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Cardiovascular Revascularization Medicine 19 (2018) 43–50

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Cardiovascular Revascularization Medicine

Right ventricular infarction☆,☆☆,★
Vinod Namana a,⁎, Sushilkumar Satish Gupta b, Anna A. Abbasi b, Hitesh Raheja b,
Jacob Shani a, Gerald Hollander a
a
b

Department of Cardiology, Maimonides Medical Center, Brooklyn, NY, USA
Department of Medicine, Maimonides Medical Center, Brooklyn, NY, USA

a r t i c l e

i n f o

Article history:
Received 27 May 2017

Received in revised form 9 July 2017
Accepted 11 July 2017
Keywords:
Right ventricular infarction
Infero-posterior myocardial infarction
Myocardial infarction
Right-sided electrocardiogram

a b s t r a c t
Coronary Heart Disease is a leading cause of morbidity and mortality worldwide. A great amount is known about
left ventricular myocardial infarction. It was not until much later (1974) that right ventricular myocardial infarction was studied as a separate entity. Isolated right ventricle myocardial infarction is rare. Around one-third of
patients with acute infero-posterior ST-segment elevation myocardial infarction, will present with concomitant
right ventricular infraction. The aim of this paper is to review the literature on the importance of early recognition
of right ventricular infarction, clinical presentation, pathophysiology, diagnostic evaluation, differential diagnosis,
treatment, complications and prognosis.
© 2017 Elsevier Inc. All rights reserved.

1. Introduction
Coronary Heart Disease is a leading cause of morbidity and mortality
worldwide. Approximately 16.5 million American adults are affected
with coronary artery disease (Myocardial Infarction - 7.9 million,
Angina Pectoris - 8.7 million) [1]. A great amount is known about left
ventricular myocardial infarction (MI). It was not until much later
(1974) that right ventricular myocardial infarction (RVI) was studied
as a separate entity [2].
Isolated RVI occurs seldom; approximately only 2% cases are reported on autopsy [3,4,5]. Around one-third of patients with acute inferoposterior ST-segment elevation MI, will present with concomitant RVI
[3,6]. The right ventricle (RV) is a volume dependent chamber; therefore any significant insult can lead to severe hemodynamic compromise.
RVI is associated with higher in-hospital morbidity and mortality related to hemodynamic and electrophysiological complications [5]. The
most common culprit vessel for causing RVI is occlusion of the right ventricular branch or acute marginal branch of the right coronary artery (or

Abbreviations: MI, myocardial infarction; RV, right ventricle; LV, left ventricle; RA,
right atrium; RVI, right ventricular infarction.
☆ Disclosures: All authors have no conflicts on interests.
☆☆ Funding: None.
★ All authors have contributed equally to the manuscript writing.
⁎ Corresponding author at: Department of Cardiology, 4802 10th avenue, Brooklyn, NY
11219, USA.
E-mail address: vnamana@maimonidesmed.org (V. Namana).
http://dx.doi.org/10.1016/j.carrev.2017.07.009
1553-8389/© 2017 Elsevier Inc. All rights reserved.



left circumflex artery in left dominant coronary circulation) [3,5,7,8].
Atrial kick plays a crucial role in RVI; loss of atrial kick can further worsen the cardiac hemodynamics [9]. RV is relatively resistant to infarction
and recovers even after prolonged occlusion [10]. RV performance improves spontaneously even in the absence of reperfusion [10]. The aim
of this paper is to review the literature on the importance of early recognition of RVI, clinical presentation, pathophysiology, diagnostic evaluation, differential diagnosis, treatment, complications and prognosis.

2. Pathophysiology and clinical presentation
Right ventricular myocardial infarction is often silent and only 25% of
patients develop clinically evident hemodynamic manifestations on
presentation [11,12]. Signs and symptoms can include some of the typical manifestations of an MI such as chest pain, diaphoresis, nausea and
vomiting. However certain manifestations that are more specific, although not sensitive for RVI include the following hemodynamic
triad: hypotension, elevated jugular venous pressure and clear lungs
[8,13]. Some additional signs and symptoms that indicate impending
hemodynamic instability include Kussmaul's sign, pulsus paradoxus
and a tricuspid regurgitation murmur [8]. The presence of elevated jugular venous pressure and Kussmaul's sign in the setting of an acute
infero-posterior MI indicate a hemodynamically significant RVI [35]
(sensitivity = 88% and specificity = 100%), particularly when it is associated with significant damage to the left ventricle and/or interventricular septum [14]. Concomitant RVI with infero-posterior MI may
initially present without evidence of hemodynamic compromise


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V. Namana et al. / Cardiovascular Revascularization Medicine 19 (2018) 43–50

characteristic of RVI, but subsequently develop hypotension precipitated by preload reduction attributable to nitroglycerine [15] or associated
with bradyarrhythmias [16,17]. Early recognition of acute RVI is very
crucial in initiation of treatment for hypotension and shock and to
avoid therapy that will lower right heart preload (nitrates and diuretics). RVI should be suspected in each and every case of inferoposterior MI and right-precordial lead electrocardiogram should be
performed to diagnose. An interesting study comparing the clinical differences between pure infero-posterior MI and RVI along with inferoposterior MI showed that patients with the latter are more likely to
present with chest pain, lower level of consciousness, hypotension
and elevated JVP [18].
Acute proximal right coronary artery occlusion decreases perfusion
to the RV free wall. However, all right coronary artery occlusions may
not result in significant RV ischemia or infarction. This could be due to
smaller RV muscle mass compared to LV, coronary perfusion of the RV
occurring both in systole and diastole, lesser RV myocardial oxygen demand and the presence of more extensive collateral vessels from left to
right [19–21]. Right ventricular hypertrophy increases the changes of
having RVI [22,23]. Ischemic or infracted RV is stiff, dilated and dyskinetic resulting in decrease in RV compliance, reduced filling and decreased RV stroke volume. This result in decrease in LV filling and
drop in cardiac output despite normal LV contractility [24,25]. The
stiff, dilated and non-complaint RV impedes RV inflow in early diastole
resulting in rapid diastolic pressure elevation resulting in interventricular septum bowing toward the volume-deprived LV [26–28]. The LV
compliance is further decreased by increased intrapericardial pressure
as a result of RV dilatation [29,30]. Biventricular diastolic dysfunction
contributes to significant hemodynamic compromise [26–28]. In addition to the diastolic filling abnormalities and changes in compliance,
the geometric changes in the LV, caused by RV dilatation due to RVI, results in a significant impairment of LV contractile function [31].
Right atrial ischemia is not infrequent; autopsy studies reported an
incidence up-to 20% of the cases of RVI and RA involvement is more
common than the left atrium [32,33]. RA gets spared when the occlusion
of the culprit right coronary artery is distal to the right atrial branch.
Augmented RA contractility enhances RV performance and offsets
some of the hemodynamic consequences of RVI [10]. The symptoms of
RVI may be more pronounced in the presence of combined right atrial
infarction with associated rate and rhythm disturbances and decreased
RA contractility [31,34]. RA dysfunction decreases RV filling resulting in
decreased global RV systolic performance, leading to further decrease in
LV preload and cardiac output. In patients with intact RA perfusion have
augmented atrial contraction resulting in enhanced A wave and X descent, but diminished Y descent on JVP. In contrast, patients with depressed RA function have higher RA and systemic venous pressures,
but depressed A wave, X descent, and Y descent [31].
When RVI develops in setting of global cardiomyopathy or LV dysfunction, the clinical picture may be dominated by left heart failure;
low cardiac output and pulmonary congestion along with right heart
failure [35].
3. Diagnostic tools
Electrocardiogram (ECG) is an important tool for the diagnosis as
signs and symptoms are not very specific. The standard 12 lead ECG
gives a better picture of the left side of the heart compared to the right
[36]. Right-sided precordial lead ECG is crucial for the diagnosis [36].
RVI is suspected when there is ST-segment elevation in lead V1 along
with infero-posterior ST-segment elevation; Leads II, III, AVF (Fig. 1A)
[5,37]. ECG using right-precordial leads will confirms the diagnosis.
However, ECG using right-sided precordial leads should always be performed if clinical suspicion for RVI is high. ST-segment elevation in V1
and V3R–V6R confirms RVI (Fig. 1B) [3,4]. ST-segment elevation V4R
is extremely sensitive and specific for RVI [3,4,36] and a strong independent predictor of major complications and in-hospital mortality

including cardiogenic shock, ventricular fibrillation, and third-degree
atrioventricular block [38–44]. ST-segment elevation in right-sided precordial leads is transient and may be absent in one half of patients with
RVI after 12 h of onset of chest pain [49,50]. Thus ECG serves as a very
important tool for the diagnosis of RVI, and it is crucial to record rightsided precordial leads in all patients with infero-posterior MI as soon
as possible [43,44].
Rarely a RVI result in ST-segment elevations in precordial leads V1 to
V5 mimicking anterior ST-elevation MI [3,4,7]. This could be misinterpreted and even missed if not suspected and could lead to the
incorrect management of the patient [3,5]. The distribution of STsegment elevation in the anterior leads is greater in leads V1–V2 and decreased toward V5–V6 in RVI compared with anterior wall MI [17]. In
such cases, performing ECG with right-sided precordial leads would
confirm the diagnosis of RVI [3]. Recently we reported a case of RVI presenting as anterior-wall MI with ST-segment elevation from V1–V3 following infero-posterior ST-segment elevation MI (Leads II, III, AVF)
percutaneous coronary intervention of the occluded right coronary artery (Fig. 2A and B) [3]. Right ventricular myocardial infraction resulted
from occlusion of RV branch due plaque shift during coronary angioplasty (Fig. 3A and B) [3]. In experimental dog models, it was found
that the absence of ST elevation in precordial leads in RVI associated
with infero-posterior MI is due to suppression of the electrocardiographic manifestations of RV injury by the dominant electrical forces
of simultaneous LV infero-posterior injury [3,7]. In prior studies, the
ST-segment elevations in precordial leads have been attributed to dilatation of the right ventricle with clockwise rotation of the heart [22]. Interestingly Q waves do not manifest or evolve in the precordial leads in
such patients [5,7,45]. The RV and AW infarcts can also be teased out by
using vector concept [34,46]. In RVI the ST-segment vector is directed
anteriorly and is more than +90° to the right (producing a downward
displacement of the ST-segment in lead I), while in the case of
anteroseptal LVMI the vector is also anterior, but is usually located
from −30° to −90° to the left in the frontal plane (producing an elevation of the ST segment in lead I) [34,46].
The right-sided precordial lead ECG is sensitive for diagnosing the
presence of RVI but could not predict the magnitude of RV dysfunction
nor its hemodynamic impact. Echocardiography can depict the severity
of RV dilation, restricted or abnormal movement of the RV free wall
(hypokinesis, akinesis or dyskinesis), the degree of concurrent paradoxical motion of the septum (interventricular and interatrial) and the
presence of RA enlargement in concomitant ischemic RA dysfunction
and or tricuspid regurgitation [8,47]. In addition, Doppler echocardiography could also detect the complications of RVI such as tricuspid
regurgitation, ventricular septal defect, and shunt flow across a patent foramen ovale [34]. Cardiac Magnetic Resonance is another imaging
study that can be used for diagnosis. It is more sensitive than physical examination, ECG and echocardiography [48]. Recent cardiac MRI studies
suggest that the extent of acute RV dysfunction and RV free
wall myonecrosis (indicated by late gadolinium enhancement and
obstruction) are independent predictors of long-term outcome [49]. Invasive hemodynamic measurements by swan gang catheter provide reliable
information about the extent and severity of right heart involvement
(atrial and ventricular). The diagnosis of RVI can be confirmed by hemodynamic data when the right atrial pressure exceeds 10 mm Hg and the
ratio of right atrial pressure to pulmonary capillary wedge pressure
exceeds 0.8 (normal value b0.6) [50,51].
Lopez-Sendon et al. reported that right atrial pressure N10 mm Hg and
with pulmonary artery wedge pressure 1–5 mm Hg, had a sensitivity of
73% and a specificity of 100% in identifying hemodynamically important
RVI [51–53]. Key findings of diagnostic tools were shown in Table 1.
4. Differential diagnosis
The important clinical scenarios to consider in patients presenting
with typical manifestations of an MI such as chest pain, diaphoresis,


V. Namana et al. / Cardiovascular Revascularization Medicine 19 (2018) 43–50

45

Fig. 1. A: Electrocardiogram showing normal sinus rhythm with ST elevations in II, III, aVF and V1. Courtesy of V. Namana et al. [37]. B: Right-sided precordial lead electrocardiogram
showing 2:1 atrioventricular block and ST elevations in leads V3R–V6R. Courtesy of V. Namana et al. [37].

nausea and vomiting with hemodynamic triad: hypotension, jugular
venous distension (JVD) and clear lungs include acute pulmonary
embolism, cardiac tamponade, constrictive pericarditis or restrictive
cardiomyopathy, severe pulmonary hypertension, right heart mass obstruction and acute severe tricuspid regurgitation [35]. Acute massive
pulmonary embolism eludes RVI in clinical presentation however lack
infero-posterior MI changes on electrocardiogram and echocardiogram
and usually generate high RV systolic pressure detected on echocardiography [35]. The acute clinical presentation, signs and symptoms of
acute infero-posterior MI, together with echocardiography demonstrating RV dilatation and dysfunction, excludes tamponade, constriction,
and restriction [35]. Severe pulmonary hypertension with RV
decompensation may mimic severe RVI. But markedly elevated PA
systolic pressures on Doppler echocardiography or invasive hemodynamic monitoring exclude severe pulmonary hypertension [35].
Acute primary tricuspid regurgitation is also evident on echocardiography and usually caused by infective endocarditis with obvious
vegetations [35].

5. Treatment
The first and the foremost step is to suspect and diagnose RVI. Early
diagnosis avoids incorrect management, improves clinical outcomes,
decreases electrical and mechanical complications, mortality and
improves over all short-term and long-term prognoses. The salient features of RVI treatment are based on its pathophysiology, which include
1. Optimization of oxygen supply and demand 2. Optimization of
ventricular preload 3. Restoration of physiologic rhythm 4. Parenteral inotropic support for persistent hemodynamic compromise 5. Reperfusion
and 6. Mechanical support with intraaortic balloon counterpulsation
and RV assist devices [35].
Dual antiplatelet therapy including aspirin and thienopyridine agents,
along with oxygen if the patient is hypoxic should be administered. Volume resuscitation remains the cornerstone of management for RVI to
maintain adequate cardiac output. However extreme volume replacement
can do more harm than good [8,13]. RV is a pre-load dependent chamber
and functions as a passive conduit [55,56]. In RVI, RV is dilated, stiff,


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V. Namana et al. / Cardiovascular Revascularization Medicine 19 (2018) 43–50

Fig. 2. A: Coronary angiogram showing complete occlusion of the mid RCA (black arrow) distal to a large right ventricular branch (white arrow). Courtesy of V. Namana et al. [3]. B:
Electrocardiogram performed following percutaneous coronary intervention showing resolution of ST-segment elevation in inferior leads and a new development of RSR pattern with
concave upward ST-segment elevation in right precordial leads V1 through V3. Courtesy of V. Namana et al. [3].

noncompliant and pre-load deprived and exquisitely preload-dependent,
as is the LV. Therefore, any factor that reduces ventricular preload tends to
be detrimental. Studies by Guiha et al. [54] and Goldstein et al. [26] on
dogs and recent studies by Brooks et al. [55] on pigs showed hemodynamic benefit from volume loading. However clinical studies have reported
variable responses to volume challenge [57–59]. Therefore, volume loading in the context of RV dilatation may not always improve the cardiac
function. Volume loading may further dilate the RV, causing a further decrease in LV compliance and systolic function. These conflicting results may reflect a spectrum of initial volume status in patients
with acute RVI. Patients who are volume-depleted may experience
benefit and those who are more volume-replete manifest a flat response to fluid resuscitation [35]. Still an initial volume challenge
with isotonic saline is appropriate if a patient has clear lungs, hypotension and a low JVP or an estimated central venous pressure
b 15 mm Hg, indicating low cardiac output, to increase the filling of
the RV which in turn will increase the filling of the under filled LV
and increase cardiac output [8,35]. For those who experience no response to an initial trail of fluids, determination of filling pressures
by central venous pressure or pulmonary/Swan-Ganz catheter and
subsequent hemodynamically monitored volume challenge may be
appropriate [59]. Caution should be exercised to avoid excessive volume administration above and beyond that documented to augment
output, because the right heart chambers may operate on a descending limb of the Starling curve, resulting in further depression of RV

pump performance and inducing severe systemic venous congestion
[35]. We should avoid agents that can decrease preload such as nitrates, opioids, and diuretics. Medications with negative inotropic
and chronotropic effect should be refrained as well [8].
Patients with acute infero-posterior MI with or without RVI (worsened with RVI) are prone to develop bradycardia, mediated by BezoldJarisch reflex [60,61] and often manifest a relative inability to increase
the sinus rate in response to low output, owing to excess vagal tone,
ischemia, or pharmacologic agents. Bradyarrhythmias may precipitate
severe hemodynamic compromise in patients with RVI. The depressed
ischemic RV has a relatively fixed stroke volume, as does the preloaddeprived LV. Therefore, biventricular output is exquisitely heart rate–
dependent, and bradycardia even in the absence of atrioventricular
dyssynchrony may be deleterious to patients with RVI. For similar
reasons, chronotropic competence is critical in patients with RVI.
Bradyarrhythmias resulting in atrioventricular dyssynchrony and loss
of RA contribution may also lead to severe hemodynamic compromise
[62,63]. Given that the ischemic RV is dependent on atrial transport,
the loss of RA contraction from atrioventricular dyssynchrony further
exacerbates difficulties with RV filling and contributes to hemodynamic
compromise [26,27].
Although atropine may restore physiologic rhythm in some patients,
temporary pacing is often required. Ventricular pacing alone may suffice, especially if the bradyarrhythmias are intermittent and atrioventricular sequential pacing may be necessary for increasing the cardiac


V. Namana et al. / Cardiovascular Revascularization Medicine 19 (2018) 43–50

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Fig. 3. A: Coronary angiogram of RCA: following percutaneous coronary intervention of mid RCA, right ventricular branch (white arrow pointing) was occluded possibly from distal
embolization of thrombus. RCA: right coronary artery. Courtesy of V. Namana et al. [3]. B: Right-sided precordial leads electrocardiogram showing ST-segment elevation N1 mm in V3R,
V4R and V5R suggestive of acute right ventricular myocardial infarction. Courtesy of V. Namana et al. [3].

output and reversing the shock associated with atrioventricular
dyssynchrony in RVI [64]. However, transvenous pacing can be difficult
because of issues with ventricular sensing, presumably related to diminished generation of endomyocardial potentials in the ischemic RV. Manipulating catheters within the dilated ischemic RV may also induce
ventricular arrhythmias [65]. There are reports that aminophylline
may restore sinus rhythm in patients with acute atrioventricular
block, suggesting the role of ischemia-induced adenosine [66,67]. This
pharmacologic maneuver may restore atrioventricular synchrony and
thereby obviate the need for transvenous pacing. In patients with atrial
fibrillation, prompt cardioversion and restoration of atrioventricular
synchrony should be considered at the earliest sign of hemodynamic
compromise.
In patients with cardiogenic shock, inotropic agents such as dobutamine can be useful [59]. If the patient is planned for percutaneous coronary intervention (PCI), then GP2b/3a agents can be used along with
intravenous unfractionated therapy if no complications are noted.
Early (PCI) and revascularization is the gold standard treatment, as it
can clearly improve the clinical outcome [10]. The effectiveness of reperfusion in patients with RVI and infero-posterior MI has been less impressive than in patients with anterior wall MI [35]. Some studies
suggest that RV function recovers only after successful reperfusion
[68–70] whereas others report improvement even in the absence of a
patent infarct-related vessel [71,72]. Study by Zehender et al. [73]
found that both mortality and major in-hospital complications were
lower in patients who received thrombolytics than in those who did

not. In another related study, Bowers et al. [24] found that patients
with right ventricular dysfunction who had incomplete reperfusion
had higher mortality (58%) and a higher rate of untoward in hospital
events (83%). In a recent study, Zeymer et al. [74] authors concluded
that reperfusion therapy in patients with acute inferior wall MI is not indicated irrespective of the presence of RVI, unless advanced heart block
or hemodynamic instability indicates a large infarct.
In patients who are not fully responsive to the volume resuscitation
and restoration of physiologic rhythm, parenteral inotropic support is
usually effective in stabilizing hemodynamics [24,75]. The mechanisms
through which inotropic stimulation improve low output and hypotension in patients with acute RVI have not been well studied. However,
studies on patients with RVI [56] experimental animal investigations
[28,31,75], suggest that inotropic stimulation enhances RV performance
through increasing LV septal contraction, which there by augments
septal-mediated systolic ventricular interactions, reducing RV cavity dilatation, thus maintaining LV cavity geometry and enhancing its contractile performance. Dobutamine is the preferred initial inotropic
agent. Dobutamine has the least deleterious effects on afterload, oxygen
consumption, and arrhythmias [34,35]. Dobutamine also can diminish
pulmonary vascular resistance and therefore reduce right ventricular
afterload [34]. Patients with severe hypotension may require agents
with pressor effects (such as dopamine) for prompt restoration of adequate coronary perfusion pressure. The inodilator agents, such as
milrinone, have not been studied in patients with RVI, but their vasodilator properties could exacerbate hypotension [35]. In patients with


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V. Namana et al. / Cardiovascular Revascularization Medicine 19 (2018) 43–50

Table 1
Showing key findings associated with diagnostic tools.
Diagnostic tool

Key findings

Symptoms
Signs

Chest pain, nausea and vomiting
Hemodynamic triad: hypotension, jugular venous distension and clear lungs
Kussmaul's sign
Pulsus paradoxus
Tricuspid regurgitation murmur
Elevated jugular venous pressure plus Kussmaul's sign in the setting of an acute
infero-posterior myocardial infarction indicate a hemodynamically significant right
ventricular infarction (sensitivity = 88% and specificity = 100%)
In patients with intact right atrial perfusion/function - enhanced A wave and X descent,
but diminished Y descent
In patients with depressed right atrial perfusion/function have higher RA and systemic
venous pressures, but depressed A wave, X descent, and Y descent
Suspect right ventricular infarction with ST-segment elevation in lead V1 along with
infero-posterior ST-segment elevation; Leads II, III, AVF
ST-segment elevation in V1 and V3R–V6R confirms right ventricular infarction
ST-segment elevation V4R is extremely sensitive and specific for right ventricular
infarction and a strong independent predictor of major complications and in-hospital
mortality including cardiogenic shock, ventricular fibrillation, and third-degree atrioventricular block
Right ventricular dilation
Restricted or abnormal movement of the right ventricular free wall (hypokinesis, akinesis or dyskinesis)
Paradoxical motion of the septum (interventricular and interatrial)
Right atrial enlargement and dysfunction Tricuspid regurgitation
Ventricular septal defect
Shunt flow across a patent foramen ovale
Diagnosis of right ventricular infarction can be confirmed when the right atrial pressure
exceeds 10 mm Hg and the ratio of right atrial pressure to pulmonary capillary wedge
pressure exceeds 0.8 (normal value b0.6)
Right atrial pressure N 10 mm Hg and with pulmonary artery wedge pressure 1–5 mm Hg,
had a sensitivity of 73% and a specificity of 100% in identifying hemodynamically
important right ventricular infarction

JVP

Electrocardiogram
Right-sided precordial lead electrocardiogram

Echocardiography

Pulmonary or Swan-Ganz catheter

persistent hypotension, intra-aortic balloon pumps can help improve
right ventricular function indirectly by improving coronary perfusion
[8]. In extreme cases, right ventricular assist devices can be used as a
destination therapy anticipating the recovery of RV function [13].
6. Complications
Hemodynamic and electrical complications are more common than
mechanical complications and dreadful complication of RV dysfunction
is arrhythmias [6]. High-grade atrioventricular block and bradycardiahypotension without atrioventricular block commonly complicate RVI
with concomitant infero-posterior and have been attributed predominantly to the effects of atrioventricular nodal ischemia and cardioinhibitory (Bezold-Jarisch) reflexes. These arise from the stimulation
of vagal afferents in the ischemic LV infero-posterior wall [76,77]. Arrhythmias are more common with proximal right coronary artery lesions inducing RV and LV infero-posterior ischemia, compared with
more distal occlusions compromising LV perfusion but sparing the RV
branches [77]. Patients with RVI are prone to ventricular tachyarrhythmias; ventricular tachycardia/fibrillation, due to massively dilated ischemic RV [65] and may develop in a trimodal pattern, either during
acute occlusion, abruptly with reperfusion, or later [65]. However, successful mechanical reperfusion dramatically reduces the incidence of
malignant ventricular arrhythmias [65] presumably through improvement in RV function, which lessens late ventricular tachyarrhythmias.
Occasionally, RVI may be complicated by recurrent malignant arrhythmias and in some cases, intractable “electrical storm” possibly because
of sustained severe RV dilatation [65].
Mechanical complications include ventricular septal defect (VSD),
stretch opening of patent formen ovale (PFO) and tricuspid regurgitation. These complications aggravate the hemodynamic compromise
and confound the clinical hemodynamic picture. Ventricular septal rupture is a dreadful complication, which increase the overload stress to the
dysfunctional RV, precipitating pulmonary edema, elevating pulmonary
pressures and resistance, and worsening the low output state [78].

Surgical repair is imperative but may be technically difficult owing to
extensive necrosis involving the LV inferior-posterior free wall, septum,
and apex. Catheter closure of these defects may be possible. Severe right
heart dilatation and elevated diastolic pressure may stretch open a patent foramen ovale, precipitating acute right-to-left shunting and manifest as systemic hypoxemia or paradoxic emboli [79]. A successful
mechanical reperfusion and recovery of RV performance will decrease
the right-heart pressure and may reduce the PFO and thus its complications; rarely some may require percutaneous closure [80]. Primary
papillary muscle ischemic dysfunction or rupture and severe RV and
tricuspid valve annular dilatation may give rise to severe primary and
secondary tricuspid regurgitation respectively and complicate RVI
[81,82].
7. Prognosis
Prognosis of patients can be grave in the short term, and it directly
corresponds to the amount of myocardium involved, arrhythmias and
cardiac arrest [83]. Emergent reperfusion with percutaneous coronary
intervention improves survival rate and the long-term prognosis [10].
Many patients spontaneously improve within 3 to 10 days regardless
of the patency status of the infarct-related artery [24,72,84] and global
RV performance typically recovers, with normalization within 3 to
12 months. And furthermore, chronic right heart failure secondary to
RVI is rare [84].
8. Summary
Isolated RVI is rare. Around one-third of patients with acute inferoposterior ST-segment elevation MI, will present with concomitant RVI.
Signs and symptoms include some of the typical manifestations of an
MI such as chest pain, diaphoresis, nausea and vomiting. However certain manifestations that are more specific, although not sensitive for
RVI include the following hemodynamic triad: hypotension, jugular venous distension (JVD) and clear lungs. Right-sided precordial lead ECG


V. Namana et al. / Cardiovascular Revascularization Medicine 19 (2018) 43–50

is crucial for the diagnosis. RVI is suspected when there is ST-segment
elevation in lead V1 along with infero-posterior ST-segment elevation
(Leads II, III, AVF). ST-segment elevation in V1 and V3R–V6R confirms
RVI. ST-segment elevation V4R is extremely sensitive and specific for
RVI. The most common culprit vessel for causing RVI is occlusion of
the right ventricular branch or acute marginal branch of the right coronary artery (or left circumflex artery in left dominant coronary circulation). All right coronary artery occlusions may not result in significant
right ventricular ischemia or infarction. This could be due to smaller
RV muscle mass compared to left ventricle, coronary perfusion of the
RV occurring both in systole and diastole, lesser RV myocardial oxygen
demand and the presence of more extensive collateral vessels from
left to right. The RV is a volume dependent chamber; therefore any significant insult can lead to severe hemodynamic compromise. Atrial kick
plays a crucial role in RVI, loss of atrial kick can further worsen the cardiac hemodynamics. Ischemic or infracted RV is stiff, dilated and dyskinetic resulting in decrease in right ventricular compliance, reduced
filling and decreased right ventricular stroke volume leading to decreased left ventricular filling and drop in cardiac output despite normal
LV contractility. Echocardiography can depict the severity of RV dilation,
restricted or abnormal movement of the RV free wall (hypokinesis,
akinesis or dyskinesis), the degree of concurrent paradoxical motion
of the septum (interventricular and interatrial) and the presence of
RA enlargement in concomitant ischemic RA dysfunction and or tricuspid regurgitation. Cardiac Magnetic Resonance is another imaging study that can be used for diagnosis. It is more sensitive than
physical examination, ECG and echocardiography. Invasive hemodynamic measurements by swan gang catheter provide reliable information about the extent and severity of right heart involvement
(atrial and ventricular).
The first and the foremost step in management is to suspect and diagnose RVI. Early diagnosis avoids incorrect management, improves
clinical outcomes, decreases electrical and mechanical complications,
mortality and improves over all short-term and long-term prognoses.
Delay in diagnosis of RV involvement will lead to increased mortality,
a complex clinical course, and lengthy hospitalization, as well as frequent mechanical and electrical complications. The salient features of
RVI treatment are based on its pathophysiology, which include 1. Optimization of oxygen supply and demand 2. Optimization of ventricular
preload 3. Restoration of physiologic rhythm 4. Parenteral inotropic
support for persistent hemodynamic compromise 5. Reperfusion and
6. Mechanical support with intraaortic balloon counterpulsation and
RV assist device.
Dual antiplatelet therapy including aspirin and thienopyridine
agents, along with oxygen if the patient is hypoxic should be administered. Volume resuscitation remains the cornerstone of management
for RVI to maintain adequate cardiac output. However extreme volume
replacement can do more harm than good. Hemodynamic and electrical
complications are more common than mechanical complications and
dreadful complication of right ventricular dysfunction is arrhythmias
[6]. High-grade atrioventricular block and bradycardia-hypotension
without atrioventricular block commonly complicate RVI with concomitant infero-posterior and have been attributed predominantly to the effects of atrioventricular nodal ischemia and cardio-inhibitory (BezoldJarisch) reflexes.
9. Conclusion
Having high index of suspicion for RVI, performing right-sided
precordial lead ECG in all patients with infero-posterior wall MI, early
diagnosis and initiation of the appropriate treatment are crucial for
the best outcomes.
Acknowledgements
None.

49

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