STUDY OF CLINICAL PROFILE OF 50 PATIENTS WITH ACUTE INFERIOR

WALL MYOCARDIAL INFARCTION IN SKBZ/CMH MUZFFRABAD

BY

SYEDA NATASHA MAQSOOD

MANSOOR AHMAD

ANILA AZAD

INSHA HAMEED

AZAM TARIQ

Session 2019-2023

Faculty of Health & Medical sciences

University of Azad Jammu & Kashmir Muzaffarabad

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STUDY OF CLINICAL PROFILE OF 50 PATIENTS WITH ACUTE INFERIOR

WALL MYOCARDIAL INFARCTION IN SKBZ/CMH MUZFFRABAD

By

SYEDA NATASHA MAQSOOD

(Reg.No. 2019-UMBD-001532)

ANILA AZAD

(Reg.No.2019-UMBD-00157)

MANSOOR AHMAD

(Reg.No.2019_UMBD-002505)

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 INSHA HAMEED

(Reg.No.2019-UMBD-001557)

AZAM TARIQ

(Reg.No.2019-UMBD-001584)

BS MEDICAL TECHNOLOGY

(Emergency Medicine & Intensive care Technology)

INSTITUTE OF MEDICAL TECHNOLOGY

FACULTY OF HEALTH & MEDICAL SCIENCES

UNIVERSITY OF AZAD JAMMU & KASHMIR

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4
Informed Consent Letter

We, Syeda Natasha Maqsood, Mansoor Ahmad, Insha Hameed, Azam Tariq, Anila Azad, Bs

Medical Technology, University of Azad Jammu & Kashmir doing our research work on the

topic entitled “STUDY OF CLINICAL PROFILE OF 50 PATIENTS WITH ACUTE INFERIOR

WALL MYOCARDIAL INFARCTION IN SKBZ/CMH MUZFFRABAD”. The purpose of this

research is to examine the consequence of inferior wall MI. We have proposed the sample of

this research on the basis of purposive sampling technique.

It is assured that all the information will be kept confidential under the academic

research ethics standards.

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 Supervisor External Examiner

Dr. Khawaja Arshad Mehmood --------------------------------

Cardiologist (SKBZ/CMH MZD)

Director

Dr. Bashir-ur-Rehman

General surgeon/ Associate professor

Institute of Medical Technology

Faculty of Health and Medical Sciences

The University Of Azad Jammu & Kashmir, Muzaffarabad

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 ACKNOWLEDGEMENT

First, we would like to express my deepest appreciation and sincerest to our gratitude to our

respected teacher, HOD Dr. BASHARAT HAYAT and other Doctors of SKBZ/CMH MZD.

Honorable supervisor, DR ARSHAD MAHMOOD gives us his invaluable advice and guidance

during the research of this thesis writing. We thank his for offering us his insight on selecting an

interesting and challenging research topic, identifying specific problems for each research phase.

We also thank his for enthusiasm and support whenever we need it.

Last, but definitely not least, we would like to thank our family members for their moral

supports and love

SAYEDA NATSHA MAQSOOD

INSHA HAMEED

ANILA AZAD

AZAM TARIQ

MANSOOR AHMAD

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 Contents
INTRODUCTION............................................................................................................................ 7

PURPOSE OF THE STUDY ........................................................................................................... 9

REVIEW OF THE LITERATURE ................................................................................................... 9

INVESTIGATIONS ........................................................................................................................ 19

MATERIALS AND METHODS ..................................................................................................... 33

RESULTS ...................................................................................................................................... 34

DISCUSSION ................................................................................................................................ 46

CONCLUSION .............................................................................................................................. 51

BIBLIOGRAPHY ........................................................................................................................... 53

ANNEXURE .................................................................................................................................. 61

PROFORMA ............................................................................................................................. 62

AMI : ACUTE MYOCARDIAL INFARCTION .................................................................. 66

CVA : CEREBRO VASCULAR ACCIDENT....................................................................... 66

MASTER CHART ...................................................................................................................... 68

ECG ……………………………………………………………………………………..91

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INTRODUCTION

Myocardial infarction (MI) is the medical term for the condition known as
ischemia, in which the myocardium experiences necrosis as a result of insufficient
blood flow. MI can present as subendocardial or transmural infarctions. Patients
with stable angina and those with acute coronary syndromes (ACS) can be
generally divided into two groups within the spectrum of ischemic heart disease.
Acute myocardial infarction with ST-segment elevation (STEMI), unstable angina
(UA), and non-ST-segment elevation MI (NSTEMI) are additional conditions
included in the ACS category.
Noteworthy traits of inferior wall infarctions include their relationship with right

ventricular infarction (RVI), tendency for bradyarrhythmias, notably sinus

bradycardia, and second-degree atrioventricular (AV) block. Regarding acute

presentation, therapeutic strategies, and long-term prognosis, RVI exhibits distinct

characteristics from left ventricular infarctions. Since the beginning of RVI's

hemodynamic effects is unpredictable and they may be lessened by the

administration of intravenous fluid loading, prompt diagnosis of RVI is crucial from

a clinical standpoint.

Although the first description of RVI was made over 60 years ago, it wasn't until
1974 when Cohn and colleagues published their important study that RVI was
recognized as a distinct clinical entity. Between 25% and 50% of patients with
inferior wall myocardial infarction (IWMI) have a reported incidence of RVI.

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The right coronary artery's atherosclerotic blockage and the right ventricle's
involvement are strongly related, and damage to the postero-inferior wall and
posterior part of the septum is frequently seen. Clinically, a patient with IWMI
who exhibits elevated jugular venous pressure (JVP), a positive Kussmaul's sign (an
abnormal increase in JVP during inspiration), hypotension, the presence of right-
sided third or fourth heart sounds, tender hepatomegaly, oliguria, and
infrequently, tricuspid regurgitation, in addition to a clear chest, raises suspicion
of RVI.

Right precordial leads have increased the significance of electrocardiography,

which was previously thought to be ineffective in the diagnosis of RVI. This lead
has remarkable sensitivity (93%) and specificity (95%) for RVI diagnosis with a 1
mm ST-segment elevation. It's crucial to remember that these ECG alterations are
frequently brief; roughly 48% of patients report symptom relief within 10 hours of
symptom start.

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PURPOSE OF THE STUDY

 This study's goal is to examine the clinical traits of 50 consecutive

individuals who have been identified as having acute inferior wall
myocardial infarction (IWMI) and right ventricular infarction (RVI). The
primary goal of our study is to undertake a thorough investigation of the
patient cohort's age and gender distribution, clinical symptomatology,
presenting clinical symptoms, complications, and final clinical outcomes.

REVIEW OF THE LITERATURE

One of the earliest recorded cases of postmortem findings correlating with clinical
observations in a patient suffering from ischemic heart disease was provided by
William Harvey in 1667, making him noteworthy. The patient, a middle-aged man,
suffered from recurrent attacks of "distressing chest pain" and passed away during
one of these attacks. An underlying left ventricular rupture was discovered during
postmortem investigation. Thomas Wills described a case that was comparable,
and it strengthened the link between clinical symptoms and pathological findings.
The left coronary artery of a patient who had passed away suddenly was later
highlighted by an autopsy in Morgagni's work "De Sedibus et Causis Morborum,"
which was published in 1761.

Heberden's description of angina pectoris, which signaled the beginning of the

modern era in the history of this field, came in 1772, marking the crucial moment
in the evolution of our understanding of coronary artery diseases. Marshall Hall
highlighted the quick demise caused by experimental coronary artery occlusion in

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1842. James B. Herrick defined the clinical symptoms related to coronary artery
blockages in 1912.

Postmortem biopsy was initially required for the diagnosis of right ventricular
infarction (RVMI). 164 myocardial infarction cases that were autopsied in 1948
included 22 cases of RVMI, according to Wartman and Hallerstein. Wade then
reported on 19 patients who had right ventricular infarction in 1959.

Despite the fact that the earliest accounts of RVMI date back more than 60 years,
its clinical importance was downplayed. The failure of animal experiments to show
appreciable changes in systemic venous pressure, pulmonary pressure, or cardiac
output in response to experimentally produced isolated right ventricular injury
contributed to this in part. However, RVMI was recognized as a separate clinical
entity in a crucial paper written in 1974 by Cohn and colleagues. Since that time,
RVMI has grown in popularity while continuing to be difficult to diagnose and treat.

The right coronary artery (RCA) is frequently blocked along with RVMI, particularly
close to the acute marginal branches. Rarely, RVMI can also develop from
obstruction of a dominant left circumflex artery, and in some cases, right
ventricular infarction can be brought on by occlusion of the left anterior
descending (LAD) artery.

Even while isolated right ventricular infarction (RVMI), which accounts for fewer
than 2% of all infarction cases, is very uncommon, it entails a sizable risk of
morbidity. RVMI may be related to various underlying issues, including:

Isolated Occlusion of Right Ventricular Branches: Isolated occlusion of right

ventricular branches is one of the etiological factors.

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Occlusion of Non-Dominant Right Coronary Artery: RVMI can also result from
obstruction of the right coronary artery that is not the major artery.

Right coronary artery dominance occlusion with collateral flow to the posterior
descending artery:

Additionally, RVMI can happen when the right coronary artery is dominant and
the posterior descending artery has efficient collateral circulation. It should be
noted that severe right ventricular hypertrophy, such as that observed in diseases
like chronic obstructive pulmonary disease (COPD), pulmonary stenosis (PS), and
pulmonary hypertension, can cause RVMI to develop even in the absence of
coronary artery disease.

Recognizing the syndrome of RVMI is of utmost clinical importance because it is a

unique clinical entity linked to high morbidity and death. Reduced right ventricular
compliance, decreased filling, reduced right ventricular stroke volume, and
ultimately reduced left ventricular filling can all result from ischemia or infarction
of the right ventricle. A decrease in cardiac output, systemic hypotension, and
shock result from this cascade effect.

Ischemic damage has the ability to alter the atrioventricular (AV) and
intraventricular conducting pathways, among other levels of the conduction
system. Specifically:

 First-Degree AV Block: Less than 15% of individuals with acute myocardial

infarction who are admitted to coronary care units have first-degree AV
block.

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  Mobitz Type I Block: Mobitz Type I block is seen in up to 10% of cases of
acute myocardial infarction, with inferior wall myocardial infarctions having
a higher prevalence than anterior infarctions.
 Mobitz Type II Block: Mobitz Type II block, which makes up around 10% of
all cases of second-degree heart block, is a rare event following acute
myocardial infarction.
 Complete Heart Block: Patients who experience anterior or inferior wall
myocardial infarctions may develop complete heart block in 5% to 15% of
cases. Patients who also have a right ventricular infarction typically have a
higher incidence of the condition.

Bundle Branch Blocks: Bundle branch blocks are widespread in the setting of
acute inferior wall myocardial infarction and are documented in 5% to 10% of
patients with acute myocardial infarction. It is interesting to note that, despite the
prevalence of morphological signs of RVMI, hemodynamically relevant RVMI
patterns do not present as frequently as would be predicted based purely on
anatomical observations.

ANATOMY OF CORONARY CIRCULATION

The coronary arteries, which emerge as the aorta's main branches, are crucial in
the myocardium's blood supply. Specifically:

 coronary artery on the left:The left anterior descending (LAD) artery and
the left circumflex artery (LCx) are the two main branches that split out
from the left coronary artery. The free wall of the left ventricle close to the
interventricular septum is largely nourished by the LAD artery's branches.
The left atrium and various areas of the posterior and lateral walls of the

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 left ventricle, on the other hand, receive blood from the LCx artery.
Importantly, in a significant majority of cases, the LCx artery also supplies
blood to the atrioventricular (AV) node (20%) and the sinoatrial (SA) node
(35%) nodes.
 Right Coronary Artery: The posterio-inferior third of the interventricular
septum, the right atrium, the right ventricle, various areas of the
diaphragmatic aspect of the left ventricle, the right coronary artery, and
the cardiac conduction system up to the proximal segments of the right
and left bundle branches are all thoroughly perfused by the right coronary
artery. Notably, the AV node is typically supplied by the right coronary
artery (80% of the time), while the SA node is frequently (65% of the time).
In around 50% of cases, the right coronary artery supplies the right atrium
exclusively, whereas the other 50% show a dual supply configuration.
 Left atrium: The left coronary artery accounts for 62% of the blood flow to
the left atrium, with contributions from the right coronary artery coming in
at 27% and a smaller fraction showing an equal contribution.

The coronary sinus, Thebesian veins, and anterior cardiac veins are a few of the
mechanisms via which venous return from the cardiac tissue enters the right
atrium.
The clinical importance of both arterial systems in the context of coronary artery
disease is highlighted by the fact that atheromatous occlusion, a common
pathological feature of coronary arteries, affects the right coronary artery with a
frequency comparable to that of the left coronary artery.

PATHOLOGICAL AND ANATOMICAL CORRELATION

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The dominant right coronary artery's (RCA) proximal blockage is the main cause of
right ventricular myocardial infarction (RVMI). However, there are several
exceptional circumstances in which RVMI can present alone:

Isolated Right Ventricular Branch Occlusion: Rarely, the right ventricular branches
of the RCA might be completely blocked to cause RVMI. The right ventricle's
anterolateral portions are predominantly affected by the infarction caused by this
disorder.

Non-Dominant Right Coronary Artery Occlusion When the non-dominant right

coronary artery is blocked, RVMI might also have this uncommon cause. The right
ventricle has an infarction in such circumstances.

Posterior Descending Artery (PDA) Effective Collateral Flow Due to Effective

Occlusion of the Dominant Right Coronary Artery: RVMI may also result from the
dominant right coronary artery being blocked. When the PDA is supplied by a strong
collateral circulation, this manifestation frequently happens. When these collateral
pathways are well-established, infarction may only affect the right ventricle's
inferior and anterolateral sides. However, there is a risk of incorporating other
areas, including those given by the PDA, if collateral circulation to the PDA is
restricted.

It's crucial to remember that the PDA is a branch coming from the RCA in 90% of
instances. As a result, the right ventricle's infarct size is dependent on how well the
collateral circulation is functioning. Unless there is sufficient collateral flow to the
PDA, which can protect this territory, in situations where the RCA is the major
artery, obstruction of the RCA's main stem may result in infarction affecting both
the anterolateral and inferior parts of the right ventricle.

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A condition known as left dominance occurs when the PDA develops as an
extension of the left circumflex artery in roughly 10% of instances. In these
circumstances, RVMI can happen even if the right coronary artery is healthy.

In conclusion, RVMI frequently co-occurs with infarction in the inferior or

anteromedial walls of the left ventricle. In rarer cases, solitary occlusion of right
ventricular branches, occlusion of the non-dominant RCA, or occlusion of the
dominant RCA with efficient collateral circulation to the PDA might result in isolated
RVMI.

The sinoatrial node artery, which comes from the right coronary artery in around
65% of people, performs the critical task of giving blood to the right atrium and
sinoatrial (SA) node. Both the right atrium and the SA node are likely to suffer
ischemia damage in the event that the right coronary artery is blocked close to its
origin. This might result in the emergence of right ventricular myocardial infarction
(RVMI) symptoms, which may intensify in the presence of a right atrial infarction,
which is frequently accompanied by rate and rhythm problems.

PATHOPHYSIOLOGY OF RVMI

1. The following remarks are made in academic language:

2. The cardiac output from the right and left ventricles is equal.
3. The low-pressure pulmonary circulation is served by the RV, which is
morphologically and functionally specialized.
4. Only 15% of the LV's muscle mass is found in the RV.
5. The RV stroke work is roughly 25% less than the LV.
6. About 10% of systemic vascular resistance is made up of pulmonary
vascular resistance.

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7. The right ventricle experiences coronary blood flow throughout both
systole and diastole when there is no right ventricular hypertrophy.
8. The right coronary artery, which serves the lateral and posterior walls as
well as the posterior interventricular septum via the posterior descending
artery, is the main coronary blood vessel for the right ventricle.
9. The conus artery and the left anterior descending artery (LAD) give blood
to the RV's anterior wall.
10. The RV has a lower afterload and myocardial oxygen demand than the left
ventricle and is physically connected to the LV by sharing the
interventricular septum and pericardium.
11. Insufficient collateral vessel creation may be to blame for the higher
frequency of right ventricular infarction in patients without a history of
preinfarction angina.
12. Between 30% and 50% of inferior wall myocardial infarctions are
complicated with right ventricular infarction.
13. ST segment elevation in the right precordial leads, especially V4R, along
with ST segment elevation in II, III, and aVF are the most dependable
electrocardiogram (ECG) findings for right ventricular infarction.
14. Systemic hypotension, high central venous pressure, and clear lung fields
are some of the clinical indicators of right ventricular infarction.
15. The RV may serve largely as a conduit between systemic veins and the
pulmonary circulation in cases of massive infarction.
16. Right ventricular infarction can cause an increase in right atrial pressure,
which can then trigger the release of atrial natriuretic factor (ANF), which
has significant vasodilatory, natriuretic, diuretic, and aldosterone-inhibiting
effects.

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 17. To maximize LV preload and improve cardiac output, right ventricular
infarction management options include volume loading and the early
administration of inotropic drugs such dobutamine.
18. Right ventricular infarction can also occur in cases with left dominant
coronary circulation when the left circumflex artery is blocked. Typically,
this occurs when the right coronary artery is blocked close to the acute
marginal branches.
19. Less frequently, blockage of the left anterior descending artery (LAD) might
cause right ventricular infarction.
20. The presence of further right ventricular infarction may be suggested by
hemodynamic insufficiency that is present in conjunction with an inferior
wall myocardial infarction.
21. Only 2% of cases of right ventricular infarction that are autopsied are
isolated cases.

HAEMODYNAMICS

1. Right ventricle ischemia or infarction causes a number of significant

alterations, including decreased right ventricular compliance, impaired
filling, decreased right ventricular stroke volume, and increased right atrial
pressure.
2. As a result of these changes, the left ventricular filling is reduced and the
cardiac output decreases.
3. The situation is made worse by acute right ventricular dilatation, which
shifts the interventricular septum to the left. This displacement lowers left
ventricular compliance and cardiac output while raising left ventricular
end-diastolic pressure.

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4. According to research by Brookes and colleagues, right ventricular
dilatation in cases of right ventricular myocardial infarction (RVMI) causes
geometric alterations in the left ventricle that considerably impair left
ventricular contractile function. Along with aberrant diastolic filling and
changes in compliance, these modifications also exist.
5. As a result, even if there are clinical signs of elevated right-sided pressure,
left ventricular filling and systolic function may be below average.
6. Due to the different pathophysiology associated with RVMI, the
management of right ventricular infarction differs dramatically from the
usual strategy for left ventricular infarction.
7. Clinicians should have a high degree of suspicion for RVMI in any patient
presenting with an acute inferior wall myocardial infarction (MI) given that
haemodynamically substantial right ventricular infarction often occurs in
individuals with such an infarction.

Clinical Diagnosis

1. In a patient with an inferior wall myocardial infarction (MI), the clinical

triad of hypotension, clear lung fields, and increased jugular venous
pressure (JVP) is almost pathognomonic for the existence of right
ventricular infarction.
2. Because of volume depletion, it is vital to use caution when relying on
these results. Additionally, right ventricular infarction physical and
hemodynamic symptoms frequently don't show up until after volume
loading.

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 3. Right ventricular myocardial infarction (RVMI) cases have been associated
with pulses paradoxus and Kussmaul's sign (an inspiratory increase in
JVP).
4. With a sensitivity of 88% and a specificity of 100%, increased JVP and
Kussmaul's sign in the setting of an acute inferior wall MI clearly suggest a
hemodynamically significant RVMI.
5. In patients with intact right atrial perfusion, atrial contraction is usually
increased, causing an elevated 'a' wave and 'y' descent in the jugular
venous pulse.
6. A reduced 'a' wave has been identified as a poor prognostic predictor in
patients with clinically severe RVMI, depressed right atrial function, or
right atrial infarction.
7. Upon clinical auscultation, a right-sided S3 and S4 heart sound may be
audible.
8. When papillary muscle dysfunction is involved, tricuspid regurgitation,

which predominantly results from right ventricular chamber dilatation, can

become severe.

INVESTIGATIONS

ECG changes of Inferior wall infarction with Right Ventricular infarction

According to research, surface electrocardiography (ECG) can be used to diagnose

right ventricular infarction (RVMI) with accuracy. RVMI is often diagnosed by
looking for increased ST segments in the extreme right leads V3R and V4R on an
ECG.

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When lead V1, lead V4R, or any of the other right precordial leads (V4R-V6R) have
a ST segment elevation of 1 mm or greater in the context of an acute inferior wall
infarction, there should be a high suspicion of RVMI.

According to the research by Braat et al., patients with inferior wall infarction who
had ST segment elevation of at least 1 mm in lead V4R had a 93% sensitivity and
95% specificity for RVMI.

The most specific and accurate RVMI diagnosis is made when the ST segment
elevation is higher in lead V4R than in leads V1 and V3R. The ST segment elevation
seen in the right precordial leads is significant since it frequently goes away 10 to
18 hours after the beginning of chest discomfort in about 50% of individuals.

A reliable and independent predictor of significant complications and in-hospital

mortality related to RVMI is the presence of ST segment elevation in lead V4R.

In some cases of RVMI, leads V1 and V2 experienced ST segment elevation,

simulating anterior wall MI. Vector principles can help to explain this occurrence.
The ST segment in lead I is displaced downward in RVMI because the ST segment
vector points anteriorly and is frequently more than +90 degrees to the right.
Contrarily, anteroseptal left ventricular infarction manifests as an anteriorly
directed vector but is often orientated between -30 and -90 degrees to the left in
the frontal plane, leading to an elevation of the ST segment in lead I.

In something like 10 hours following the beginning of side effects, 48% of patients
in a single series revealed that their ECG modifications had settled. Hence, to get
these changes, it is fundamental for record the ECG using beneficial right
precordial leads straightaway.

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The utilization of lead V4R is the suggested request procedure since it is urgent to
comprehend the fleeting idea of ST section rise. The most dependable ECG finding
for RVMI is still ST section rise in lead V4R.
RVMI is generally joined by conduction peculiarities such right group branch block
and complete heart block. Moreover, RVMI patients' ECGs show mood
irregularities incorporate atrial fibrillation and sinus bradycardia.
Use of 18 lead ECG in diagnosing RVMI and posterior wall MI in patients with
acute inferior wall MI

In individuals with acute inferior wall myocardial infarction (IWMI), the diagnosis
of right ventricular (RV) and posterior wall involvement is critical.

Right-sided leads like V4R, V5R, and V6R are used to determine RV participation.
Leads V7 to V9 (particularly, V7 is located along the left posterior axillary line, V8 is
positioned at the inferior angle of the left scapula, and V9 is located in the left
paravertebral area) are used to evaluate the posterior wall.

Mirror image changes in leads V1 and V2 can also be used to detect posterior wall
myocardial infarction (MI). Indicators of these changes include significant "R"
waves, ST segment depression, and upright "T" waves.

The results of Anderson's study show that high sensitivity (88%) and specificity
(91%) for the diagnosis of RVMI are demonstrated by the presence of ST elevation
in lead III greater than that in lead II. Based on the idea that lead III is anatomically
orientated further toward the right ventricle than lead II is, this diagnostic
premise.

Enzyme Study

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The evaluation of the enzymes that irreparably injured myocardium cells release
into the bloodstream is crucial in the identification of acute myocardial infarction
(AMI). Serum Creatine Kinase (CK) levels among these enzymes have a specific
temporal pattern. After the commencement of AMI, CK becomes detectable
between 4 and 8 hours later, reaches its highest concentration within 24 hours, and
then returns to normal levels between 3 and 4 days after the initial onset of chest
pain.

The most useful marker for detecting myocardial necrosis among the several
isoenzymes of CK is CK-MB. Compared to total CK, CK-MB is less common in
substantial amounts in extracardiac tissues, making it a more accurate marker of
myocardial damage. It is important to remember that cardiac procedures
including surgery, myocarditis cases, and electrical cardioversion can result in high
serum levels of CK-MB.

When evaluating myocardial injury, an indicator called the "CK-MB mass index,"
which measures the ratio of CK-MB mass to CK activity, becomes especially
important. When this index reaches a value of 2.5 or higher, it strongly suggests
that myocardial damage may be present.

Serum Markers for Myocardial Infarction

Important biomarkers used in the evaluation of myocardial damage include

cardiac troponin-T (cTnT) and cardiac troponin-I (cTnI). Together with other
proteins related to the heart contractile apparatus, these biomarkers are released
into the bloodstream when the integrity of the myocardial cell membrane is
compromised.

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With a rate of 100% for the correct diagnosis of acute myocardial infarction (AMI),
the presence of cTnT in the serum has demonstrated outstanding diagnostic
sensitivity. Additionally, cTnT provides a longer diagnostic window because it can
be detected up to 12 days after myocardial infarction has occurred. This increased
window of detection helps to assess the effectiveness of reperfusion therapy and
is especially useful for the delayed diagnosis of AMI.

Myoglobin

The first serum marker to show an elevation after an acute myocardial infarction
(AMI) is this biomarker. Since elevated levels can also be found in cases of renal
disease or muscular injury, it has a poorer specificity for cardiac tissue.

Notably, this biomarker rapidly leaves the body by urine elimination, returning the
blood to normal levels within 24 hours of the start of myocardial infarction.

Echocardiography

A useful diagnostic method for determining cardiac anomalies linked to right

ventricular infarction is two-dimensional echocardiography. The right ventricle
was dilated, the right ventricular wall was asynthesized, and the interventricular
septum was moving irregularly. The reversal of the transseptal pressure gradient
caused by increased right ventricular end-diastolic pressure is thought to be the
cause of this motion anomaly.

In particular, the short-axis view has shown greater sensitivity, measuring at 82%,
with specificity levels ranging from 62% to 93% in detecting right ventricular
infarction that is hemodynamically important.

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The interatrial septum's bowing toward the left atrium is another important
prognostic indicator in right ventricular infarction. This finding indicates that the
pressure gradient between the right and left atriums has increased. When
compared to patients without this trait, individuals who exhibit it frequently have
higher rates of heart block, higher levels of hypotension, and higher fatality rates.

The detection of problems resulting from right ventricular infarction is where

Doppler echocardiography is especially useful. These issues could include tricuspid
regurgitation, ventricular septal abnormalities, and early pulmonary valve
opening, which is a sign of an uncooperative right ventricle.

Other Imaging Modalities

Nuclear Imaging

 By focusing on viable cardiac tissue, myocardial perfusion imaging using

TL201 or 99mTC-sestamibi provides insightful information about the
distribution of myocardial blood flow. These imaging methods usually
identify a defect, frequently referred to as a "cold spot," during the first few
hours after a transmural infarction develops.
 The ability to distinguish between acute infarcts and chronic scar tissue
means that perfusion scanning lacks specificity for the accurate diagnosis of
acute myocardial infarction (MI), despite its high sensitivity.
 34 Patients with ST-elevation myocardial infarction frequently show
anomalies in ventricular wall motion and a decrease in ventricular ejection
percentage while undergoing radionuclide ventriculography utilizing
99mTC-labeled red blood cells. Even though this method is useful for
determining the hemodynamic effects of infarction and supporting the

24
 diagnosis of Right Ventricular (RV) infarction when RV ejection fraction
declines, it is non-specific because other cardiac abnormalities besides MI
can also cause the radionuclide ventriculogram to change.
 In order to evaluate patients with ST elevation myocardial infarction, a
number of imaging modalities, such as radionuclide angiography, perfusion
imaging, scintigraphy, and positron emission tomography, have been used.

Nuclear Imaging

In the assessment of myocardial infarction, cardiac radionuclide imaging has

numerous important functions. It makes it easier to determine the size of the
infarct.

 It offers information on collateral blood flow.

 It facilitates the assessment of cardiac tissue in danger.
 It enables the assessment of how the infarction affects ventricular function.
 It contributes to the creation of prognostic indicators.

It's crucial to recognize that the need to transfer critically ill patients from the
coronary care unit to the nuclear medicine department can restrict the practical
deployment of these imaging modalities. Consequently, in specific, limited
circumstances where clinical history, ECG abnormalities, and serum cardiac
markers provide conflicting results should cardiac radionuclide imaging be used to
diagnose myocardial infarction.

64 slice CT scanning:

The technology has the potential to generate high-resolution images while

simultaneously doing a thorough scan in a remarkable 10-second time frame. This

25
outstanding competence enables the prompt and non-invasive detection of
coronary artery disease. It also makes it possible to directly see the presence of
atherosclerotic plaque inside the arterial structure in addition to the coronary
artery luminal area.

Magnetic resonance imaging

Various vital uses of magnetic resonance imaging (MRI) in the treatment of acute
myocardial infarction (AMI) include:
 It helps in locating the infarcted area and estimating its size.
 It evaluates how serious the ischemia insult is.
 It assesses the degree of perfusion in both infarcted and uninfarcted
cardiac tissue, as well as in myocardium that has undergone reperfusion.
 Myocardial edema, fibrosis, wall thinning, and hypertrophy are all
recognized.
 It sheds light on the size of the ventricular chamber and the mobility of the
segmental walls.
Both MRI and CT scanning have useful capabilities, but because AMI patients must
be transported to the radiological department, their practical applications are
rather constrained.

Management:
AMI mortality has significantly decreased since the introduction of coronary care
units, with about 40% of the decrease in mortality attributable to interventions
like these, pre-hospital resuscitation, and improvements in mechanical and
medical therapies for coronary artery disease.

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Pain Relief:
For AMI patients, effective pain management is crucial, and morphine is the
analgesic of choice. However, care should be taken when giving morphine to
people who have had a right ventricular myocardial infarction (RVMI). Systemic
hypotension is a common presenting symptom in patients with inferior wall MI
and RVMI, for whom volume loading is the main therapy strategy.

A few people, particularly those with a significant right ventricular dilatation,

probably won't answer volume stacking as well as they ought to. Volume
implantation is many times finished with saline or colloids over a time of 5 to 10
minutes, in additions of 200 ml. Until the hypotension is revised, the narrow
wedge pressure arrives at 15 to 20 mm Hg, or the right atrial tension surpasses 15
mm Hg, volume extension ought to proceed.
Dobutamine is encouraged to work on right ventricular systolic capability and
expand forward cardiovascular result in the event that heart yield doesn't
improve with painstakingly managed volume implantation. Moreover,
dobutamine raises left ventricular result. Despite the fact that inotropic
medications could raise the oxygen interest of an ischemic myocardium, the
better cardiovascular record and stroke volume might compensate for this by
raising myocardial blood stream.
By expanding volume development, contractile power, systolic compression
strength, and stroke volume through the organization of crystalloids as well as
colloids, the left ventricle is provided with oxygenated blood.

Arrhythmia Management:
The control of arrhythmias is essential for raising survival rates. Bradyarrhythmias
are common in inferior wall MI linked to RVMI. Bradyarrhythmias that result in
loss of right atrial contribution and atrioventricular dyssynchrony can have serious

27
effects on hemodynamics. Atrioventricular sequential pacing may be required to
keep the heart beating in cases of severe atrioventricular blockages.

When addressing inferior wall MI with RVMI, as opposed to standard care for left
ventricular infarction, vasodilators, nitrates, and diuretics must be avoided.

Early Reperfusion:
In patients with inferior wall MI with RVMI, early reperfusion of the right coronary
artery has been shown to greatly improve right ventricular mechanical
performance and decrease in-hospital mortality. A thrombolytic agent or an
angioplasty can achieve reperfusion.

Strategies in Treatment of Right ventricular Infarction

1. Maintain Right Ventricular Preload

 Volume load, such as intravenous saline or colloids

 Volume loading raises RAP and PCWP, but it also raises cardiac output.

 Steer clear of nitrates, diuretics, and morphine boluses (they lower

preload).

 Keep the atrioventricular rhythm in sync:

 AV sequential pacing in the event of a total heart block

 Quick cardioversion in the event of atrial fibrillation

2. Inotropic Support

28
  Preference for dobutamine
 Recommendations
 Process of Action
3. Reducing Right ventricular after load

 Counterpulsation of the intraaortic balloon

 Vasodilators (Nitrosol sodium)

 These could also lower LV preload and, in turn, cardiac output.

4. Reperfusion

 Thrombolytic agents

 Direct angioplasty
5. Temporary pacing

Patients who have any of the following conditions should undergo temporary
pacing:

a. Sinus bradycardia that is resistant to medication

b. Second-degree atrioventricular block of Mobitz type II
c. Heart block of the third degree
d. bidirectional bundle branch block
e. Block of a newly acquired bundle branch
f. A first-degree atrioventricular block along with a right or left bundle branch
block.

Immediate surgical intervention may be required when percutaneous transluminal

coronary angioplasty (PTCA) is unsuccessful and patients continue to complain of

29
persistent chest discomfort or show hemodynamic instability. This is especially
important for individuals who are already known to have mechanical problems,
such as papillary muscle rupture (leading in mitral regurgitation) or ventricular
septal defects, that cause significant pulmonary congestion or hypotension.
Emergency surgery is recommended in such circumstances.
Management of Atrioventricular (AV) Block: AV block is a right ventricular
infarction (RVI) consequence that is frequently observed. Patients with junctional
rhythms or AV block generally need brief pacing. In these patients, AV sequential
pacing is advised to guarantee optimum heart rhythm and function.

COMPLICATIONS

Right Ventricular Infarction (RVI)-Related Complications

1. Cardiogenic shock:
occurs in RVI patients and denotes a serious and potentially fatal disease.
2. Atrioventricular (AV) Block in Advanced Stages:
A 2nd or 3rd degree heart block, which can occur in up to 48% of RVI cases, is a
dire prognostic indicator.
3. Atrioventricular Fibrillation:
Patients with RVI may experience atrial fibrillation, which can lead to
arrhythmias and hemodynamic instability.
4. Ventricular Rhythm Disorders
Ventricular arrhythmias that result from RVI may complicate the clinical
picture further.
5. Ventriculo-Septal Rupture
seen in individuals with RVI, especially when transmural posterior septal
infarction is present.

30
 6. Pulmonary embolism with Right Ventricular Thrombus Formation:

The problem is made more complicated by the possibility of pulmonary embolism

from thrombus formation within the right ventricle.
7. tricuspid regurgitation
Right ventricular dilatation can cause tricuspid regurgitation, which affects cardiac
function.
8. pericarditis
The comparatively thin-walled right ventricle may sustain transmural damage,
which could result in pericarditis.
9. A right-to-left shunt through the patent foramen oval
Patients with hypoxemia who don't respond to oxygen therapy should be
examined for the possibility of a right-to-left shunt through a patent foramen
ovale.

Management of AV Block:
RVI frequently involves varying degrees of AV block, which frequently calls for
short-term pacing. In individuals exhibiting AV block or junctional rhythms, AV
sequential pacing is advised for best therapy.

PROGNOSIS

In the middle somewhere in the range of 25% and 53% of people with
substandard wall myocardial localized necrosis (IWMI), right ventricular
myocardial dead tissue (RVMI) for the most part follows IWMI. The clinical
conclusion of RVMI is habitually made utilizing a gathering of side effects that
highlight right-sided cardiovascular breakdown. These incorporate a third or
fourth heart sound coming from the right ventricle, raised jugular venous strain

31
with an unmistakable 'y' plunge, the presence of the Kussmaul's sign, blood vessel
hypotension, and clear lung fields on X-beam and actual assessment. Also, the ECG
of most of patients with RVMI shows ST section rise, especially in lead V4R on the
right-sided precordial leads.

Rarely, RVMI may present as tricuspid regurgitation or an interventricular septal

rupture. Shock is typically only noticed when RVMI affects two or more left
ventricular walls and causes transmural infarction of the right ventricle.

Atrioventricular (AV) block is more common in patients with RVMI and concurrent
IWMI, and there is a possible link with an increased risk of pulmonary embolism,
although conclusive evidence for this consequence is yet lacking.

In patients with RVMI, reperfusion of the right coronary artery by angioplasty can
result in a remarkable restoration of right ventricular function as well as
outstanding clinical results. On the other hand, a poor recovery of right ventricular
function, ongoing hemodynamic impairment, and a significant death rate are
associated with failed reperfusion.

Right ventricular dysfunction following a myocardial infarction has been shown in

numerous studies to be an independent predictor of increased long-term
mortality. However, right ventricular dysfunction usually becomes better with
time in the majority of RVMI survivors. Even patients who had right ventricular
failure for weeks or months at a time tend to recover their normal function with
time. This recovery can be attributed to either gradual stretching of the
pericardium, which lessens the restricting impact of the pericardium, or alleviation
of concurrent left ventricular dysfunction, which reduces right ventricular
afterload.

32
 MATERIALS AND METHODS

MATERIALS AND METHODS

Between July 2023 and Sep.2023, a cohort of 50 patients who had been hospitalized
to the coronary care unit with a confirmed diagnosis of acute inferior wall infarction
participated in this study.
Every subject got a thorough ECG assessment, which went beyond the usual 12-
lead ECG to include leads V3R and V4R. The study also included evaluation of
extended leads V7 through V9 on the ECG. Rhythm strips were acquired for
patients who were having arrhythmias. while patients were in, on day two, and
while they were being discharged, ECGs were carefully examined.

Only instances with hyperacute inferior wall infarction, indicated by the presence
of ST segment elevation in leads II, III, and aVF, were included in the research.
When the ST elevation in lead V4R was equal to or more than 1 mm, a right
ventricular infarction was determined to have occurred. The diagnosis of posterior
wall myocardial infarction, meanwhile, depended on the presence of tall 'R'
waves, ST segment depression, and upright 'T' waves in leads V1 and V2, as well as
ST segment elevation equal to or surpassing 1 mm in extended leads V7 to V9.

A thorough clinical and electrocardiographic evaluation of every patient was

performed, with an emphasis on the patient's presenting symptoms, risk factors,
vital signs, arrhythmias, and mortality. Following up with patients didn't stop after
they left the hospital.

33
Patients who presented more than 24 hours after the onset of their chest
discomfort were subject to exclusion criteria since ST alterations in right
ventricular infarction may be temporary in such circumstances. As the criteria for
identifying right ventricular infarction using ECG would not be applicable in these
cases, people with a history of chronic lung illness, prior myocardial infarction,
rheumatic heart disease, pericardial disease, or left bundle branch block were also
excluded.

34
 RESULTS

OBSERVATIONS

The observations made in a cohort of 50 individuals with acute inferior wall

myocardial infarction are summarized in this section with descriptive data and

tabular data.

Age Distribution:

The patients were divided into groups with an age difference of five years to make
it easier to compare the distribution of gender and age.

 The research identified two separate peak incidence groups with mean
ages of 42 and 62 years, respectively.
 The youngest patient in the study group was a man who was 31 years old,
while the oldest patient was a female who was 82 years old.
 they were 50 patients, and they were 41 men and 9 women.

35
TABLE – 1

AGE AND SEX DISTRIBUTION OF PATIENT

36
PRESENTING SYMPTOMS (TABLE – 2)

49 of the 50 participants who took part in the study reported having

retrosternal chest pain as their primary complaint. The lone exception among
these patients came with dyspnea as the main complaint rather than chest
discomfort.

TABLE – 2

PRESENTING SYMPTOMS

Radiation

29 out of 50 patients (58%) had symptoms that were radiated. 40% of individuals
who experienced radiation said it reached their left upper limb, 6% said it
reached their epigastric area, and a further 6% said it reached their right upper
limb. Less frequently, patients (4%) and 2%, respectively, experienced radiation
to the jaw.

37
TABLE – 3

TIME OF ONSET OF SYMPTOM

38
Past History

Eight (16%) of the subjects in the research had experienced unstable angina
before developing an acute myocardial infarction. It's noteworthy that the
majority of these cases of unstable angina happened within the two weeks
before the myocardial infarction.

Furthermore, four patients (8%) said they had exertion angina prior to the start
of their present myocardial infarction. It's important to note that all of these
patients had recently reported experiencing exertion angina.
TABLE – 4

RISK FACTORS

Diabetes Mellitus:

In the study cohort, a total of 11 patients (22%) had a confirmed diagnosis of

diabetes mellitus, and they were all using oral hypoglycemic medications. When
accessible, every effort was made to check their prior medical records.
Systemic Hypertension:
Antihypertensive drugs were prescribed as a result of either a prior diagnosis of
hypertension by a medical practitioner or a history of persistently high blood
pressure readings while in the hospital. 17 participants (or 34%) in this study met
the criteria for hypertension.

Smoking:
No female patients reported a smoking habit, but 28 of the 41 male patients were
active smokers. The majority (85%) of the male smokers were still smoking
40
regularly, averaging 10 to 20 cigarettes or beedies per day for at least 15 to 30
years.
Alcohol:
14 of the 41 male patients admitted to regularly consuming alcohol, compared to
no female patients who did so. The male patients who drank had been doing so
for at least 10 to 18 years, and they frequently drank every day.
Obesity:
Based on their body mass index (BMI), which was assessed for each participant, 6
patients (12%) were identified as obese.
Dyslipidemia:
Dyslipidemia was discovered in five patients (10%) after routine examinations
carried out elsewhere. None of these patients were taking any drugs to decrease
their cholesterol levels.
Family History:

Ten patients (20%) had a family history of diabetes mellitus, seven patients (14%)
had a history of hypertension, and nine patients (18%) had a history of coronary
artery disease.

Occupation:

26 patients (or 52%) of the study participants worked in physical labor, whereas
the rest participants had sedentary jobs.

Treatment History:

The 11 diabetes patients were divided into 7 who consistently used oral
hypoglycemic medications, 1 who was taking both oral hypoglycemic medications
and insulin therapy, and 3 who inconsistently followed their treatment plan. The
three angina patients received aspirin, nitrates, ACE inhibitors, and beta blockers
as part of their treatment. Eight of the 17 hypertensive patients were actively
receiving regular antihypertensive therapy, which frequently included a mix of
beta blockers, ACE inhibitors, and calcium channel blockers.

42
Clinical Examination

In 9 patients (18%), pallor was noted, while in 14 patients (28%) bradycardia was
present. Six patients (12%) had tachycardia, and fifteen patients (30%) had
hypotension. In 16 individuals (32%), elevated jugular venous pressure (JVP) was
observed. Additionally, 10 patients (20%) had auscultated right-sided third or
fourth heart sounds. Notably, right ventricular infarction was detected
electrocardiographically in all patients. Hepatomegaly was seen in two patients
(4%) in a tender state.

TABLE – 5

CLINICAL SIGNS AT THE TIME OF PRESENTATION

Electrocardiogram (ECG) Findings:

In 19 individuals (38%), right ventricular infarction was visible on the ECG. Eight
patients (16%) had true posterior wall infarction, which is indicated by tall 'R'
waves in V1 with ST segment depression and upright 'T' waves. These different
changes often become apparent after a day.

Arrhythmias:

Three patients (6%), four (8%), three (6%), and seven (14%), all had first-degree
atrioventricular (AV) blocks, second-degree Mobitz type I blocks, and third-
degree Mobitz type II blocks, respectively. In one instance, a transient complete
right bundle branch block (RBBB) that later developed into a total heart block was
the initial presentation. Additionally, a left anterior hemiblock was seen in 1
patient (2%) of the total. The majority of these arrhythmias were of a transitory
character and didn't require any special care. Tragically, three patients who were
hospitalized with right ventricular myocardial infarction, hypotension, and total
heart block passed away. Two individuals (4%) experienced atrial fibrillation,
which both experienced during the first 24 hours. In addition, 2 individuals (4% of
the total) had papillary muscle dysfunction.

Mortality:

Three patients experienced hospital mortality; two of them passed away within
24 hours of admission due to right ventricular infarction, extreme hypotension,
and total heart block. The patient who was still alive had a right-sided hemiplegia
due to a cerebrovascular accident (CVA), right ventricular infarction, hypotension,
and total heart block. The left middle cerebral artery (MCA) area was the site of
infarction, according to a computed tomography (CT) brain scan.

44
TABLE – 6

COMPLICATION DEVELOPED DURING FOLLOW UP

 DISCUSSION

This study examined risk variables, clinical characteristics, and complication rates
in 50 confirmed instances of acute inferior wall myocardial infarction (IWMI).
Within 24 hours after the onset of symptoms, all patients were admitted to the
hospital and received a thorough evaluation that included an ECG examination of
the V3R, V4R, extended leads V7 to V9, and rhythm strips as necessary.

Analysis of Patient Demographics:

According to the study, 96% of patients who were 40 or older and 82% of whom
were men over the age of 40 had IWMI. The patients ranged in age from 31 years
old for a male patient to 82 years for a female patient.

Clinical Presentation:

Almost all patients (98%) had classic retrosternal chest pain when they first
arrived. Of them, 22% had bouts of pain that lasted under an hour, the remaining
78% had episodes that lasted over an hour, however they were all chest pain
episodes that lasted longer than 30 minutes. The most typical symptom that was
present in 86% of patients in addition to chest pain was perspiration, which was
frequently accompanied by cold extremities.

Other symptoms included vomiting, which was frequently accompanied by

nausea and was reported by 52% of patients. A history of syncope or presyncope
was reported by 14% of patients, and right ventricular infarction was present in
six of these cases. 16% of patients reported experiencing palpitations; two of

46
these cases involved atrial fibrillation and five involved right ventricular
infarction.

Temporal Patterns:

The study found a substantial diurnal trend in the start of symptoms, with
symptoms appearing more frequently in the morning. This finding is consistent
with past research that indicates chest pain is more common in the morning.

Risk Factors for Coronary Artery Disease:

The majority (56%) of patients who were active smokers (all male) had this risk
factor. Furthermore, 28% of patients admitted to using alcohol, while 34% had
hypertension and 22% had diabetes. 10% of patients were found to have
dyslipidemia, and 12% of patients had obesity as measured by body mass index.

Comparison with Previous Studies:

Although exact percentages differed, comparison with earlier studies revealed a

similar incidence of risk variables. For instance, in earlier investigations, smoking
was mentioned in 63% of cases, diabetes mellitus in 23%, and hypertension in
45% of cases.

Medical History:

Twelve patients had a history of coronary artery disease; eight of them had
unstable angina in the past, and four experienced effort angina in the past. Three
of these individuals were taking consistent anti-anginal drugs.

Family History:

47
18% of patients had a family history of coronary artery disease.

Clinical Signs:

Upon admission, 30% of patients had systolic blood pressure below 100 mm Hg,
28% of patients had bradycardia, and 18% of patients had pallor. 38 percent of
patients displayed right ventricular myocardial infarction (RVMI) on the
electrocardiogram (ECG), with ST elevation more than 1 mm in V3R and V4R.
Between 25% and 53% of patients with IWMI have been documented to have
RVMI.

Kussmaul's Sign:

With high jugular venous pressure (JVP) and a positive Kussmaul's sign, 16 of the
19 patients with ECG indications of RVMI demonstrated RV failure. According to
earlier accounts, positive Kussmaul's signs occurred somewhere between 20%
and 90% of the time.

Additional Clinical Findings:

Ten patients reported right-sided third and fourth heart sounds (S3 and S4) and
two patients experienced painful hepatomegaly among the 19 patients with ECG
evidence of RVMI. Intravenous fluids and inotropic support were given to these
individuals with RVMI and hypotension as part of their treatment.

Posterior Wall Myocardial Infarction:

True posterior wall myocardial infarction, which is indicated by tall 'R' waves in
the V1 and V2 and ST depression, upright 'T' waves, and ST elevation in the V7,

48
V8, and V9, was found in nine patients. These individuals exhibited conduction
issues in five of them.

Arrhythmias:

A number of arrhythmias were observed, with total heart block occurring in 14%
of patients. In 4% of individuals, transient atrial fibrillation developed. One
patient experienced a complete right bundle branch block (RBBB), whereas
another patient experienced a left anterior hemiblock.

Pericardial Friction Rub and Papillary Muscle Dysfunction:

Three patients (or 6%) had pericardial friction rub, while two patients (or 4%) had
papillary muscle dysfunction with pansystolic murmur. These results were
frequently linked to slight hemodynamic instability.

Treatment:

The remaining patients were treated conservatively, with 60% of patients

receiving thrombolytic treatment. Three patients died while receiving treatment;
two of them had severe RVMI, full heart blocks, and chronic hypotension, while
the third suffered from an infarct in the left middle cerebral artery area that
caused right-sided hemiplegia.

Outcomes:

The remaining patients were released without any serious issues.These results
support earlier studies on IWMI and add new information about risk factors,
clinical manifestations, and outcomes.

49
50
 CONCLUSION

1. There is a clear gender difference in the prevalence of acute inferior wall

myocardial infarction, with males experiencing the condition far more
frequently than females. As people get older, this gender disparity tends
to close.
2. According to the results of this study, there is a noticeable increase in
incidence among males after the age of 40.
3. The most common symptoms among patients were retrosternal chest pain
that lasted longer than 30 minutes and was frequently accompanied by
excessive sweating.
4. With 56% of patients, smoking appeared as the primary risk factor.
5. The majority of patients (60%) said their symptoms started between 6 and
12 o'clock in the morning.
6. In this study, 38% of patients had right ventricular infarction, which
represents a sizable fraction of cases.
7. Patients who also had a right ventricular infarction frequently experienced
syncope or presyncope.
8. In 15 patients (30%), a triad of clinical symptoms that included high Jugular
Venous Pressure (JVP), hypotension, and clear lung fields was seen.
9. Using right-sided leads during an ECG examination is crucial in all cases
with inferior wall infarction, and it should be done very away.
10. The prognosis is often good when Right Ventricular Myocardial Infarction
(RVMI) is correctly diagnosed and early management is started.

51
11. A real posterior wall myocardial infarction occurred 16% of the time,
according to the study.
12. Compared to patients who do not encounter this complication, people
who develop right ventricular infarction have much higher mortality rates.

52
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47. CD Morgan, Haq A, Brobac M, Baigrie RS. Spectrum of right ventricular
involvement in the inferior wall myocardial infarction. J Am Coll Cardiol
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48. Vas Gorselen, Vorsheugt, BT. J Meursing, AJ Mondi. Posterior wall

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16 – 21.

49. Recharia E, Strasbery B, Mager A et al. The incidence of atrial arrhythmias

during inferior wall myocardial infarction with and without right ventricular
myocardial infarction. Am Heart J 1992; 124: 387 – 391.
50.Peter Berger, James L Orford, Complications of acute myocardial infarction:
ACP medicine: 2006.

51. Philip Podrid, Evaluation and management of rhythm and conduction

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52. Mauri, Zaputovi, Kuci, Roje, Marinovi. Prognostic significance of complete

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Am Heart J 1990, 119(4); 823 – 828.

53. Adgey AAJ, Geddes JS, Pautridge JF; Incidence significance and management
of bradyarrhythmia complicating acute myocardial infarction.

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prognostic implications of heart block complicating IWMI. J Am Coll Cardiol
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55. Tans A, Durrer D. Clinical setting and prognostic significance of high degree
atrioventricular block in acute IWMI, a study of 144 patients. Am Heart J.
1980; 99: 4 – 8

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56. Strasberg B, Prichas A, Arditti A. Left and right ventricular function in acute
myocardial infarction and significance of advanced atrioventricular block.
Am J Cardiol 1984; 54: 985 – 989.

57. David Harpaz, Solomon Behac, Michel Elder, Valentina Boyko. Complete AV
block complicating acute myocardial infarction. J Am Coll Cardiol 1999; 34:
1721 – 1728.

58. Robert A Levine, Judy Hung. Ischaemic MR, the dynamic lesion. J Am Coll
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59. Leonardo Zornoff, John Sutton, Eugene braunnwald. Right ventricular

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failure in patient with myocardial infarction. J Am Coll Cardiol 2002; 39:

1400 – 55.
60.Alice K Jacobs, Jane A Leopold, Ravin Davidoff (Shock registry) Cardiogenic
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60
 ANNEXURE

61
PROFORMA

Name : Age : Sex:

I.P. No : Date of Admission:

Complaints of:
Chest pain : Y/N

Radiation : Y/N
Sweating : Y/N
Dyspnoea : Y/N
Vomiting : Y/N
Palpitation : Y/N
Syncope : Y/N

Past History of:

Diabetes Mellitus : Y/N

Hypertension : Y/N
Coronary Artery Disease : Y/N
Dyslipidemia : Y/N

Family History of:

Diabetes Mellitus : Y/N

Hypertension : Y/N
Ischemic Heart Disease : Y/N
Personal History of:
Smoking : Y/N

Alcohol : Y/N
Occupation

62
 Sedentary / Non Sedentary :

On Examination

BP : PR :
Pallor : CVS :
JVP : RS :
Abdomen :
Investigation

RBS : Urea
:

Creatinine :

CPK :

CPK MB :

Sr.Cholesterol :

Hb% : ECG :

Chest X ray – PA view :

Treatment

Conservative

Thrombolysis

Anticoagulants

Complications

63
 Shock :

Rhythm disturbance :

Death :

Discharge :

ABBREVIATIONS

ACS : ACUTE CORONARY SYNDROME

64
RVI : RIGHT VENTRICULAR INFARCTION

IWMI : INFERIOR WALL MYOCARDIAL INFARCTION

AWMI : ANTERIOR WALL MYOCARDIAL INFARCTION

TR : TRICUSPID REGURGITATION

RCA : RIGHT CORONARY ARTERY

LAD : LEFT ANTERIOR DESCENDING

COPD : CHRONIC OBSTRUCTIVE PULMONARY DISEASE

PS : PULMONARY STENOSIS

AV : ATRIO VENTRICULAR

SA : SINO ATRIAL

RV : RIGHT VENTRICLE

LV : LEFT VENTRICLE

65
AMI : ACUTE MYOCARDIAL INFARCTION

PTCA : PERCUTANEOUS TRANSLUMINAL CORONARY

ANGIOPLASTY

CVA : CEREBRO VASCULAR ACCIDENT

MCA : MIDDLE CEREBRAL ARTERY

CK : CREATINE KINASE

RAP : RIGHT ATRIAL PRESSURE

PCWP : PULMONARY CAPILLARY WEDGE PRESSURE

JVP : JUGULAR VENOUS PRESSURE

RBBB : RIGHT BUNDLE BRANCH BLOCK

LAHB : LEFT ANTERIOR HEMI BLOCK

66
ANF : ATRIAL NATRIURETIC FACTOR

67
 MASTER CHART

SYMPTOMATOLOGY

1 2 3 4 5 6 7 8 9 10 11 1 1 1 1
2 3 4 5

1 MAQSOOD 45 M 6.07.23 7.00 N 4409 + + + - - + -

a.m. S 1

2 MUSHTAQ CH. 66 M 12.07.23 9.00 N 4611 + - + - - + +

a.m. S 6

3 HAFIZ GULL 60 M 15.07.23 10.00 N 4662 + - + + - - -

KHAN a.m. S 6

4 HABIBA 65 F 25.07.23 7.00 S 4697 + + + - - - -

IKRAM a.m. 9

5 SAHIB JAN 64 M 25.07.23 10.00 S 567 + - - - - + -

a.m.

6 WAJIHA 72 F 26.07.23 10.05 S 3721 + - + + + - +

ZAMAN p.m.
7 ABDULLAH 63 M 28.07.23 7.40 N 4097 + + + - - + -
a.m. S

8 RAJA 68 M 29.07.23 12.20 S 4397 + - - + + + +

TABASUM p.m.

9 MUJAHID 60 M 30.07.23 3.30 N 4722 + - + - - - -

AWAN a.m. S

10 ISHAQ 74 M 1.08.23 3.00 S 5406 + + - - - - -

GILLANI a.m.

11 SHAHID 60 M 02.08.23 3.50 S 5407 + - - + - + -

a.m.

12 AHMAD 53 M 04.08.23 9.30 S 6050 + - + - - - -

MUSHTAQ a.m.

13 NOOR GILLANI 55 M 06.08.23 6.35 N 6250 + - + - - + -

a.m. S

14 GULLAB DIN 45 M 12.08.23 7.40 N 6508 + + + + - - -

a.m. S

15 SHAZAD 48 M 17.08.23 2.30 N 6778 + + + - - + -

p.m. S

16 SAKEEB 41 M 19.08.23 10.15 N 7469 + + + - - - -

MUGHAL a.m. S

11.25 N
17 MANI KHAN 38 M 21.08.23 7813 + + + - - + -
a.m. S
 SYMPTOMATOLOGY

1 2 3 4 5 6 7 8 9 10 11 1 1 1 1
2 3 4 5

18 ASHIQ 47 M 26.08.23 7.00 N 7922 + + + - - + -

HUSSAIN a.m. S

19 SYED ISMAIL 48 M 29.08.23 3.00 N 8244 + + + - - + -

a.m. S

20 MAHIRA BIBI 82 F 30.08.23 11.20 S 8463 - - - - + + +

a.m.

21 MUJHID 55 M 31.08.2023 1.40 S 8767 + + + - - - -

AWAN p.m.

22 GULL KHAN 64 M 01.09.23 3.30 S 9191 + - + - - + -

p.m.

23 HABEEB 55 M 01.09.23 12.30 S 9617 + + + - - - -

a.m.

24 AYESHA BIBI 55 F 02.09.23 12.35 S 1044 + + + - - + -

a.m. 7
25 KAMALA 60 F 02.09.23 11.30 S 1084 + - + + - - +
a.m. 2

26 AHMED 58 M 02.09.23 1.50 S 1126 + - + - - - -

BASHA p.m. 2

27 NOOR UL 49 M 03.09.23 3.45 N 1127 + - + - - - -

ALAM a.m. S 1

28 ARSHAD 50 M 04 .09.23 10.20 S 1182 + + + - - + -

GILLANI a.m. 0

29 MEHMOOD 54 M 04.09.07 9.00 S 1234 + + + - - - -

GILLANI p.m. 3

30 BEGUM 43 F 05.09.2023 4.00 N 1324 + + + - - - -

a.m. S 3

31 BABU 42 M 05.09.2023 9.30 N 1326 + - + - - + -

a.m. S 7

32 MANI 42 M 06.09.2023 11.15 N 1368 + + + - - + -

p.m. S 2

33 SHAKOOR 58 M 07.09.2023 1.20 N 1458 + + + + - - -

a.m. S 6

AHMAD 9.10 N 1541

34 40 M 07.09.2023 + + + - - + -
AWAN a.m. S 6

SYMPTOMATOLOGY
1 2 3 4 5 6 7 8 9 10 11 1 1 1 1
2 3 4 5

35 ASHIQ KHAN 40 M 08.09.2023 2.30 N 1553 + + + - - - -

a.m. S 4

36 MAHBOB 63 M 08.09.2023 8.45 S 1579 + - + + - + -

MUGHAL a.m 0

37 SAQIB ABBASI 74 M 08.09.2023 9.00 S 1582 + + - - + + +

p.m. 0

38 RAJA ILYAS 55 M 09.09.2023 5.45 S 1618 + + + - - - -

p.m. 8

39 TABASSUM 31 M 09.09.2023 9.35 N 1619 + + + - - + -

p.m. S 5

40 SHAFIQ 56 M 10.09.2023 9.00 N 1620 + + - - - - -

a.m. S 0

41 MEHWISH 60 F 10.09.2023 11.00 S 1680 + - + - - - -

p.m. 3

42 MOHD. 48 M 11.09.2023 9.00 N 1870 + + + - - - -

FAROOQ a.m. S 5
43 RAJA ALI 40 M 11.09.23 10.50 N 1915 + - + - - + -
a.m. S 4

44 FAIZ BUTT 40 M 12.09.23 8.20 N 2105 + + + - - - -

a.m. S 4

45 TAJMUL KHAN 42 M 12.09.2023 2.30 N 2172 + - + - - + -

p.m. S 8

46 ASAD RAZA 44 M 12.09.23 10.50 N 2268 + + + - - - -

S 1

47 ABDULKADAR 66 M 13.09.2023 8.25 S 2271 + - + - - + +

a.m. 6

48 GULL NAZZ 63 F 14.7.07 10.30 S 2343 + + + - - + -

a.m. 7

49 ADNAN 78 M 14.09.23 2.45 S 2543 + + + - - + -

KHALIL p.m. 4

50 ANAYA 71 F 15.09.2023 8.00 S 2546 + - + - - - -

a.m. 5

RISK FACTORS FAMILY ON EXAMINATION

HISTORY
 16 1 1 19 2 21 2 23 2 2 26 27 28 2 3 31 3 3 3 3
7 8 0 2 4 5 9 0 2 3 4 5

1 + + + - - + + - + + + 50 80/ + ↑ + - - N -
60

2 - - - - - + + - - - - 80 170/ - N - - - N -
100

3 - + - - - + + - - - - 82 90/ - ↑ + - + N +
50

4 - - - - - - - + - - - 54 130/ - N - - - N -
80

5 - - - - - + - - - - - 78 180/ - N - - - N -
90

6 - - - - - - - + - - - 50 70/ + ↑ + - - N -
50

7 - + + - - + - - - + - 90 160/ - N - PS - N -
80 M

8 - - - - - + - - - - - 110 80/ - ↑ - - - N -
60

9 + + + + - + - - + - + 84 150/ - N - - - N -
70

1 - - - - + - - - - - - 52 80/ - ↑ + - - N -
0 50
1 - + + - - + - - - + - 121 120/ - N - - + N -
1 70

1 - - - - - + - - - - - 84 120/ - N - - - N -
2 80

1 - - - - - + - - - - - 86 130/ - N - - - N -
3 80

1 + + - - + - - - - - 128 110/ - N - - - N -
4 80

1 - + + - - + + - - - - 82 190/ - N - - - N -
5 110

1 - - - - - - - - - - - 80 130/ - N - - - N -
6 80

1 90/
+ + + + + - - - + - + 54 + ↑ - - - N -
7 50

FAMILY
RISK FACTORS HISTORY ON EXAMINATION

16 1 1 19 2 21 2 23 2 2 26 27 28 2 3 31 3 3 3 3
7 8 0 2 4 5 9 0 2 3 4 5
1 - - - - - + + - - - - 42 80/ - ↑ + - - N +
8 60

1 - - - - - + + - - - - 81 116/ - N - PS - N -
9 80 M

2 - - - - - - - + - - - 68 80/ + ↑ + - + N -
0 60

2 - - - - - - - - - - - 91 120/ - N - - - N -
1 80

2 - - - - - + - - - - - 93 110/ - N - - - N -
2 70

2 - + + + + + + - + + + 41 80/ - ↑ + - - N -
3 60

2 - - - - - - - + - - - 84 120/ - N - - - N -
4 70

2 + + + - - - - + + + 40 80/ + ↑ - - - N -
5 50

2 - - - - - + + - - - - 83 140/ - N - - - N -
6 80

2 - - - - - + + - - - - 82 140/ - N - - - N -
7 90

2 - - - - - + - - - - - 41 70/ - ↑ - - - N -
8 50
2 + - - - - - - - + - - 53 80/ + ↑ + - - N -
9 60

3 - + - - - - - - - - - 123 170/ - N - - - N -
0 100

3 + - + - - + + - + - + 74 110/ - N - - - N -
1 80

3 - - - - - + - - - - - 41 80/ + ↑ - - - N -
2 50

3 - - - - - + + - - - - 76 120/ - N - - - N -
3 80

3 130/
- - - - - + - - - - - 84 - N - - - N -
4 80

FAMILY
RISK FACTORS HISTORY ON EXAMINATION

16 1 1 19 2 21 2 23 2 2 26 27 28 2 3 31 3 3 3 3
7 8 0 2 4 5 9 0 2 3 4 5

3 + + + + + - - - + + + 88 170/ - N - - - N -
5 120
3 - + - - - - - - - - - 120 106/ - N - - - N -
6 70

3 - - - - - - - - - - - 81 130/ - N + - - N -
7 80

3 - - - - - - - - - - - 56 110/ - N - - - N -
8 70

3 - + - - - - - - - - - 95 200/ - N - - - N -
9 130

4 + - - - + + + - - - - 94 190/ - N - - - N -
0 100

4 - - - - - - - + - - - 90 130/ - N - - - N -
1 80

4 + + + + - + + - - - - 42 80/ + ↑ - - - N -
2 50

4 - + + - + - - - + + + 86 120/ - ↑ - - - N -
3 80

4 - - - - - - - - - - - 51 100/ - N - - - N -
4 70

4 - - - - - + - - - - - 88 110/ - N - - - N -
5 70

4 - - - - - + + - - - - 85 140/ - N - - - N -
6 90
4 + + - - - + - - + + + 130 110/ - N - - - N -
7 70

4 - - - - - - - + - - - 82 160/ + N - - - N -
8 100

4 - - - - - - - - - - - 83 80/ - ↑ + - - N -
9 60

5 - - - - - - - + - - - 84 150/ - N - - - N -
0 80

COMPLICATIONS

36 37 38 39 40 41

1 IWMI + RVI + - + Second degree AVB Type -

1

2 IWMI - + - _ -

3 IWMI + RVI - + + _ -

4 IWMI - + - _ -

5 IWMI - + - _ -

6 IWMI + RVI + - + CHB +

7 IWMI + DMI - + - _ -

8 IWMI + RVI - + + Second degree AVB Type -

1

9 IWMI - + - _ -

10 IWMI + RVI + DMI + - + Second degree AVB Type -

2

11 IWMI - + - AF -

12 IWMI + DMI + - - Second degree AVB Type -

1

13 IWMI - + - _ -

14 IWMI + - - AF -

15 IWMI + - - Second degree AVB Type -

2

16 IWMI - + - _ -

Second degree AVB Type

17 IWMI + RVI + DMI + - + -
1

COMPLICATIONS
 36 37 38 39 40 41

18 IWMI + RVI + - + CHB -

19 IWMI - + - _ -

20 IWMI + RVI + - + CHB +

21 IWMI - + - _ -

22 IWMI - + - _ -

23 IWMI + RVI + DMI + - + First Degree AVB -

24 IWMI - + - _ -

25 IWMI + RVI + - + CHB -

26 IWMI - + - _ -

27 IWMI - + - _ -

28 IWMI + RVI + - + CHB -

29 IWMI + RVI + - + Second Degree AVB Type -

2

30 IWMI + DMI + - - _ -

31 IWMI - + - _ -

32 IWMI + RVI + - + CHB -

33 IWMI - + - _ -

34 IWMI + DMI - + - _ -
CHB : Complete Heart Block

AVB : Atrio Ventricular Block

LAHB : Left Anterior Hemi Block

RBBB : Right Bundle Branch Block

AF : Atrial Fibrillation

PSM : Pan Systolic Murmur

IWMI : Inferior Wall Myocardial Infarction

RVI : Right Ventricular Infarct

DMI : Dorsal Wall Myocardial Infarction

NS : Non Sedentary

S : Sedentary
 COMPLICATIONS

36 37 38 39 40 41

35 IWMI + - - _ -

36 IWMI + RVI - + - _ -

37 IWMI + RVI + - - First Degree AVB -

38 IWMI - + - _ -

39 IWMI + DMI + - - _ -

40 IWMI - + - _ -

41 IWMI - + - _ -

42 IWMI + RVI + - + CHB +

43 IWMI +RVI - + - First Degree AVB -

44 IWMI - + - _ -

45 IWMI + DMI - + - LAHB -

46 IWMI - + - _ -

47 IWMI + RVI - + - _ -

48 IWMI - + - _ -

49 IWMI + RVI + - + RBBB -

50 IWMI - + - _ -