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Right ventricular myocardial infarction:
pathophysiology, diagnosis, and management
Nicholaos Kakouros,
1
Dennis V Cokkinos
2
ABSTRACT
Right ventricular (RV) ischaemia complicates up to 50%
of inferior myocardial infarctions (MIs), though isolated
RV myocardial infarction (RVMI) is extremely rare.
Although the RV shows good long term recovery, in
the short term RV involvement portends a worse
prognosis to uncomplicated inferior MI, with
haemodynamic and electrophysiologic complications
increasing in-hospital morbidity and mortality. Acute RV
shock has an equally high mortality to left ventricular (LV)
shock. Identification of RV involvement, particularly in the
setting of hypotension, can help anticipate and
prevent complications and has important management
implications which are distinct from the management
of patients presenting with LV infarction. Reperfusion
therapy, particularly by primary percutaneous
coronary intervention, hastens and enhances RV
functional recovery that occurs to near normality in most
patients. The diagnostic methods for RVMI are
discussed, including clinical, electrocardiographic, and
various imaging modalities as well as the RV
pathophysiology that underpins the specifics of RVMI
management.
INTRODUCTION
Despite the clinical observation of right ventricular
(RV) infarction by Sanders almost 80 years ago,
1
this condition had received little clinical attention
until recent years, as early animal studies suggested
it to be of low haemodynamic significance.
2
It was
first described as a distinct clinical entity by
a seminal paper by Cohn et al 36 years ago.
3
Post-
mortem studies reveal that there is RV involvement
in 14e60% of patients dying with acute infer-
oposterior myocardial infarctions (MIs).
45
Non-invasive studies also suggest the presence of
RV ischaemic dysfunction in about 50% of patients
with acute inferior MI
67
and in #10% of patients
with anterior infarcts, whereas isolated RV infarc-
tion is rare, accounting for <3% of all cases of fatal
infarction.
8
The prognosis of right ventricular myocardial
infarction (RVMI) is generally thought to be goodda
view corroborated by the observation that the
outcome of inferior myocardial infarction is more
favourable than that of anterior infarction. Multiple
studies have, however, described increased acute
mortality in patients with acute inferior infarcts
complicated by RV involvement.
9e12
In a recent
meta-analysis of 22 studies involving a total of 7136
patients with acute MI, the presence of RVMI was
associated with a 2.6-times increased risk of
mortality as well as statistically significant increases
in secondary end points of morbidity such as
ventricular arrhythmias, high grade atrioventricular
(AV) block, and mechanical complications.
13
The early recognition of RVMI in a patient with
acute MI is of prime importance, not only for
prognostication purposes, but also because it can
guide specific therapy, including aggressive primary
percutaneous coronary intervention (PCI), with
particular attention to RV branch revascularisation,
in order to limit the deleterious effects of this
diagnosis.
In this review we first discuss the pathophysi-
ology of RVMI, as this underpins the specific
management decisions for RVMI patients. We then
aim to provide an overview of clinical, electrocar-
diographic, and several imaging diagnostic tech-
niques, their strengths and limitations as well as
the applicability of each modality in the various
clinical settings of RVMI presentation. Finally, we
discuss the management implications of RVMI.
RV PATHOPHYSIOLOGY
The RV has about one sixth the muscle mass and
performs about one quarter of the work of the left
ventricle (LV) yet, with the exception of small
physiologic shunts, provides the same cardiac
output.
14
This is achieved through the pulmonary
circulation providing a much lower afterload than
systemic resistance.
15 16
RV myocardial oxygen
consumption is approximately half that of the LV
and oxygen extraction at rest is lower than the LV,
with capacity to increase on stress.
17
Anatomic
blood supply is dual with predominant supply from
the right coronary artery (RCA) and nearly one
third of RV free wall blood flow derived from the
left coronary branches.
18
Unlike the LV, RV coro-
nary perfusion occurs in systole as well as diastole
in the absence of severe RV hypertrophy,
19
and
there is also potential for more extensive subacute
collateral formation from left to right coronaries.
20
Consequently, the supplyedemand profile of the
RV is more favourable than that of the LV.
The RV acts as a volume pump by its free wall
(RVFW) longitudinally shortening and contracting
towards the interventricular septum from apex to
RV outflow tract.
20
The septal contraction
contributes about one third of RV stroke work even
under physiological conditions,
21 22
with the LV
assisting further by providing traction on the RV
free wall at their attachment points.
23
The RV
pressureevolume loop has relatively brief periods of
isovolumic contraction and relaxation and
a sustained ejection period during pressure devel-
opment but also pressure decline. This low pres-
sure, volume pump system can adapt well to
volume overload states such as tricuspid regurgita-
tion or atrial septal defect,
24
but is very sensitive to
1
Interventional Cardiology
Fellow, JohnsHopkins Hospital,
Baltimore, Maryland, USA
2
Biomedical Research
Foundation of the Academy of
Athens, Greece
Correspondence to
Dr Nicholaos Kakouros,
Interventional Cardiology Fellow,
Johns Hopkins University, Ross
Research Building 1165/1167,
1721 East Madison Street,
Baltimore, MD 21205, USA;
nkakouros@gmail.com
Received 1 June 2010
Accepted 10 August 2010
Published Online First
18 October 2010
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increases in afterload to which the RV can respond only by
compensatory dilatation to maintain stroke volume, albeit at
a reduced ejection fraction.
14 25
OCCURRENCE OF RVMI
RVMI occurs principally due to occlusion of the RCA proximal
to the major RV branches in the context of an inferior MI.
26
It
may also occur by occlusion of the left circumflex artery in
patients with a left-dominant circulation but also, less
commonly, in anterior infarcts as the anterior part of the RV free
wall is supplied by collaterals from the left anterior descending
artery.
18
The conus artery, that has a separate ostium to the
RCA in 30% of cases, supplies the infundibulumdwhich
explains the sparing of this region even in proximal RCA
occlusions.
Although ischaemic dysfunction occurs initially, the
ischaemic RV usually recovers its function in the long term even
in many non-revascularised patients.
27
Recovery is so common
as to have led some clinicians to believe that the term ‘right
ventricular infarction’is a misnomer and that RV ‘stunning’
with viability is more appropriate.
28
As might be expected, RV
hypertrophy with consequent increased oxygen demands may
predispose to more RV infarction.
52930
RVMI is associated with clinically evident haemodynamic
manifestations in <50% of affected patients. Nonetheless, even
in the absence of evident haemodynamic compromise, the
potential of RV ischaemia should be recognised so as to avoid
treatment that will further lower RV preload and compromise
the patient’s condition.
RV ischaemia causes depressed RV contractility and RV dila-
tation as well as impaired relaxation. This leads to decreased RV
compliance, reduced filling, and decreased RV stroke volume,
resulting in reduced transpulmonary delivery of LV preload that
leads to lower total cardiac output despite intact (or mildly
reduced) LV contractility. RV dysfunction, however, has a more
pronounced effect on cardiac output than would simply be
expected by the reduced LV preload. The elevated RV volume
and RVend diastolic pressure (RVEDP) also displaces the septum
towards the volume deprived LV, further impairing LV compli-
ance and limiting LV filling.
20
Moreover, RV dilatation within
the non-compliant pericardium leads to elevated intrapericardial
pressure, causing further restraint of LV filling and to equal-
isation of diastolic pressures.
31
Notably, the early animal studies,
that had found no significant haemodynamic compromise from
experimentally induced isolated RV damage, had used an open
pericardial model.
232
Associated ischaemia of the interventricular septum, with loss
of its significant contribution to global RV systolic function,
may further exacerbate haemodynamic compromise.
33
In the
acute setting, coexisting LV MI may cause pulmonary capillary
wedge pressure to rise, increasing RV afterload and further
embarrassing RV function.
If the right atrium (RA) is spared, it may demonstrate
increased contractility through increased preload. This leads to
enhanced atrial relaxation, facilitated atrial inflow and may
enhance RA performance to the extent of offsetting some of the
haemodynamic consequences of RV ischaemia. The forceful RA
contractions can cause the pulmonary valve to open before RV
systole, a phenomenon initially detected by M mode echocar-
diography.
34
The increased loading conditions on the RA,
however, increase RA oxygen demands while the increased intra-
atrial pressure tends to diminish transmural perfusion. These
features, in addition to the RA blood supply being related to that
of the RVand consequently likely to be compromised, make RA
ischemic involvement not uncommon in RVMI; it is documented
in up to 20% of RVMI cases on autopsy studies.
20 35
Right atrial ischaemia may further compound RV ischaemia
by leading to rate and rhythm disturbances that impair RA and
RV function as well as AV synchrony in as many as 50% of
RVMIs, especially in patients with proximal RCA occlusion.
36 37
High degree AV block is often due to AV nodal ischaemia and is
associated with poorer prognosis,
38
whereas atrial fibrillation
(AF) may occur secondary to atrial wall stretch by the elevated
RA pressures.
Afferent vagal stimulation by receptors on the inferior and
posterior walls of the heart, commonly affected in RVMI, as
well as baroreceptors from the RV lead to enhanced para-
sympathetic tone and the cardioinhibitory BezoldeJarisch reflex.
Reperfusion of the acutely occluded RCA by thrombolysis or
primary PCI may paradoxically lead to severe yet transient
bradycardia hypotension, which is thought to be due to this
right heart reflex mechanism. AV nodal block occurring beyond
the first 24 h of infarction tends to be atropine insensitive; it has
been suggested to be secondary to adenosine release by the
ischaemic myocardium
39 40
and may therefore respond to
aminophylline.
41
Ventricular tachyarrhythmias from the dilated
RVare common in the acute setting, complicating up to a third
of cases
10 11 42 43
particularly in the absence of coronary reper-
fusion,
28
though late scar-related arrhythmias are unlikely.
20
DIAGNOSIS OF RVMI
The diagnosis of RVMI is commonly made from the physical
examination, electrocardiography, echocardiography, and
haemodynamic measurements. Chest radiography may be useful
in determining the presence or absence of pulmonary oedema
but is not useful for the detection of RVMI related chamber
dilatation, as the RV is an anterior cardiac structure occupying
little of any heart border.
44
Radionuclide angiography was
previously considered the gold standard (next to autopsy) for
detection of haemodynamically significant RV dysfunction,
4
but
has now been superseded by cardiac MRI (CMR). Electrocardi-
ography and echocardiography remain the most readily available
and simplest of these techniques in the acute setting.
Clinical and haemodynamic findings
Clinically, the triad of hypotension, elevated jugular venous
pressure (JVP), and clear lung fields is recognised as a marker of
RVMI in patients with acute inferoposterior wall infarction,
with high specificity (96%) but low sensitivity (25%).
45
Simi-
larly, the haemodynamic correlate of RA pressure (RAP) $10
mm Hg with an RAP: pulmonary capillary wedge pressure
(PCWP) ratio of $0.86 is highly specific (97%) for RV necrosis
determined on postmortem examination, and persists after
diuresis or use of inodilators.
34
Pulsus paradoxus and Kussmaul’s sign may also occur with
RV ischaemia.
46
The combination of elevated JVP and Kuss-
maul’s sign in a patient with acute inferior wall MI is highly
specific and sensitive for RV ischaemia.
45
Auscultation may
reveal a right-sided S3 and S4 gallop.
46
If the atrial perfusion is
not compromised, the a-wave and x descend waveforms of the
JVP are enhanced but y descent is blunted due to pandiastolic RV
dysfunction, giving rise to a ‘W’pattern waveform.
47e49
In
patients with associated RA infarction, the RA and central
venous pressures are higher but with depressed a-wave, and x
and y descent, forming an ‘M’pattern.
48
Dilatation of the RV
may lead to functional tricuspid regurgitation such that the
RA pressure tracing reveals a systolic wave that precedes and
may fuse with the venous filling wave.
50
Severe tricuspid
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regurgitation may occur in cases of ischaemic papillary muscle
dysfunction or rupture.
51
In these cases the RA waveform
progressively approximates the RV waveform.
Occasionally, a ventricular septal defect may accompany RV
infarction, causing a holosystolic murmur and often leading to
severe acute haemodynamic compromise.
52
The left-to-right
shunt reduces effective for ward LV output and further overloads
the dysfunctional RV leading to hypotension and precipitating
pulmonary oedema. Surgical repair or percutaneous device
closure is imperative, albeit high risk.
53
Elevated right heart
pressures due to ischaemia may also stretch open a patent
foramen ovale or cause a right-to-left shunt via an atrial
septal defect, clinically evident as oxygen resistant systemic
hypoxaemia or paradoxic emboli.
54e56
Electrocardiography
The precordial leads of the classic 12 lead ECG provide a wealth
of information on the LV, but yield limited information on the
electrical activity of the right heart. Only lead V1 and possibly
V2 may provide a partial view of the RV free wall as shown in
figure 1. ‘Right precordial’leads are obtained by placing the
precordial electrodes over the right chest in positions mirroring
their usual arrangement (figure 1). The presence of acute ST
segment elevation, Q waves or both in the right precordial leads
(V3R to V6R), is highly reliable in the diagnosis of RVMI.
57e59
ST segment elevation $0.1 mV in the right precordial leads,
especially V4R, is observed in 60e90% of patients with acute
RVMI.
58 60e64
It correlates with reduced RVejection fraction and
is strongly associated with major complications and in-hospital
mortality.
43 65 66
Nonetheless, right precordial ST segment
elevation is a transient event that may be absent in up to half of
patients with RV infarction 10e12 h after the onset of pain,
64 67
and is also associated with other cardiac diseases including acute
anteroseptal MI, previous anterior MI with aneurysm, LV
hypertrophy, and acute pulmonary embolus, and may mimic
Brugada syndrome.
68
STelevation from the RV free wall may also be detected by ST
elevation in lead III being more than that in lead II or by
reciprocal ST depression in leads I and aVL >2 mm in total
(figure 2).
69 70
The positive predictive value of both these find-
ings is about 70e80%.
71 72
Similarly, reciprocal ST depression in
the lateral leads is a sensitive predictor of RV ST elevation,
though specificity is understandably low.
73
In inferior infarction involving the LV posterior wall in addi-
tion to the RV, right precordial ST elevation or R wave loss have
low sensitivity and only moderate specificity. The opposing
vectors generated by the thicker LV posterior wall dominate,
creating prominent R waves and reciprocally depressed ST
segments on the right precordial leads. The individual contri-
bution by each of these vectors may be resolved by comparing
ST elevation in aVF with ST depression in V2, which is roughly
orthogonal to the standard limb plane and reflects posterior wall
contribution. More specifically, elevation in aVF exceeding the
depression in V2 is suggestive of additional RV involvement.
Similarly a ratio of <0.5 between ST depression in lead V3 and
ST elevation in lead III has approximately 90% sensitivity and
specificity in diagnosing infarction related to occlusion of the
proximal RCA.
74
It has been suggested that slurring of the ‘r’wave in either
right precordial leads or lead aVR is both sensitive and specific
for RV involvement in cases of inferoposterior infarction (70%
and 94%, accordingly
75
). This is thought to arise by focal
conduction block and depolarisation heterogeneity in the RV
free wall caused by RV ischaemia. This conduction block can
also lead to the development of isolated islands of viable
myocytes, delayed depolarisation of which can lead to the post-
excitation ECG phenomenon called ‘epsilon wave’, more
commonly recognised as a major diagnostic criterion of
arrhythmogenic RV dysplasia.
76
Isolated ST segment elevation in V1 to V3 (and possibly V4),
with decreasing levels of elevation from V1 onwards and
without Q wave formation, has also been reported in a few cases
of RV infarction.
77e80
This seems unrelated to septal damage,
but is rather a correlate to the rare entity of isolated RV
infarction. In the clinical setting, isolated RV infarction has been
reported after acute occlusion of the RV branches after
angioplasty,
81e84
occlusion of a rudimentary or non-dominant
RCA,
80
and good left coronary supply to the inferoposterior
LV
85 86
or if the inferior wall has already previously been
infarcted.
82 87 88
In patients with RV infarction, in contrast to
basal interventricular septal infarction, ST segment elevation in
V4R is greater than that in V1 to V3.
78
The relatively small
representation of this isolated RVMI ECG entity in the literature
may be partly due to misdiagnosis as anteroseptal infarction,
and stresses the importance of performing right precordial ECG
recordings in patients with isolated V1 to V3 ST elevation.
Echocardiography
Two dimensional echocardiography provides an assessment of
RV function, wall motion abnormalities, valve lesions and LV
Figure 1 (A) Placement of right
precordial leads in a mirror arrangement
to the left precordial leads, and (B)
simplified schematic demonstrating the
relation of the leads to the ventricles.
Note that, of the common left precordial
leads, V1 is best placed to view any
right ventricular free wall injury
currents. LV, left ventricle; RV, right
ventricle.
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function.
27
Nonetheless, heavy RV trabeculations make endo-
cardiac surface definition difficult and volume calculations are
hindered by the complex geometry of the RV, while echocar-
diographic imaging windows can be limited by the retrosternal
position of the chamber.
Several different echocardiographic features have been used as
surrogates of global RV function. Assessment of RV free wall for
hypokinesia or akinesia, performed qualitatively by operator
real-time evaluation, is a sensitive assessment for detecting RV
dysfunction.
89 90
Nonetheless, this visual assessment leads to
underestimation of dysfunction due to a visually misleading
asymmetric contraction of the RV walls toward its centre, and is
best combined with demonstration of RV dilatation in order to
define RVMI accurately.
91
A semiquantitative method based on
RV wall motion score indexing (assigning points to parts of the
wall) has been found to correlate well with radionuclide derived
RVEF.
92
Additional features of RV involvement include paradoxical
septal motion due to increased RV end diastolic pressure,
91 93
tricuspid regurgitation which can be assessed by Doppler echo-
cardiography, and severe RA enlargement.
94
The increased RA
pressure may cause deviation of the interatrial septum with
convexity toward the left atrium in up to 80% of RVMI
patients.
93
Doppler echo may also detect flow across a patent
foramen ovale opened by the increased right heart pressures as
well as an acute ventricular septal defect.
M mode measurements of the systolic displacement of the
lateral portion of the tricuspid annular plane (TAPSE: tricuspid
annular plane systolic excursion) have been advocated as
a measure of RV base-to-apex shortening during systole and
a correlate of RV ejection fraction, with the rationale that, in
contrast to the LV, the RV contraction involves predominantly
longitudinal shortening. TAPSE has been shown to be highly
reproducible and of prognostic value in patients with congestive
cardiac failure.
95 96
TAPSE as an estimate of RVEF has been
shown to correlate well with RVEF measured by first pass
ventriculography and CMR.
95 97 98
There are limited data on the
application of TAPSE in the early diagnosis and assessment of
RVMI. In a study by Kidawa et al, patients with RCA occlusion
on angiography who presented >2 h after onset of symptoms
had significantly reduced TAPSE and worse long term prognosis
compared with patients who presented earlier than 2 h.
99
In
a recent study by Engstrom et al of patients with ST elevation
MI (STEMI) complicated by cardiogenic shock, a low TAPSE
(#14 mm) was an independent predictor of long term
mortality.
12
It is noteworthy, however, that TAPSE is not only
affected by RV systolic function but may also be reduced by
impaired LV systolic function.
100
Echocardiography: tissue Doppler imaging
Tissue Doppler imaging (TDI) can provide information on
myocardial wall motion during the cardiac cycle. Annular
velocities towards the apex reflect the contraction and relaxation
of longitudinal myocardial fibres in both ventricles. As most RV
muscle fibres run in an oblique or longitudinal direction,
101
this
is a good measure of global RV function.
97 102e104
Figure 2 Summary of ECG features of right ventricular myocardial infarction (MI) complicating inferior MI. Coronary angiography confirmed proximal
occlusion of the right coronary artery with minor left anterior descending artery disease.
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TDI has been used to assess RV function in patients with
RVMI complicating inferior infarction. Significantly reduced
systolic lateral tricuspid velocities are found in patients with
concomitant RV infarction.
94 105e107
The TDI derived RV
systolic strain also correlates with RVEF, is lower in patients
with RVMI, and has prognostic value in AMI patients.
108e110
Lateral tricuspid annulus TDI can also detect ischaemic RV
diastolic dysfunction.
111
In particular, the early diastolic annular
velocities (Em) show a significant and steady decrease with
progressive diastolic dysfunction, which appears unaffected by
preload state.
107 112
Reduced early diastolic tricuspid annular
velocities have been demonstrated in patients with RV infarction
complicating inferior MI.
94 105e107
Echocardiography: myocardial perfusion index
The concept of myocardial perfusion index (MPI), initially
described by Tei in 1995, has also been applied to assess RV
function.
113 114
This simple index of combined systolic and
diastolic myocardial performance is defined as the sum of the
isovolumetric contraction and relaxation periods divided by
ejection time which can be derived from pulse wave Doppler
interrogation of the tricuspid inflow and RV outflow or from the
TDI signal of the tricuspid annulus.
107 115
As MPI encompasses the energy dependent processes of RV
relaxation, contraction and ejection, it is well poised to be
a sensitive marker of RV ischaemia. RV MPI is higher in patients
with inferior acute MI and RV involvement than in patients
with no RV involvement,
93 115
such that a TDI derived MPI of
>0.70 is both highly sensitive and specific in detecting RV
ischaemia in the setting of an acute inferior MI.
107
Notably, RV
MPI may be increased by left heart disease, cor pulmonale,
pulmonary valve stenosis, and thromboembolism which need to
be excluded. We have recently demonstrated that combining the
peak lateral tricuspid annulus systolic velocity (S’) data with
MPI, as the novel S’/MPI index, yields good sensitivity and
specificity in detecting RVMI both in the acute and late phase of
RVMI.
116
Echocardiography: three dimensional
Three dimensional echocardiography (3DE) has been available
for some years, from 3D reconstruction of 2D images and more
recently with real-time 3D echo imaging, and can provide
volumetric images of the RV in most patients. Although early
results suggested poor correlation with CMR volumes,
98
there
have since been significant improvements in hardware and
modelling software.
117
In a recent study by Leibundgut et al,
although the 3DE derived volumes were lower than CMR, the
two modalities correlated very well.
118
Nonetheless, despite
these improvements, the technique applicability remains limited
in dyspnoeic patients and irregular cardiac cycles whereas new
hardware as well as expertise in the semi-automated post-
processing is required. Currently, the utility of 3DE in the acute
setting of RVMI remains unknown.
Radionuclide techniques
Radionuclide angiography used to be the gold standard for the
assessment of RV end diastolic and end systolic volumes and
calculation of RVejection fraction, as assessment of radionuclide
count density is not geometry dependent.
119
Segmental RV wall
motion abnormalities in association with a reduced RVEF (to
<40%) on first pass ventriculography are highly sensitive and
specific for RVMI or RV ischaemia.
89
These radionuclide tech-
niques have now been superseded by CMR which is accurate
and does not require radiation exposure.
CMR
CMR is a volumetric technique based on visualisation of the
anatomy of the RV that can directly evaluate RV size, mass,
morphology, and function in an accurate and reproducible
manner.
44 120
It can additionally detect other right sided
myocardial disease such as arrhythmogenic RV dysplasia,
complex congenital disease, pericardial disease, as well as medi-
astinal pathology. Manual or semi-automated volume measure-
ments by CMR show high reproducibility and very good
agreement between calculated LV and RV stroke volumes.
119
CMR is now considered the gold standard for non-invasive
assessment of RV function, particularly as it provides additional
information on RV anatomy and myocardial mass.
Gadolinium late hyperenhancement of RVFW on CMR has
been demonstrated in cases of RVMI
121e123
and may persist at
least 6 months after the ischaemic event.
124
Advances in tech-
nology including shorter acquisition times and more widespread
availability of equipment and expertise is likely to lead to the
increased utilisation of this modality.
CT
CT has been used in the assessment of RV function in the
setting of pulmonary embolism, with better sensitivity and
specificity than echocardiography when compared with a 40%
pulmonary occlusion standard.
125
Delayed enhancement multi-
slice cardiac CT (MSCT) has been shown to have good agree-
ment with delayed enhancement cardiac MRI and postmortem
evaluation in determining myocardial infarct size at 3e7 days in
an animal model.
126
Despite high spatial resolution, soft tissue
contrast is poor and radiation exposure remains significant,
rendering its utility in the diagnosis of RVMI very limited above
the previously discussed imaging techniques. Notably, however,
MSCT angiography can provide increasingly higher quality
coronary images which can be helpful, particularly for congenital
malformations such as anomalous RCA origin.
127
OUTCOME OF RVMI
Successful intervention by primary PCI in patients with RVMI
has been shown to normalise the RV ejection fraction and is
associated with improved in-hospital mortality compared with
patients in whom angioplasty is unsuccessful.
28 128
Reperfusion
within 1 h of occlusion leads to immediate recovery of RVFW
function and consequent improved LV filling and performance.
20
Delayed reperfusion after 4e8 h is associated with a higher
degree of RV dysfunction and complications, but still results in
significant, yet slower, recovery of RV function.
129 130
Failure to
reperfuse the RCA, and in particular the RV branches, leads to
lack of recovery in the acute setting and consequent haemody-
namic compromise, which is associated with high in-hospital
mortality. Similarly, thrombolysis leads to functional RV
recovery and imparts a survival benefit in patients sustaining an
inferior MI with RV involvement, but only as long as it is
successful in achieving RCA patency.
131 132
This is an important
caveat as the proximal RCA lesion, which frequently presents
with high clot burden in association with reduced coronary
delivery of fibrinolytic agent due to associated hypotension,
leads to a higher incidence of primary thrombolytic failure as
well as a higher incidence of reocclusion.
131
A study of unse-
lected patients who presented with acute MI, and received
thrombolysis with tissue plasminogen activator, found the
infarct related artery more likely to be occluded in patients with
RVMI than in those without. In view of the above, thrombolysis
is not an appropriate treatment modality in this group of
patients if primary angioplasty is available.
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In the SHOCK (Should we emergently revascularize Occluded
coronaries for Cardiogenic shock) trial registry, the cardiac index
was depressed to a similar extent in patients with RV shock as in
patients with LV shock, albeit with higher RA pressures and
lower pulmonary artery pressures for a similarly elevated LV
filling pressure.
133
Furthermore, mortality of cardiogenic shock
associated with RVMI was equivalent to mortality of shock due
to LV infarction (55% and 60% in-hospital mortality, respec-
tively) despite the patients’younger age, lower rate of anterior
MI, and higher prevalence of single vessel coronary disease.
134
Even though significant haemodynamic compromise and
arrhythmias associated with RV ischaemia lead to increased
early mortality,
10 11 43
in the longer term most patients with
acute RV ischaemia improve spontaneously even in the absence
of reperfusion of the infarct related artery.
89 135
Clinical
improvement occurs within 3e10 days whereas RV ejection
fraction returns to near normal within 3e12 months.
89 132 135 136
Recovery is thought to be due the favourable supplyedemand
characteristics of the RV and is, predictably, less pronounced in
the presence of RV hypertrophy.
29 30
The employment of right
sided chest leads during stress testing may, however, reveal latent
post-infarction RV ischaemia.
137 138
FURTHER MANAGEMENT IMPLICATIONS OF RVMI
The accurate diagnosis of RVMI is vital as both the treatment
and the prognosis of RV infarction substantially differ from that
of LV infarction (see box 1). Early work on experimentally
induced RV ischaemia found that volume loading led to an
increment in RV filling pressures and increased systolic arterial
pressure and cardiac output.
90
Furthermore, treatments
commonly employed in predominantly LV infarction, such as
the use of diuretics, intravenous nitrates, ACE inhibitors or even
opiates, may reduce RV preload and cause catastrophic haemo-
dynamic compromise. In the clinical setting, the beneficial effect
of fluid loading is not universal but is dependent on the degree of
RVafterload and baseline volume status of the patient. Excessive
volume loading can increase wall tension, decrease contractility,
and impair LV filling through interventricular dependence
mechanisms discussed earlier, and lead to reduced systemic
cardiac output.
139
Nonetheless, in the absence of pulmonary
oedema or evidence of notably increased right sided preload,
a trial of volume loading is appropriate.
20
Should cardiac output fail to improve after fluid loading, the
common inotrope of choice is dobutamine.
140 141
Dobutamine
may enhance RV performance through its inotropic effect,
reduce pulmonary vascular resistance and hence RV afterload,
and improve AV conduction. Its utility is limited by arrhyth-
mias, systemic vasodilation, and hypotensive response. The
‘inodilator’milrinone may reduce preload and exacerbate
hypotension, but also reduces RV afterload by lowering pulmo-
nary resistance. In severely hypotensive patients the addition of
a pressor (such as dopamine) to aid maintenance of coronary
perfusion pressure may be beneficial.
Levosimendan, a calcium sensitiser inotrope, appears to
improve RV contractility in patients with chronic LV failure
without detriment to diastolic function or an apparent increase
in myocardial oxygen demand.
142e144
Levosimendan may also
reduce RV afterload by activation of ATP sensitive potassium
channels in the pulmonary vasculature, leading to dilatation,
while reducing LV afterload and improving coronary perfusion
by a similar mechanism on systemic and coronary vessels.
145 146
In an experimental animal model of acute RVMI, levosi-
mendan improved global haemodynamics, increased RV
contractility, and mildly reduced RV afterload.
147
In a recent
study of 56 patients with cardiogenic shock secondary to MI, an
improvement in RV function and a reduction in pulmonary
vascular resistance was noted with levosimendan and persisted
after the end of the infusion.
148
Although no specific RVMI
criteria were applied in the study, patients with inferior MI had
lower RV function indices and showed significant improvement
in both right and left cardiac function in response to levosi-
mendan. Interestingly, in an animal model of RV ischaemia/
reperfusion injury, both levosimendan and milrinone appeared
to have additionally cardioprotective properties.
149
Mechanical support with intra-aortic balloon pumping may
increase coronary perfusion pressure, enhance coronary fibrino-
lytic delivery, and improve LV performance in hypotensive
patients with RVMI and depressed LV function, thus reducing
RV afterload. Percutaneous cardiopulmonary support and, more
recently, assist devices have also been successfully used to
provide support for patients with refractory RV failure
secondary to RVMI.
150e153
Main messages
<Right ventricular (RV) ischaemia occurs in up to half of inferior
myocardial infarctions (MIs).
<RVMI portends increased mortality and morbidity to acute
infarction.
<Prompt revascularisation improves outcomedprimary percu-
taneous coronary intervention (PCI) is superior to thrombol-
ysis.
<Diagnosis of RV involvement can be challenging. Electrocar-
diography and echocardiography are the methods of choice in
clinical practice during the acute setting assessment.
<Identification of RV involvement prompts specific manage-
ment considerations (see box 1).
<The RV tends to recover to near normality in the long term.
Box 1 Right ventricular (RV) myocardial infarction
management: summary
<Prompt diagnosis
– Clinical signs, ECG (figure 2)drecord right precordial leads
in all patients with inferior ST elevation or isolated V1eV3
ST elevation, echocardiographic imaging
<Reperfusion therapy
– Primary percutaneous coronary intervention preferable to
thrombolysis
<Optimise RV preload
– Avoid : morphine, diuretics,
b
-blockers, nitrates
– Trial of judicious fluid administration in the absence of
pulmonary oedema
<Reduce RV afterload
– Inotropes, pulmonary vasodilators (nitric oxide, prostacy-
cline), intra-aortic balloon pump
<Maintain chronotropic competence and atrioventricular
synchrony
– Avoid:
b
-blockers in patients with proximal right coronary
artery occlusion
– Consider dual-chamber temporary pacing
<If above fails consider
– RV assist device, emergency percutaneous cardiopulmo-
nary support
724 Postgrad Med J 2010;86:719e728. doi:10.1136/pgmj.2010.103887
Review
group.bmj.com on June 15, 2013 - Published by pmj.bmj.comDownloaded from
The acutely ischaemic RV and consequently preload deprived
LV have a relatively fixed stroke volume, and output is therefore
strongly heart rate dependent.
37
Maintenance of chronotropic
competence, which is frequently compromised by mechanisms
discussed previously, is therefore of great importance. Atropine
may restore physiological rhythm, but ventricular pacing may be
required. AVasynchrony leads to loss the of the atrial transport
contribution to RV filling and may precipitate tricuspid regur-
gitation further impairing effective forward RV output. Some of
these patients may, therefore, require sequential dual chamber
temporary AV pacing.
47 154
Unfortunately, transvenous pacing
may prove problematic due to poor ventricular sensing from the
ischaemic RVas well as difficult lead positioning in the ischaemic
and often dilated RA.
20
In these cases rapid administration of
intravenous aminophylline has been reported to restore sinus
rhythm in patients unresponsive to atropine, presumably by
reversing the negative chronotropic effects of ischaemia induced
adenosine production.
155e157
The salutary effects of reperfusion
therapy and the particular importance of flow restoration to the
major RV branches have been discussed earlier.
CONCLUSION
The pathophysiology of the RV makes it resistant to infarction,
but acute ischaemia can lead to severe haemodynamic
consequences. RVMI worsens the short term prognosis of infe-
rior MI, but has an excellent long term prognosis in the absence
of associated severe LV dysfunction.
The diagnosis of RVMI can be challenging; the 12 lead ECG
with supplemental right precordial recordings remains the
principal diagnostic tool in the acute setting, but the findings
may be transient. The previously described echocardiographic
techniques, particularly the application of TDI, are most useful
in the acute and later phase of assessment, whereas the utility of
3DE is unknown. In the subacute setting, modern cardiac MRI
techniques may also be used to detect RV free wall scarring and
have become the gold standard for assessment of RV ejection
function, superseding nuclear techniques.
Identification of RVMI is important to guide initial manage-
ment of fluid, inotropic, and chronotropic support with rapid
reperfusion therapy, and to raise awareness of potential
complications.
SELF ASSESSMENT QUESTIONS (TRUE/FALSE; ANSWERS
AFTER THE REFERENCES)
1. Patients with RVMI and high central venous pressures
(elevated JVP) should be treated with furosemide even in
the absence of pulmonary oedema to reduce pressure load on
the ischaemic RV.
2. ST elevation $0.1 mV in the right precordial lead V4R can be
used to diagnose concomitant RV infarction in patients with
inferior MI.
3. Cardiogenic shock due to RV infarction has a better prognosis
than shock due to LV infarction.
4. In patients presenting with ST elevation MI, CMR is the gold
standard for the diagnosis of RV infarction.
5. Echocardiographic techniques such as TAPSE and systolic
tricuspid annular velocities by TDI only assess longitudinal
RV shortening and do not take into account circumferential
RV function.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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<Can the prompt identification of RV infarction lead to more
specific treatment that can further impact on prognosis? Does
aggressive primary PCI with revascularisation of the branches
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<What is the utility of 3D echocardiography in the assessment
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<What is the prognostic significance of an old RVMI (eg, as
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ANSWERS
1. False. On the contrary, the elevated central venous pressures have the salutary
effect of providing increased RV preload that helps maintain output. Treatment
with furosemide or other venodilators can lead to catastrophic decompensation
and haemodynamic collapse.
2. True. ST elevation in the right precordial leads and particularly V4R is
a sensitive (albeit transient) diagnostic ECG finding in patients with RVMI
complicating inferior STEMI.
3. False. Although inferior infarction, which RVMI usually complicates, overall has
a better prognosis than anterior LV infarction, cardiogenic shock due to RVMI has
a prognosis that is as poor as that due to LV infarction.
4. False. Although CMR has superseded radionuclide techniques as the gold
standard for RV volume assessment, ECG and echocardiography remain best
suited for the acute assessment of patients presenting with AMI.
5. True. Although this is true, both of these measures correlate very well with
global RV systolic function as most RV free wall muscle fibres run in an oblique or
longitudinal direction. Additionally, assessment of diastolic velocities from TDI can
provide information on RV diastolic function.
728 Postgrad Med J 2010;86:719e728. doi:10.1136/pgmj.2010.103887
Review
group.bmj.com on June 15, 2013 - Published by pmj.bmj.comDownloaded from
doi: 10.1136/pgmj.2010.103887
18, 2010 2010 86: 719-728 originally published online OctoberPostgrad Med J
Nicholaos Kakouros and Dennis V Cokkinos
management
pathophysiology, diagnosis, and
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