Right ventricular myocardial infarction-

Hemodynamics, Diagnosis for management

Dr Rudresh M G
Chair: Prof Dr Prabha Nini Gupta
 Introduction

• Infarction of the right ventricle with or without left ventricular

involvement is becoming a more commonly diagnosed entity
as the tools for diagnosis and options for treatment evolve.

• First described in 1974 in a series of six patients by Cohn JN,

Guiha NH
 Background

• Right ventricular infarction was recognized in a subgroup of

patients with inferior wall myocardial infarctions

• emphasizes the clinical significance of the right ventricle to

total cardiac function.
• Interest in recognizing RVMI noninvasively has grown

• Higher rates of significant hypotension, bradycardia requiring

pacing support, and inhospital mortality than isolated inferior
infarctions.
 Epidemiology

• The incidence of RVMI co-existing with inferior wall left

ventricular dysfunction - 30-50%.

• Cases of isolated RVMI or dysfunction - very rare (exception of

iatrogenic causes i.e. interventional procedures or cardiac
surgery).

• The incidence of clinically evident right ventricular infarction

is considerably less than that found at autopsy
 Pathophysiology

The right ventricle less susceptible to infarction than the left

ventricle because -

• The RV is a thin-walled chamber that functions at low oxygen

demands and pressure.
• It is perfused throughout the cardiac cycle in both systole and
diastole,
• its ability to extract oxygen is increased during hemodynamic
stress.
• RV may have rich collaterals from left coronary artery
• Rv receives direct blood supply from RV cavity through
thebesian veins
 Pathophysiology

• The RV supplied by the right

coronary artery (RCA),
which arises from the right
coronary cusp of the aorta.

• Conus artery - RVOT.

• The sinoatrial node (SA) - from
the second division. Coursing
in the atrioventricular groove,
the RCA then gives off
multiple, small branches to
supply the anterior RV before
dividing terminally into the
acute
marginal branch (AM) that runs
anteriorly along the diaphragm,
and the posterior descending
artery (PDA) that
runs posteriorly.
• The PDA also supplies the AVN in 90% of patients, with a
branch of the left circumflex artery providing flow in the
remainder of patients.

• The PDA supplies the inferior wall of both ventricles, and is a

terminal branch of the RCA in 85% of patients, but may arise
from the left coronary circulation in 15% of the population.
• A direct correlation exists between the anatomic site of right
coronary artery occlusion and the extent of right ventricular
infarction.

• Studies have demonstrated that more proximal right coronary

artery occlusions result in larger right ventricular infarctions.

• On occasion, the right ventricle can be subjected to infarction

from occlusion of the left circumflex coronary artery.
• the right ventricular diastolic pressure increases substantially
and systolic pressure decreases.

• In such a scenario, concomitant left ventricular dysfunction,

with an increase in right ventricular afterload is possible.

• In such a setting, right ventricular output can decrease

dramatically, and right atrial pressure increases.

• In this circumstance, the right ventricle serves as a poorly

functioning conduit between the right atrium and the
pulmonary artery.
Mechanism of decrease in right and secondarily
left ventricular output

RVMI

Increaser RA pressure

Stimulates ANP release

Vasodilatation
Diuretic
Natruritic
Antialdosterone

Worsening clinical syndrome

unusally sensitive to diminished preload and loss of

AV synchrony
• Early reperfusion of the occluded coronary artery resulting in
right ventricular infarction is associated with prompt
reduction in right atrial pressure.

• The extent of right ventricular infarction varies greatly and is

dependent on the site of occlusion of the right ventricular
arterial supply.

• If the occlusion occurs before the right ventricular marginal

branches and if collateral blood flow from the left anterior
descending coronary artery is absent, then the size of
infarction is generally greater.
• The primary effects of RV ischemia and infarction result from
decreased RV contractility. This leads to a reduction in blood flow
from the venous system to the lungs, and finally to the left side of
the heart.

• The clinical signs

-Increased right sided heart pressures
-Increased pulmonary artery (PA) systolic pressures
-Decreased left ventricular preload.
• Symptoms
-Peripheral edema
-Distention of the jugular vein
-Hypoxemia
-Hypotension.
• As the RV dilates - motion and function of the interventricular
septum is altered.

• If the RV is dilated secondary to overload or if the septal

myocardium is jeopardized by simultaneous left ventricle (LV)
ischemia the symptoms of hypotension and cardiac failure
may be pronounced.

• If the septum shifts leftward during diastole it impedes left

ventricular filling and as a result cardiac output is decreased.
This is termed loss of biventricular interdependence.
 History and Physical Examn
• Patients with RV infarction present with symptoms commonly
seen in left side infarction.

• Rhythm abnormalities ranging from bradycardia to complete

heart block.

• Other signs of right heart failure -Hypotension, acute

peripheral edema and jugular venous distention.
• The triad of jugular vein distention, clear lung fields, and
hypotension is the classic picture of right ventricular
dysfunction.
• A pan-systolic murmur best heard at the left lower sternal
border may indicate tricuspid regurgitation, but due to the
lower filling pressures of the right heart, this is not always
present.
 History and Physical Examn
• Patients may describe symptoms consistent with hypotension.
A subtle clue to the presence of hemodynamically significant
right ventricular infarction is a marked sensitivity to preload-
reducing agents such as nitrates, morphine, or diuretics.

• Other presentations include high-grade atrioventricular block,

tricuspid regurgitation, cardiogenic shock, right ventricular
free wall rupture, and cardiac tamponade.
 Evaluation
*Electricardiography
• Electrocardiogram (ECG) is the first diagnostic test to be performed.

• If LV is involved - evidence of ischemia/infarction in leads II, III, and

AVF.

• Disproportionate ST-elevation in lead III>II is pathognomonic for

RVMI

• ST elevation in lead aVF is greater than THE ST depression in lead

V2.

• ST elevation in the V1 lead is also highly suspicious for RVMI and is

even more specific when coupled with ST-depression in lead V2.
 ECG contd...
• Overall, conventional left sided ECG is a poor indicator of RV
ischemia/infarction due to the position of the right side of the
heart.

• If right side dysfunction is suspected, a right-sided ECG is the

most sensitive and specific, as ST elevation in V4R >1.0 mm
has 100% sensitivity, 87% specificity, and 92% predictive
accuracy.

• ST elevation in lead V4R is also associated with other cardiac

conditions such as acute anteroseptal MI, previous anterior
wall MI with aneurysm, LVH, acute pulmonary embolus
• Right precardial ST segment elevation is transient event
–absent in upto half of the patients with RVMI 12 hrs
after the onset of chest pain

• ST-elevation in lead V4R correlates with reduced RV EF

and associated with major complications and inhospital
mortality.

• Conduction abnormalities such as right bundle branch

block, bradycardia or complete heart block can also
manifest themselves in the ECG but may also be non-
specific.
 Echocardiography
• Echocardiography has a high threshold for detecting right-sided
myocardial dysfunction, and its increasing availability and fidelity
has made it a rising diagnostic modality in a variety of settings such
as the emergency department and the operating room.

• The sensitivity and specificity of echo may be as high as 82% and

93%, respectively, for detection of right ventricular infarction.

• Signs - RV wall dyskinesia/hypokinesia

- Paradoxical septal motion
- Tricuspid regurgitation
- Pulmonary regurgitation

• Other measurements such as tricuspid annular plane excursion

(TAPSI) are currently being evaluated and may indicate a poor
prognosis.
 Angiography and hemodynamic study

• Coronary angiography and ventricular scintigraphy are the

gold standards for definitive diagnosis. These procedures are
invasive, require a large use of resources, and are often
performed during intervention; their place in the initial
evaluation and work up are limited.
• RCA . LCX, LAD
• Hemodynamically significant RVMI is associated with
 increased RAP(>10mm Hg)
 RAP:PCWP > 0.8
 RAP within 5mm Hg of the PCWP
 Reduced cardiac index
Angiography and hemodynamic study
• PAPi = (systolic PA pressure-diastolic PA pressure)/
mean RA
• Value of < 0.9 provides 100% sensitivity and 98.3 %
specificity for predicting outcomes for high risk
patients with acute RVMI
• Cardiac power output is the single most predictive
marker of prognosis in cardiogenic shock
• Prominent y decent of RAP, increased RAP and drop of
systemic arterial pressure >10mm Hg witrh inspiration ,
‘dip and plateau’ morphology and equalisation of
diastolic pressures, and pericardial pressures due to
increased RV volume
 Angiography and Scintigraphy
• Tomala et al suggest that the angiographic result of index
primary percutaneous coronary intervention (PCI) determines
the presence of right ventricular (RV) infarction in patients
with acute inferior myocardial infarction (MI).

• In a multivariate regression analysis, thrombolysis in MI

(TIMI) flow score below 2 in at least one RV branch after PCI
was an independent angiographic predictor of RVMI, and TIMI
flow below 3 in at least one RV branch before PCI was an
independent angiographic predictor of ST-segment elevation
of at least 1 mm in V4R.

• The only predictor of RVMI was TIMI flow less than 2 in at

least one RV branch after PCI.
• In the case of radionuclide angiography, the
right ventricle is demonstrated to be enlarged
and poorly contractile, with a reduced
ejection fraction. When technetium 99m
pyrophosphate is employed, the right
ventricular free wall is "hot," indicating
significant infarction
 Others

• Cardiac enzymes will be elevated in RVMI, similarly to LVMI

scenarios.

• Chest radiography also has limited specificity and diagnostic

capability. Findings of an enlarged heart silhouette, dilation of
the inferior or superior venae cavae, and clear lung fields may
be present.

• The presence or absence of pulmonary edema may be useful

in determining the presence or extent of concomitant left
ventricular dysfunction or to further evaluate for the presence
of a pulmonary embolus (PE)
Contrast enhanced cardiovascular MRI
of RVMI
• Late enhancement cardiovascular MRI (LE-CMR) can be
performed safely in patients with ACS and visualises in vivo
areas of necrosis in acute LVMI and fibrous scar in chronic
chronic LVMI
• Its high spatial resolution allows for detection of very small
irreversibly injured areas of the LV and small fibrous lesions
of the RV
• Andreas Kumar MD et al., from Germany studied the role of
LE-CMR in detecting RVMI in pts with acute IWMI
• They performeds 4 diagnostic tests for RVMI i.e. physical
examination, ECG with right precardial leads,
echocardiography and LE-CMR
• The results were compared with agreement
statistics
• Concluded that findings consistent with RVMI
were more frequently observed on LE-CMR
than on ECG, Physical examination or
echocardiography
• LE-CMR imaging findings for irreversible injury
of the RV in the acute phase persisted at 13
months of follow up
• As opposed to all the other investigational methods, LE-CMR
specifically diagnoses irreversible injury and therefore infarction per
se, whereas all other methods investigate other facets of
pathophysiology
• Ecg measures ischemic currents directed towards RV wall, which
can be a result of ischemia as well as infarction
• Echocardiography examines wall motion abnormalities due to RV
failurewhich might be caused by reversible or irreversible RV injury
• Physical exam relies on hemodynamic consequences of failing RV
which might be due to reversible as well as irreversible RV injury or
might even be secondary to LV failure
• Therefore one might argue that LE-CMR seems to be more specific
for irreversible RV injury and most specific test for diagnosing true
RV RV infarction
 Treatment
Clinically significant decreased
right heart function

Decreased LV preload

Systemic hypotension

• One approach to the treatment of suspected RVMI - fluid challenge

of 500 ml of crystalloid fluid.
• It is important to monitor for improvement in hemodynamics as
patients may present with variable volume statuses ranging from
hypovolemia to fluid overload.
• Treatment with nitrates may be harmful, as the ventilation and drop
in preload can worsen RV dysfunction and systemic flow.
 Treatment

Fluid challange
Nitric oxide + Dobutamine
Suboptimal response
Added benefit
Ionotropes(Dobutamine)
Reduces PVR
Improved cardiac index
Decreases RV after load
Improved RV stroke volume
Decrease myoardial work load
Improves left ventriculaar function
promoting forfward flow
 Treatment

• The combination of inhaled nitric oxide combined with dobutamine

also has the added benefit of reducing pulmonary vascular
resistance (PVR), thereby decreasing RV afterload and myocardial
work.

• Milrinone, a phosphodiesterase III inhibitor, may also improve RV

dysfunction. The increased cAMP levels from milrinone
administration led to increased RV contractility and decreased PVR.

• However, milrinone is not a selective pulmonary vasodilator, and its

use must be weighed against the risk of exacerbating systemic
hypotension.
 Treatment
• A class of agents known as calcium sensitizers may also
improve RV function

• One such agent, levosimendan, has been shown to improve

RV function. The mechanism of action involves improving
cardiac contractility by increasing cardiac myocyte sensitivity
to intracellular calcium without increasing calcium
concentrations.

• The clinical effects of this drug are increased inotropy, as well

as peripheral vasodilation.
 Treatment
• Due to the location of the conduction system of the heart,
arrhythmias ranging from bradycardia to complete heart block
may arise in patients with RVMI.

• The decreased preload and relatively fixed LV stroke volume

mean that systemic cardiac output is somewhat rate-
dependent.

• Additionally, it has been shown that AV pacing in patients

presenting with RVMI and complete heart block can improve
survival, while ventricular pacing alone does not.
• Similar to the treatment of LV infarction, time of
revascularization is the primary factor dictating survival and
recovery. Earlier intervention is favored in either instance.

• It is the only treatment modality targeted at treating the

cause of RVMI, while the other treatment options mentioned
here are for symptomatic management of the sequelae.

• The use of ventricular assist devices (VADs), both surgical and

percutaneous, have been shown to improve survival, but data
is limited primarily to case reports and small studies.

• An intra-aortic balloon pump is also a treatment option.

• In addition to augmenting left heart function, the elevation of

diastolic flow and coronary perfusion may help improve blood
flow to the right heart distribution.
 Prognosis

• Short term prognosis: RVMI is worse than those with isolated

LVMI. Both in-hospital morbidity and mortality are increased.
This is likely due to the critical complications that can occur
from significant RV infarction, which may require additional
invasive procedures and manipulation (i.e. placement of ICDs,
placement of VADs, arrhythmias).

• Long-term prognosis: Patients who are discharged from the

hospital after treatment and resolution of RVMI is similar to
that of patients with LVMI.
 Pearls and Other Issues
• Diagnosis of RVMI - requires a high threshold of suspicion.

• Findings from the initial evaluation of patients presenting with

chest pain may not clearly show the evolving ischemia in the
right heart.

• The possibility of other etiologies such as pulmonary

embolism, pulmonary hypertension, and causes of
hypovolemia may cloud the clinical picture.

• When possible, the employment of non-invasive diagnostic

modalities such as echocardiography may help detect
problems sooner than traditional tests of myocardial
ischemia.