulation 1986;
74:1379-1389
67. Arnold AER, Werf FV, Simoons ML, Lubsen J, Verstraete
M: Intravenous rt-PA for acute myocardial infarction: Which
patients benefit most (abstract)? Circulation 1988;78(suppl
II):II-212

Downloaded from http://circ.ahajournals.org/ by guest on December 28, 2015

410

Circulation Vol 81, No 2, February 1990

68. Bates ER, Clemmensen PM, Gorman LE, Aronson LG:

Precordial ST segment depression predicts a worse prognosis
in inferior infarction despite reperfusion therapy (abstract).
Circuilation 1988;78(suppl II):II-211
69. Little WC, Rogers EW, Sodums MT: Mechanism of anterior
ST segment depression during acute inferior myocardial
infarction: Observations during coronary thrombolysis. Ann
Intem Med 1984;100:226-229
70. Starr I, Jeffers WA, Meade RH Jr: The absence of conspicuous increments of venous pressure after severe damage to
the right ventricle of the dog, with a discussion of the relation
between clinical congestive failure and heart disease. Am
Heart J 1943;26:291-301
71. Sawatani S, Mandell G, Kusaba E, Schraut W, Cascade P,
Wajszczuk WJ, Kantrowitz A: Ventricular performance following ablation and prosthetic replacement of right ventricular myocardium. Trans Am Soc Artif Int Organ 1974;
20:629-636
72. Cohn JN, Gulha NH, Broder MI, Limas CJ: Right ventricular
infarction: Clinical and hemodynamic features. Am J Cardiol
1974;33:209-214
73. Dell'ltalia LJ, Starling MR, Crawford MH, Boros BL,
Chaudhuri TK, O'Rourke RA: Right ventricular infarction:
Identification by hemodynamic measurements before and
after volume loading and correlation with noninvasive techniques. JAm Coll Cardiol 1984;4:931-939
74. Lopez-Sendon J, Garcia-Fernandez MA, Coma-Canella I,
Yanguela MM, Banuelos F: Segmental right ventricular
function after acute myocardial infarction, two-dimensional
echocardiographic study in 63 patients. Am J Cardiol 1983;
51:390-396
75. Reduto LA, Berger HJ, Cohen LS, Bottschalk A, Zaret BC:
Sequential radionuclide assessment of left and right ventricular performance after acute transmural myocardial infarction. Ann Int Med 1978;89:441-447
76. Starling MR, Dell'Italia LJ, Chandhuri TK, Boros BL,
O'Rourke RA: First transit and equilibrium radionuclide
angiography in patients with inferior transmural myocardial
infarction: Criteria for the diagnosis of associated hemodynamically significant right ventricular infarction. J Am Coll
Cardiol 1984;4:923-930
77. Verani MS, Tortoledo FE, Batty JW, Raizner AE: Effect of
coronary artery recanalization on right ventricular function in
patients with acute myocardial infarction. JAm Coll Cardiol
1985;5:1029-1035
78. Nishumura T, Yasuda T, Gold HK, Leinbach RC, Boucher
CA, McKusick KA, Strauss HW: High-risk subgroup of
inferior infarction: Importance of anterior wall motion and
right ventricular function. Radiol Med 1986;4:112-118
79. Braat SH, Brugada P, deZwaan C, denDulk K, Wellens HJJ:
Right and left ventricular ejection fraction in acute inferior
wall infarction with or without ST segment elevation in lead
V4 R. JAm Coll Cardiol 1984;4:940-944
80. Sharpe ND, Botvinick EH, Shames DM, Schiller NB, Massie
BM, Chatterjee K, Parmley WW: The noninvasive diagnosis
of right ventricular infarction. Circulation 1978;57:483-490
81. Lew AS, Laramee P, Shah PK, Maddahi J, Peter T, Gann W:
Ratio of ST segment depression in lead V2 to ST segment
elevation in lead aVF in evolving inferior acute myocardial
infarction: An aid to the early recognition of right ventricular
ischemia. Am J Cardiol 1986;57:1047-1051
82. Shah PK, Maddahi J, Berman DS, Pichler M, Swan HJC:
Scintographically detected predominant right ventricular dysfunction in acute myocardial infarction: Clinical and hemodynamic correlates and implications for therapy and prognosis. JAm Coll Cardiol 1985;6:1264-1272
83. Wartman WB, Hellerstein HK: The incidence of heart
disease in 2000 consecutive autopsies. Ann Intem Med 1948;

28:41-65
84. Isner JM, Roberts WC: Right ventricular infarction complicating left ventricular infarction secondary to coronary heart
disease: Frequency, location, associated findings and significance from analysis of 236 necropsy patients with acute or
healed myocardial infarction. Am J Cardiol 1978;42:885-894

85. Dell'Italia LJ, Starling MR, O'Rourke RA: Physical examination for exclusion of hemodynamically important right
ventricular infarction. Ann Intemn Med 1983;99:608-611
86. Cabin HS, Clubb KS, Wackers FJT, Zaret BL: Right ventricular myocardial infarction with anterior wall left ventricular
infarction: An autopsy study. Am Heart J 1987;113:16-22
87. Ratliff NB, Hackel DB: Combined right and left ventricular
infarction: Pathogenesis and clinicopathologic correlations.
Am J Cardiol 1980;45:217-221
88. Anderson HR, Falk E, Nielson D: Right ventricular infarction: Frequency, size and topography in coronary artery
disease: A prospective study comprising 107 consecutive
autopsies from a coronary care unit. J Am Coll Cardiol
1987;10:1223-1232
89. Haupt HM, Hutchins GM, Moore GW: Right ventricular
infarction: Role of the moderator band artery in determining
infarct size. Circulation 1983;67:1268-1272
90. Forman MB, Wilson BH, Sheller JR, Kopelman HA, Vaughn
WK, Virmani R, Friesinger GC: Right ventricular hypertrophy is an important determinant of right ventricular infarction complicating acute inferior left ventricular infarction. J
Am Coll Cardiol 1987;10:1180-1187
91. Kopelman HA, Forman MB, Wilson BH, Kolodgie FD,
Smith RF, Friesinger GC, Virmani R: Right ventricular
myocardial infarction in patients with chronic lung disease:
Possible role of right ventricular hypertrophy. J Am Coll
Cardiol 1985;5:1302-1307
92. Wade WG: The pathogenesis of infarction of the right
ventricle. Br Heart J 1959;21:545-554
93. Zone DD, Botti RE: Right ventricular infarction with tricuspid insufficiency and chronic right heart failure. Am J Cardiol
1976;34:445-448
94. D'Arcy B, Nanda NC: Two-dimensional echocardiographic
features of right ventricular infarction. Circulation 1982;
65:167-173
95. Lloyd EA, Gersh BJ, Kennelly BM: Hemodynamic spectrum
of "dominant" right ventricular infarction in 19 patients. Am
J Cardiol 1981;48:1016-1022
96. Lorrell B, Leinbach RC, Pohost GM, Gold HK, Dinsmore
RE, Hutter AM, Pastore JO, DeSanctis RW: Right ventricular infarction: Clinical diagnosis and differentiation from
cardiac tamponade and pericardial constriction. Am J Cardiol
1979;43:465-471
97. Erhardt LR, Sjogren A, Wahlberg I: Simple right-sided
precordial lead in the diagnosis of right ventricular involvement in inferior myocardial infarction. Am Heart J 1976;
91:571-576
98. Croft CH, Nicod P, Corbett JR, Lewis SE, Huxley R,
Mukharji J, Willerson JT, Rude RE: Detection of acute right
ventricular infarction by right precordial electrocardiography. Am J Cardiol 1982;50:421-427
99. Baigrie RS, Haq A, Morgan CD, Rakowski H, Drobac M,
McLaughlin P: The spectrum of right ventricular involvement
in inferior wall myocardial infarction: A clinical, hemodynamic and noninvasive study. J Am Coll Cardiol 1983;
1: 1396-1404
100. Dell'italia LJ, Starling MR, Blumhardt R, Lasher JC,
O'Rourke RA: Comparative effects of volume loading, dobutamine, and nitroprusside in patients with predominant
right ventricular infarction. Circulation 1985;72:1327-1335
101. Dell'italia LI, Lemro NJ, Starling MR, Crawford MH, Simmons RS, Lasher JC, Blumhardt R, Lancaster J, O'Rourke
RA: Hemodynamically important right ventricular infarction:
Follow-up examination of right ventricular systolic function
at rest and during exercise with radionuclide ventriculography and respiratory gas exchange. Circulation 1987;
75:996-1003
102. Marmor A, Geltman EM, Biello DR, Sobel BE, Siegel BA,
Roberts R: Functional response of the right ventricle to
myocardial infarction: Dependence on the site of left ventricular infarction. Circulation 1981;64:1005-1011
103. Barrillon A, Chaignon M, Guizel L, Berbaux A: Premonitory
sign of heart block in acute posterior infarction. Br Heart J
1975;37:2-8

Downloaded from http://circ.ahajournals.org/ by guest on December 28, 2015

Berger and Ryan Inferior Myocardial Infarction

104. Nistor-Hemmert D, Ciplea A: The predictive value of V3RV4R precordial leads in the occurrence of conduction disturbances in inferior acute myocardial infarction (AMI). Physiologie 1982;19:87-90
105. Polak JF, Holman L, Wynne J, Colucci WS: Right ventricular
ejection fraction: An indicator of increased mortality in
patients with congestive heart failure associated with coronary artery disease. JAm Coll Cardiol 1983;2:217-224
106. Pfisterer M, Emmenegger H, Soler M, Burkhart F: Prognostic significance of right ventricular ejection fraction for
persistent complex ventricular arrhythmias and/or sudden
cardiac death after first myocardial infarction: Relation to
infarct location, size, and left ventricular function. Eur Heart
J 1986;7:289-298

411

107. Gadsboll N, Hoilund-Carlsen PF, Madsen EB, Marving J,

Pedersen A, Lonborg-Jensen H, Dige-Petersen H, Jensen
BH: Right and left ventricular ejection fractions: Relation to
one-year prognosis in acute myocardial infarction. Eur Heart
J 1987;8:1201-1209
108. Schuler G, Hoffman M, Schwarz F, Mehmel H, Manthey J,
Tillmanns H, Hartmann S, Kubler W: Effect of successful
thrombolytic therapy on right ventricular function in acute
inferior wall myocardial infarction. Am J Cardiol 1984;
54:951-957
109. Berger PB, Ruocco NA, Timm CT, Zaret BL, Wackers FJ
Th, and the TIMI Investigators: The impact of thrombolytic
therapy on right ventricular infarction complicating inferior
myocardial infarction: Results from TIMI II (abstract).
Circulation 1989;80(suppl II):II-313

(Circulation 1990;81:401-411)

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Inferior myocardial infarction. High-risk subgroups.

P B Berger and T J Ryan
Circulation. 1990;81:401-411
doi: 10.1161/01.CIR.81.2.401
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright 1990 American Heart Association, Inc. All rights reserved.
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