490122

2013
ACC2310.1177/2048872613490122European Heart Journal: Acute Cardiovascular CareInohara et al.

EUROPEAN
SOCIETY OF
Review CARDIOLOGY ®

European Heart Journal: Acute Cardiovascular Care

The challenges in the management 2(3) 226­–234

© The European Society of Cardiology 2013
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DOI: 10.1177/2048872613490122
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Taku Inohara1, Shun Kohsaka1, Keiichi Fukuda1 and Venu Menon2

Abstract
In recent years, right ventricular (RV) infarction seems to be underdiagnosed in most cases of acute myocardial ischaemia
despite its frequent association with inferior-wall and, occasionally, anterior-wall myocardial infarction (MI). However, its
initial management is drastically different from that of left ventricular MI, and studies have indicated that RV infarction
remains associated with significant morbidity and mortality, even in the mechanical reperfusion era. The pathophysiology
of RV infarction involves the interaction between the right and left ventricle (LV), and the mechanism has been clarified
with the advent of diagnostic non-invasive modalities, such as echocardiography and cardiac magnetic resonance. In
recent years, considerable progress has been made in the treatment of RV infarction; early revascularization remains
the cornerstone of the management, and fluid resuscitation, with appropriate target selection, is necessary to maintain
appropriate preload. Early recognition in intensive care with clear understanding of the pathophysiology is essential to
improve its prognosis. In terms of management, the support strategy for RV dysfunction is different from that for LV
dysfunction since the former may often be temporary. Along with early reperfusion, maintenance of an adequate heart
rate and atrioventricular synchrony are essential to sustain a sufficient cardiac output in patients with RV infarction. In
refractory cases, more intensive mechanical support is required, and new therapeutic options, such as Tandem-Heart or
percutaneous cardiopulmonary support systems, are being developed.

Keywords
Disease management, myocardial infarction, reperfusion, right ventricle, ventricular interaction

Received: 6 February 2013; accepted: 23 April 2013

Introduction Incidence and diagnosis

Right ventricular (RV) infarction rarely occurs in isolation,1 Physical examination
with approximately between one-third and half of the
The clinical triad of hypotension, clear lung fields, and
patients with inferior-wall myocardial infarction (IWMI)
elevated jugular venous pressure has been traditionally
having some RV involvement. The reported incidence of
considered as a maker of RV infarction in patients with
RV infarction varies widely, depending on the criteria and
IWMI. However, this triad has high specificity (96%) but
methodology of the study in question. RV infarction can be
very low sensitivity (25%).2 Kussmaul’s venous sign (dis-
defined pathologically, haemodynamically, echocardio-
tension of the jugular vein on inspiration), a feature of con-
graphically, electrocardiographically, or by cardiac mag-
strictive pericarditis, may also occur with RV infarction.3
netic resonance (CMR). In this manuscript, we first discuss
Electrocardiography and other non-invasive imaging
the incidence and diagnosis of RV infarction, with focus on
modalities continue to be the cornerstones of the diagnosis
the non-invasive modalities, such as CMR. Then, we aim to
provide an overview of its prognosis with respect to changes
between the fibrinolytic and mechanical reperfusion era. 1Keio University School of Medicine, Tokyo, Japan.
Finally, we discuss the management of RV infarction focus- 2Heart and Vascular Institute, Cleveland Clinic, Ohio, USA.
ing on biventricular interdependence, which is expected to
Corresponding author:
promote the understanding of optimal volume replacement, Shun Kohsaka, Department of Cardiology, Keio University School of
early revascularization, and utilization of newly developing Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo160-8582, Japan.
treatment modalities. Email: kohsaka@cpnet.med.keioac.jp
Inohara et al. 227
of RV infarction because of the high specificity but low
sensitivity associated with physical examination.
Electrocardiography
In clinical practice, RV infarction is frequently diagnosed
electrocardiographically. An ST-segment elevation of >1
mm in lead V4R is considered significant and correlates
closely with other noninvasive evidences of RV dysfunc-
tion.4–7 This electrocardiographic finding is also a strong
independent predictor of major complications and in-hospi-
tal mortality.8 This ST-segment elevation is thought to rep-
resent an ischaemic injury of the posterobasal septum, since
this area of contiguous myocardium is invariably damaged
in patients who have pathological evidence of IWMI
involving the RV.9
Notably, most of the so-called RV ‘infarctions,’ indi-
cated by right-sided ST-segment changes or pathological Q
waves, do not progress to an actual infarction (e.g. myocar-
dial necrosis and scar formation); these electrocardio-
graphic findings usually represent an early, transient
phenomenon.10 This has been demonstrated recently in a
study with sequential CMR imaging.11 Several unique ana-
tomic and physiological characteristics of the right ventri-
cle contribute to recovery from RV infarction. First,
pulmonary circulation is approximately one-tenth the
length of systemic circulation, and a 5-mmHg perfusion
gradient is sufficient to propel blood across the pulmonary
circuit.12 Second, unlike diastolic flow in the left ventricle
(LV), the thin RV free wall allows the biphasic perfusion of
coronary blood, with approximately equal contributions
during systole and diastole.12 Third, the right ventricle has
rich collaterals from the left anterior descending artery in
addition to right coronary artery (RCA) blood flow. Thus,
RV infarcts may be clinically suspected in many patients
with a stunned or hibernating RV free wall.
Echocardiography
Since the late 1980s, considerable progress has been
achieved in echocardiography and radionuclide techniques;
these modalities revealed that RV involvement may be pre-
sent in as much as 59% of the patients with IWMI at the
initial presentation.13–15 In particular, echocardiography is a
widely available and inexpensive tool for the comprehen-
sive evaluation of the size and function of the right ventri-
cle. However, echocardiographic imaging of the RV has
technical challenges due to the chamber’s complex shape;
the RV cannot be completely visualized in any single two-
dimensional (2D) echocardiographic view. Furthermore,
although RV infarction inherently complicates the initial
management in cases of acute infarction, echocardiographic
abnormalities can be temporary and resolve within a few
hours.16,17 Therefore, information from all available acous-
tic windows is necessary for the complete assessment of the
RV. Although not validated in acute situations, three-
dimensional (3D) echocardiographic RV volumes are com-
parable to those derived by CMR and are probably more
accurate than 2D echocardiographic volumes.18
Cardiac magnetic resonance
CMR using late gadolinium enhancement imaging ena-
bles the accurate characterization of ischaemic myocar-
dial injury (Figure 1). CMR studies have indicated that
RV infarction occurs in a high number of cases in patients
with IWMI (47–57%) and that some patients with anterior
MI (11–65%) also have RV involvement to some
extent.11,19,20 Indeed, two observational reports comparing
the frequency of RV involvement between different
modalities in patients with acute MI indicated that RV
involvement was detected significantly more frequently
with CMR than with electrocardiography or echocardiog-
raphy.19,20 Although the recent advances in CMR may
contribute to understanding the pathology as well as pro-
viding a more accurate diagnosis of RV infarction, further
investigations are essential to establish the usefulness of
the CMR technique, since the numbers of patients included
in these observational studies were limited.
Prognosis
Short-term prognosis
Patients with acute IWMI have a substantially increased
risk of death during hospitalization if RV involvement is
present. In a meta-analysis from the fibrinolytic era, the
mortality rate was noted to be higher in the presence of RV
infarction (17%) than in its absence (6.3%), thereby corre-
sponding to an overall pooled relative risk mortality
increase of 2.6 (95% confidence interval, 2.0–3.3).21 The
worse outcome is mainly attributable to the high incidence
of refractory cardiogenic shock. In a typical scenario,
infarcted RV tissue fails to offer a sufficient preload, which
is essential for adequate LV performance, and consequently,
a low cardiac output will lead to systemic hypoperfusion.
The revascularization strategy has improved the overall
short-term mortality rate of acute MI (7 vs. 9%) compared
with that associated with the fibrinolytic strategy.22
However, although the number of patients with RV infarc-
tion is small, these patients seem to have a higher risk of
in-hospital mortality in the mechanical reperfusion era than
during the fibrinolytic era. Figure 2 shows the changes in
the in-hospital mortality rate and relative risk of RV infarc-
tion for in-hospital mortality between the fibrinolytic and
mechanical reperfusion era;8,23–36 An increase in the rela-
tive risk of RV infarction from 2.29 (95% CI 1.67–3.14) to
2.98 (95% CI 1.41–6.31) also occurred during this period.
The precise explanation for the paradox remains unknown.
Despite the advances in therapeutic strategy, including
228 European Heart Journal: Acute Cardiovascular Care 2(3)

Figure 1.  Contrast-enhanced cardiovascular magnetic resonance image of right ventricular myocardial infarction (a) and cine
angiogram before (b) and after (c, d) percutaneous angioplasty in the corresponding case.
Enlarged short-axis view with infarction of the right ventricular wall (red arrows) and the inferior left ventricle. The occluded proximal right coro-
nary artery was recanalized with percutaneous angioplasty, and the major right ventricular branch (white arrows) was recognized.

mechanical reperfusion for acute MI, improvement in the
in-hospital mortality could not be achieved even by
mechanical reperfusion in patients with fatal RV infarction,
and therefore, the relative risk of in-hospital mortality in
such a population might have been highlighted.
Long-term prognosis
The prognosis associated with RV infarction is worse in the
short term, but those patients who survive hospitalization
have a relatively good long-term prognosis.37 This is in con-
cordance with the findings in patients with LV cardiogenic
shock; in the SHOCK study, 1 year after revascularization,
the survival curves remained relatively stable with an annual
mortality rate of 8–10 deaths per 100 patient-years. This
annual mortality rate is comparable to that reported in a broad
cohort of post-percutaneous coronary intervention patients.38
Therapy
The management of RV infarction should be started with
volume replacement, and recent studies have highlighted
the adverse effect of excessive volume loading. Early
revascularization is also applied to RV infarction, in which
the complete revascularization of the affected vessels,
including the major RV branch, plays an important role in
the recovery of RV function. Electrical stabilization,
including adequate heart rate and the maintenance of atri-
oventricular synchrony, is another key factor for preserv-
ing cardiac output in RV infarction. Furthermore, various
Inohara et al. 229

Figure 2.  Changes of in-hospital mortality rate and relative risk of RV infarction for in-hospital mortality between the fibrinolytic
and mechanical reperfusion era.
These data were derived from previously published meta-analyses,21 which included many prospective or retrospective studies, assessing the impact
of RV infarction in patients with acute MI up to June 2007,8,23–30,33–36 and two additional observational studies that met the same inclusion criteria up
to June 2012.31,32

extracorporeal support devices have been used to support
RV failure secondary to RV infarction and contributed to
the improvement of RV shock.
Volume replacement
When RV infarction is complicated by acute MI, it is
widely recognized that adequate therapy can be achieved
only by expanding the plasma volume, ideally with the aid
of invasive monitoring. However, fluid replacement can be
challenging in some patients with RV infarction, particu-
larly in the presence of severe RV dysfunction.39 The con-
cept of fluid replacement was first described as a treatment
option approximately 25 years ago with the development
of pulmonary artery catheterization. Since then, several
studies have validated the usefulness of volume loading
for ischaemic RV dysfunction.40–43 Therefore, the initial
therapy for hypotension in patients with RV infarction
without pulmonary congestion has traditionally been vol-
ume expansion, particularly if the estimated central venous
pressure was <15 mmHg.44
In previous studies, maintenance of the RV preload with
volume loading and normal saline alone was thought to
resolve the accompanying hypotension and improve the
cardiac output.45 The typical regimen consisted of normal
saline (40 ml/min, up to total of 2 l, intravenously), while
maintaining the right atrial pressure (RAP) at <18 mmHg to
prevent volume overload.46 However, later clinical studies
reported variable responses to aggressive fluid therapy with
a target pulmonary wedge pressure (PWP) of 18–24 mmHg
(Figure 3).47–51 Some studies, including two prospective
ones, showed that volume loading further elevates the
right-sided filling pressure without improving cardiac out-
put.47,50,51 Berisha and associates,52 in a study of 41 patients
who fulfilled the diagnostic electrocardiographic and
haemodynamic criteria for RV infarction, reported that the
maximal RV stroke work index occurred when the filling
pressure was 10–14 mmHg, and a mean RAP of >14 mmHg
was almost always associated with a reduced RV stroke
work index (Figure 3). Although the haemodynamic char-
acteristics of RV infarction may be extremely variable,
depending on the patient’s state of hydration and the degree
230 European Heart Journal: Acute Cardiovascular Care 2(3)
Figure 3.  Responses before and after volume replacement
therapy in patients with right ventricular myocardial infarction.
The association between mean right atrial pressure (mRAP) and the right
ventricular systolic work index (RVSWI) is shown by a blue line. An mRAP
of 10–15 mmHg seems to be an optimal target for right-sided filling pres-
sure.52 Changes of pulmonary wedge pressure (PWP) and cardiac index
from smaller studies are shown by a red line. There is a wide variation in
its response, but no clear linear association was noted between PWP and
cardiac index with a higher right-sided filling pressure target.47–51
of concomitant LV involvement, this study indicated that
the mean optimal PWP, which corresponded to the maxi-
mum LV stroke work index in each patient, was 16 mmHg.
Clinical implications of biventricular
interdependence
Two physiological concepts explain the detrimental effect
of excessive volume loading in patients with RV infarction
(Figure 4). First, data from animal studies suggest that
excessive RV dilatation can further compromise LV output
because of pericardial restraining effects.53 Biventricular
interdependence is mediated by the shared interventricular
septum and the surrounding pericardium. The dispropor-
tionate elevation of RV filling pressure because of surplus
volume loading can lead to marked RV dilatation, elevation
of intrapericardial pressure, and subsequent equalization of
RV and LV diastolic pressures. By compromising LV fill-
ing, this situation will precipitate a low-output state. The
resultant impairment of interventricular septal motion can
further aggravate this condition.54,55
In addition, in isolated RV infarction, RV performance
can be largely attributed to a force generated by the inter-
ventricular septum.56 Patients with intact LV-septal contrac-
tion would be expected to manifest a pattern of paradoxical
septal motion with preserved septal thickening,57 portending
a better prognosis. Damage to the interventricular septum
significantly impairs RV emptying and exacerbates diastolic
dysfunction, with an increase in the filling pressure. In RV
infarction associated with septal dysfunction, compensation
from LV-septal contraction transmitted through systolic
ventricular interaction is lacking, and these patients usually
present with hypotension and low cardiac output that are
refractory to initial volume loading. Under these circum-
stances, inotropic stimulation of contractility, usually with
dobutamine, has consistently improved RV performance by
enhancing global LV contraction and increasing paradoxical
septal displacement into the right ventricle.58 These impor-
tant impacts of the interventricular septum on RV perfor-
mance after acute MI were observed in a study using
echocardiography, in which the recovery of RV function
was best correlated with the improvement of the interven-
tricular septum wall.59
In earlier studies, RV infarction was defined by haemo-
dynamic criteria, such as an elevated RAP or PWP. At pre-
sent, in most coronary units, physicians are able to identify
RV infarction more precisely using non-invasive imaging
techniques (e.g. echocardiography, radionuclide imaging,
cardiac magnetic resonance), as discussed earlier. With
these non-invasive modalities, the extent of interventricular
involvement is essential for the precise assessment of fluid
balance, early risk stratification, and prognostic evaluation.
Early revascularization
In the typical situation of a haemodynamically significant
RV infarction, RCA occlusion compromises right atrial and
RV branch perfusion, resulting in RV ischaemic dysfunc-
tion related to the loss of the critical compensatory contri-
bution of augmented right atrial contraction. Patients with
proximal RCA culprit lesions have worse baseline charac-
teristics, less spontaneous recanalization, and a greater clot
burden than those without.60
Although the relative prognostic impact of RV infarction
has been more prominent, successful mechanical reperfu-
sion has improved the absolute clinical outcome as a whole,
in relation to RV infarction (Figure 2). Because of the
higher reperfusion rate achieved with primary angioplasty,
the mortality among patients treated with this method has
been relatively low. In addition, the clinical outcomes have
been acceptable in patients with proximal RCA culprit
lesions, despite their worse baseline characteristics; these
outcomes have been similar to those of patients with non-
proximal RCA culprit lesions.60 Technically, a shorter time
taken to reperfusion and complete revascularization of the
affected vessels, including the major RV branch, play an
important role in the recovery of RV function. Early revas-
cularization leads to an immediate recovery of RV function;
conversely, late revascularization is associated with higher
RV dysfunction and complications.61,62 Asalli and col-
leagues30 reported that complete revascularization of the
RCA, including the major RV branch, was more closely
Inohara et al. 231

Figure 4.  Two physiological concepts explaining the detrimental effects of excessive volume loading. (a) Normal ventricle: at end-
systole (ES), the right ventricular (RV) free wall moves toward the septum. (b) Pericardial restraining effects (above, before volume
loading; below, after excessive volume loading): RV dilatation, as a result of excessive volume loading, can lead to the elevation of
intrapericardial pressure, increase in pericardial constraint (red arrow), and change of geometry due to interventricular septum
shift. These changes contribute to the low-output state by decreasing left ventricular (LV) distensibility, preload, and ventricular
elastance. (c, d) Role of the interventricular septum (c, pure RV infarction; d, RV infarction with septal ischaemia). (c) At ES, the
RV free wall moves toward the septum. At end-diastole (ED), the RV dilates during diastole and the septum reverse curves toward
the volume-reduced LV. At ES, the septum thickens but moves paradoxically into the RV, displacing the RV volume despite RV
free wall dyskinesis. (d) Septal ischaemia depresses septal contraction and global LV function, resulting in LV dilatation. The septum
stops thickening and there is increased systolic septal displacement into the RV. Pansystolic septal thinning and more extensive
paradoxical displacement are associated with further depression of RV performance.

associated with a higher recovery rate of RV function by
echocardiography and better 30-day mortality than incom-
plete revascularization in patients with RV infarction.
Further, in cases of complication with ventricular arrhyth-
mia, reperfusion results in a better prognosis.63 Thus,
prompt, successful, complete revascularization seems to
benefit all patients with RV infarction.
Other treatment modalities
The current treatment of RVMI patients, other than the opti-
mization of RV and LV preload with intravenous fluids, the
administration of inotropic agents, and revascularization,
includes the maintenance of atrioventricular synchrony, intra-
aortic balloon pump counterpulsation, and more intensive
mechanical support, including an emergent cardiopulmonary
bypass and use of a ventricular assist device (VAD). In this
section, we summarize the newly developing modalities for
patients with RV shock as follows: (1) electrical stabilization
device, including adequate heart rate and the maintenance of
atrioventricular synchrony; (2) percutaneous implantable
VAD (especially focused on Tandem-Heart); and (3) percuta-
neous cardiopulmonary support (PCPS).
An adequate heart rate and the maintenance of atrioven-
tricular synchrony can play an important role in sustaining
a sufficient cardiac output. Patients with RV infarction tend
to have bradyarrhythmia. In addition, the ischaemic right
ventricle and, consequently, the preload-deprived left ven-
tricle have a relatively fixed stroke volume, and cardiac
output strongly depends on the heart rate.64,65 Therefore, an
adequate heart rate with pacing is essential for patients with
RV infarction, regardless of the presence or absence of
bradyarrhythmia. Moreover, several investigators have
shown that atrioventricular sequential pacing in patients
with a complete atrioventricular block associated with RV
infarction leads to a significant improvement in the cardiac
output and recovery from shock when ventricular pacing
alone has no benefit.66 Unfortunately, transvenous pacing
may prove problematic due to ventricular sensing failure
from the ischaemic right ventricle and difficulties with lead
positioning after right atrial enlargement.
Surgically implanted right VADs have been used mostly
for the support of surgical or pre-transplant patients. They
have been less commonly used in the management of shock
or for the post-cardiopulmonary arrest syndrome. However,
in recent years, very few papers have described the use of
percutaneous VAD implantation using Tandem-Heart
(Cardiac Assist, Pittsburgh, PA, USA) for RV infarction.67–72
Tandem-Heart is a temporary, external, continuous-flow,
centrifugal pump that is placed nonsurgically in the cathe-
terization laboratory through the femoral vein; it was origi-
nally intended for stabilizing critically ill patients who
require short-term left heart support. The cannulas can be
placed in the right atrium and pulmonary artery to support
the right ventricle, as indicated in case reports. Percutaneous
VADs are expected to allow time for the recovery of RV
function in acute conditions or to serve as a bridge to other
interventions, such as surgical VAD implantation.
232 European Heart Journal: Acute Cardiovascular Care 2(3)
PCPS has also been used successfully to provide sup-
port for patients with refractory RV failure secondary to
RV infarction.73 A PCPS is a compact, portable heart-
lung machine that can be quickly installed using a thin-
walled cannula inserted via the femoral vessels. Cannulas
are advanced in the right atrium and femoral artery, and
oxygenated blood is transmitted from the femoral artery
in a retrograde fashion. Although the installation of the
Tandem Heart for left ventricular support requires a
trans-septal puncture to place the blood removal cannula
into the left atrium, such techniques are not required to
install a PCPS, which has been used to apply shock or for
cardiopulmonary arrest due to accessibility issues. Suguta
and colleagues74 reported the first case of cardiogenic
shock caused by RV infarction treated with a PCPS,
which is now recognized as one of the therapeutic options.
Conclusion
In patients with MI, especially those with IWMI, RV
involvement is an important contributor to shock, which
significantly increases the risk of mortality. The recent
advances in non-invasive modalities, such as CMR, pro-
vide a more accurate diagnosis of RV infarction, which in
turn helps elucidate the precise pathophysiology. Although
volume loading has long been considered the cornerstone
of management in these cases, we can apprehend the
harmful aspects of this therapy by understanding its effect
on the interventricular septum. Early successful reperfu-
sion, especially using revascularization, contributes to the
recovery from shock associated with RV infarctions,
which thus results in an improved prognosis. On the other
hand, the importance of RV infarction is highlighted in
this mechanical reperfusion era. The maintenance of an
adequate heart rate and atrioventricular synchrony is
another key factor for sustaining a sufficient cardiac out-
put in patients with RV infarction. In refractory cases,
more intensive mechanical support, including Tandem-
Heart or PCPS, has been applied and is recognized as new
therapeutic options.
Acknowledgements
We appreciate the critical review of this manuscript by Dr Judith
S Hochman from the Cardiovascular Clinical Research Center,
Leon Charney Division of Cardiology, New York University
School of Medicine, New York, USA.
Funding
This research received no specific grant from any funding agency
in the public, commercial, or not-for-profit sectors.
Conflict of interest
The authors declare that there is no conflict of interest.
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