1

CORRELATION BETWEEN SERUM URIC ACID

AND KILLIP CLASS IN ACUTE MYOCARDIAL
INFARCTION

A Dissertation Submitted to
THE TAMILNADU DR. M.G.R MEDICAL UNIVERSITY
CHENNAI

In Partial Fulfillment of the Regulations

For the Award of the Degree of

M.D. (GENERAL MEDICINE) - BRANCH – I

GOVERNMENT KILPAUK MEDICAL COLLEGE

CHENNAI

MAY 2018
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BONAFIDE CERTIFICATE

This is to certify that “CORRELATION BETWEEN SERUM

URIC ACID AND KILLIP CLASS IN ACUTE MYOCARDIAL

INFARCTION is a bonafide work done by Dr. KARTHIKEYAN V A.

Post graduate student, Department of General Medicine, Kilpauk Medical

College, Chennai-10, under my guidance and supervision in partial

fulfillment of rules and regulations of the TamilNadu Dr. M.G.R Medical

University, for the award of M.D. Degree Branch I (General Medicine)

during the academic period from MAY 2015 To MAY 2018.

PROF. DR. K.V. RAJALAKSHMI M.D.

Guide for the study,
Professor and Head of the Department,
Department of Medicine,
Govt. Kilpauk Medical College,
Chennai.

Prof.Dr. P. VASANTHAMANI,
M.D., D.G.O.,MNAMS.,DCPSY.,MBA
The DEAN
Govt. Kilpauk Medical College
Chennai - 600 010
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DECLARATION

I solemnly declare that this dissertation “CORRELATION

BETWEEN SERUM URIC ACID AND KIILLIP CLASS IN

ACUTE MYOCARDIAL INFARCTION” was prepared by me at

Government Kilpauk Medical College and Hospital, Chennai, under the

guidance and supervision of Prof.Dr.K.V.RAJALAKSHMI, M.D.,

Professor and Head of the Department, Department of Internal Medicine,

Government Kilpauk Medical College and Hospital, Chennai. This

dissertation is submitted to The Tamil Nadu Dr. M.G.R. Medical

University, Chennai in partial fulfillment of the University regulations

for the award of the degree of M.D. Branch I (General Medicine).

Place: Chennai-10 Dr. KARTHIKEYAN V A

Date:
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ACKNOWLEDGEMENT

At the outset, I would like to thank my beloved Dean, Kilpauk

Medical College, Prof.Dr.P.VASNTHAMANI, M.D., D.G.O.,

MNAMS., DCPSY., MBA. for her kind permission to conduct the study

in Kilpauk Medical College.

I express my indebtedness to . Dr. K. V. RAJALAKSHMI M.D.

my thesis guide and Professor & HOD of Medicine for her continuous

motivation, affectionate guidance, valuable suggestions, sympathetic,

helping nature and encouragement enabled me to complete the

dissertation.

I am extremely thankful to my unit Assistant Professors,

Dr.M.Bathragiri, M.D., Dr.T. Mohanasundaram MD.,

Dr.P.Boopathy Rajan, M.D., D.T.C.D., for their valuable suggestions

and guidance.

I sincerely thank Dr.V.Meera, M.D.,D.G.O., Professor and head

of the department, Department of Biochemistry, Kilpauk Medical

College, for providing valuable time, knowledge & assistance without

which it would not have been possible to have this study started.
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I would always remember with extreme sense of thankfulness for

the valuable time, co-operation , criticism and support provided by my

fellow post graduates, juniors , C.R.R.I’s and friends.

I also extend my thanks to all the laboratory technicians for their

valuable support throughout my dissertation work.

I would like to take this opportunity to show gratitude to my

friends & family for their never ending support in completing this thesis.

Finally, I wholeheartedly thank all my patients for their active

cooperation in this study, without whom this would not have become a

reality.
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CERTIFICATE – II

This is to certify that this dissertation work titled entitled

dissertation “CORRELATION BETWEEN SERUM URIC ACID

AND KIILLIP CLASS IN ACUTE MYOCARDIAL INFARCTION”

of the candidate Dr.KARTHIKEYAN V.A. with Registration Number

201511156 for the award of M.D degree in the branch of GENERAL

MEDICINE. I personally verified the urkund.com website for the

purpose of plagiarism check. I found that the uploaded thesis file contains

from introduction to conclusion pages and result shows 5% of

plagiarism in this dissertation.

Guide & Supervisor sign with Seal.

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LIST OF ABBREVATIONS

ACS Acute coronary syndrome

AHA American Heart Association
ACC American college of Cardiology
cTn Cardiac troponin
CABG Coronary Artery Bypass grafting
CHF Congestive heart failure
ECG ElectroCardioGram
ESC European Society of Cardiology
EF Ejection Fraction
LAD Left Anterior Descending artery
LCX Left Circumflex artery
LCA Left Coronary Artery
LBBB Left Bundle Branch Block
MI Myocardial Infarction
STEMI ST Elevation Myocardial Infarction.
NSTEMI Non ST Elevation Myocardial Infarction
AWMI Anterior Wall Myocardial Infarction
LWMI Lateral Wall Myocardial Infarction
IWMI Inferior Wall Myocardial Infarction
RVMI Right Ventricular Myocardial Infarction.
Trop Troponin
UA Unstable Angina
TIMI Thrombolysis In Myocardial Infarction
WHO World Health Organization
CK Creatine Kinase
S3 Third Heart Sound
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CONTENTS

S.No CONTENTS PAGE No.

1 INTRODUCTION 1

2 AIM AND OBJECTIVES 3

3 REVIEW OF LITERATURE 4

4 MATERIALS AND METHODS 53

5 STATISTICS & RESULTS 58

6 DISCUSSION 73

7 CONCLUSION 75

8 BIBLIOGRAPHY

9 ANNEXURES

 PROFORMA

 MASTER CHART

 CONSENT FORM

 ETHICS COMMITTEE APPROVAL

CERTIFICATE
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INTRODUCTION

Coronary Artery disease is epidemic in our country. It is reported

that CHD accounts for 32% of adult death in 2010-2013 in our country.

In India there has been 4 fold increase in prevalence of coronary heart

disease in last 40 year. Important risk factors are diabetes, hypertension,

smoking, dyslipidemia, abdominal obesity, unhealthy diet, physical

inactivity. Rapid urbanisation and change in life style in last two decade

have led to growing burden of coronary heart disease.

Acute Coronary Syndrome (ACS) is a broad collection of condition

 Acute Myocardial Infarction which manifest either as ST Elevation

MI (STEMI) and Non ST Elevation myocardial infarction

(NSTEMI).

 Unstable angina( UA).

Notably, the clinical presentation and symptoms may be similar

for all these syndromes.

The primary goals of treatment in ACS are relieve or limit

ischemia, prevent reinfarction, improves outcome and well being.

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Acute Myocardial infarction manifests as either ST segment

elevation myocardial infarction (STEMI) or Non ST segment elevation

myocardial infarction (NSTEMI).Risk stratification of acute myocardial

infarction are done by various clinical assessment and score .KILLIP

Classification is used assess the severity and prognosis in acute

myocardial infarction .Serum uric acid which is a metabolite of purine

often used as a biomarker of inflammation. Hyperuricemia are associated

with various diseases such as chronic kidney disease, stroke,

cardiovascular disease. The purpose of this study is to assess the

correlation between serum uric acid and killip class in acute myocardial

infarct.
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AIM AND OBJECTIVES

AIM:

To study the association between Serum Uric acid level and killip

class in acute myocardial infarction.

OBJECTIVES

1. To assess the serum uric acid in level in acute myocardial

infarction.

2. To study the association between serum uric acid level an killip

class in acute myocardial infarction

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REVIEW OF LITERATURE

ACUTE MYOCARDIAL INFARCTION

The current universal definition for acute myocardial infarction

adopted by ESC/ACF (American Cardiology Foundation) as evidence of

myocardial necrosis in a clinical setting consistent. Under these

condition any of following criteria meet the diagnosis of MI

1. Detection of rise and/or fall in cardiac biomarkers preferably

troponin c with at least one value above the 99 th percentile of upper

reference limit with one of the following

 Ischemic symptoms.

 New significant ST segment T wave changes or new left bundle

branch block.

 Pathological Q wave on the ECG.

 Imaging evidence of new loss of viable myocardium or regional

wall motion abnormality.

 Intracoronary thrombus identification by angiography or autopsy.

2. PCI related MI-Elevation of cardiac troponin to >5 times of 99th

percentile of upper normal limit.

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3. CABG related MI-Elevation of cardiac troponin to >10 times of

99th percentile of the upper normal limit.

The patients included in acute myocardial infarction are either have

 ST segment elevation MI(STEMI)

 Non ST segment elevation MI(NSTEMI).

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EPIDEMIOLOGY

 Acute Myocardial Infarction is the leading cause of mortality in

both developed and developing nation such as India.

 A significant proportion of these patients will die from sudden

cardiac death due to ventricular arrhythmia prior to arriving at the

hospital.

 The success of the medical community’s concerted efforts has led

to 26% reduction in mortality since 1990

 The risk factors are hypertension, diabetes, smoking, dyslipidemia,

abdominal obesity, sedentary life style, male gender.

 90% of acute myocardial infarction are attributed to modifiable risk

factors.

 Overall survival rates in majority of good Indian centers are >

90%.

 There are various predictors of mortality in acute myocardial

infarction such as killip class,TIMI score by baseline clinical data.

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BLOOD SUPPLY OF HEART

 Coronary artery are the first branch that arises from the aorta, it

arise from the sinuses of Valsalva just above the aortic valve.

 Right coronary artery (RCA) arises from the anterior sinus

and supplies

1. Right atrium.

2. Greater part of Right ventricle.

3. Posterior region of inter ventricular septum

4. Conduction system in 40% of the patients

5. Small part of left ventricle adjacent to posterior inter ventricular

groove.
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 Left coronary artery (LCA) arises from left posterior sinus,

divides into the left anterior descending artery and circumflex

artery. It supplies

1. Left atrium.

2. Greater part of left ventricle.

3. Anterior region of interventricular septum

4. Small part of right ventricle adjacent to anterior inter ventricular

groove.

5. Part of left branch of AV bundle.

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PATHOPHYSIOLOGY OF STEMI

 STEMI occurs due to sudden decrease in coronary blood flow after

thrombotic occlusion of coronary artery.

 STEMI occurs when coronary artery thrombus develops quickly at

the site of vascular injury produced by various factors such as

smoking, hypertension, accumulation of lipid.

 In many cases atherosclerotic plaque surface will be disrupted

which leads to thrombogenesis by activation of coagulation

cascade, generation of thromboxane A2, activation of platelets.

 Other condition that can cause STEMI are

1. Severe coronary vasospasm.

2. Coronary artery embolisation.

3. Spontaneous coronary dissection.

 These conditions should be considered in a patient whose clinical

findings suggest a process other than acute plaque rupture.

 The factors responsible for myocardial damage are territory

supplied by culprit vessel, duration of occlusion, percentage of

occlusion, blood supplied by collaterals, myocardial oxygen

demand,
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PATHOPHYSIOLOGY OF NSTEMI

 Pathogenesis of NSTEMI four processs:

1. Rupture of unstable atheromatous plaque.

2. Vasoconstriction of coronary artery.

3. Imbalance between myocardial oxygen supply and demand

4. Gradual intra luminal narrowing of epicardial coronary artery

 Plaque ruptue or erosion leads to formation of superimposed

thrombus along with impaired myocardial perfusion and

vasoconstriction leads to myocardial necrosis.

 Activation of coagulation cascade and platelet plays a important

role in both STEMI and NTEMI.

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SPECTRUM OF ACUTE CORONARY SYNDROME

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ATHEROSCLEROSIS

 Endothelial cells activated by risk factors which include

hyperlipoproteinemia, usually express adhesion and chemo

attractant molecules, recruit inflammatory leucocytes such as

monocytes and T lymphocytes. Extracellular lipid begins to

accumulate in intima.

 Fibrofatty stage- monocyte recruited to artery wall becomes

macrophages and express scavenger receptors that bind modified

lipoproteins. Macrophages become lipid laden foam cells by

engulfing modified lipoproteins. Leucocytes and resident vascular

wall cells can secrete cytokines and growth factors that increase

leucocyte migration and smooth muscle cell migration and

proliferation.

 As lesion progress, inflammatory meditors causes expression of

tissue factors, a potent pro-coagulant and matrix degrading

proteinases that weaken fibrous cap of plaque.

 When fibrous cap rupture at the point of weakness,coagulation

factors have access to thrombogenic tissue factors causing

thrombosis and non occlusive plaque.

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 If balance between prothrombotic and firinolytic mechanism

prevailing at that particular region and at that particular time is

unfavourable occlusive thrombus causing myocardial infarction.

FEATURES OF VULNERABLE PLAGUE:

Lipid rich core ( > 30-40% of plague).

Fibrous cap covering the lipid rich core.

Thikness of plague<100 µm.

Many macrophages.

Few smooth muscle cells.

Outward remodelling preserving the lumen.

Neovascularisation from vasa vasorum.

Adventitial/perivascular inflammation.
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CLINICAL FEATURES

 Predisposing factors

1. 50% of the patients with STEMI usually have an identifiable

precipitating factors and prodromal symptoms.

2. Unusually heavy exercise and emotional stress would precipitate

STEMI.

3. Other precipitating factors are lung infections, hypoxemia,

pulmonary embolism, hypoglycaemia, administration of ergot,

serum sickness, sympathomimetics, allergy.

4. Onset of STEMI have a circadian periodicity, with peak incidence

of events occurring in the morning, these early morning hours are

associated with increase cortisol and catecholamines, aggregation

of platelet. These circadian rhythm will be absent in patients on

beta blockers and aspirin.

 Symptoms

1. Chest pain generally lasts more than half an hour, pain usually

described as constricting, crushing, compressing or sensation of

heaviness on chest.
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2. Chest pain localised to retrosternal region and spread to both

anterior chest wall commonly left side, pain radiates to left

shoulder, neck, jaw and interscapular region.

 Nausea and vomiting can occur, due to vagal reflex activation,

stimulation of left ventricular receptors. This symptoms are

commonly seen inferior wall myocardial infarction. This

symptoms can be confused with gastritis, peptic ulcer,

cholecystitis.

 Other associated symptoms are dizziness, palpitations, cold

perspiration, sense of impending doom.

 ATYPICAL PRESENTATION

1. Features of heart failure.

2. Classical angina pain.

3. Atypical pain location.

4. Sudden onset of mania and psychosis

5. Syncope.

6. Features resembling of stroke.

7. Apprehension and nervousness.

 Clinical features of NSTEMI resembles same as STEMI.

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PHYSICAL EXAMINATION

 Physical examination is important in determining other sources of

chest pain, assessing prognosis and establishing a baseline that will

aid in early recognition of complications.

 The goal is to determine hemodynamic instability, presence of

cardiogenic pulmonary edema, or mechanical complication such as

papillary muscle dysfunction, free wall rupture, ventricular septal

defect and to exclude other causes of chest pain.

 Physical examination should include intial assessment of vital

signs,oxygenation, bilateral blood pressure and jugular venous

pulse, bilateral crepitation for pulmonary edema, murmur or

friction rub and gallop for mechanical complication and heart

failure, and neurological examination.

 Fundus examination may provide underlying vascular status due to

hypertension and diabetes. Abdomen examination may provide

right heart failure features such as hepatomegaly and positive

abdominojugular reflex. Examination of extremities will be useful

in identifying peripheral vascular disease and cyanosis in severe

LV failure.
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DIAGNOSTIC TESTS

ELECTROCARDIOGRAM (ECG)

 The ECG should be performed and interpreted within 10 mins of

presentation.

 Serial standard 12-lead ECG is extremely useful in detection and

localisation of myocardial infarction

 Analysis of the constellation of ECG showing ST changes will be

useful in identifying the site of occlusion in the infarct artery.

 In addition to diagnostic and prognostic information,serial 12-lead

ECG monitoring will provide non invasive information about the

success of reperfusion therapy.

 ECG CRITERIA FOR DIAGNOSIS STEMI:

 New ST ELEVATION at J point in two or more contiguous

leads with (in the absence of LBBB)

 >1mm(.1Mv ) in all leads except V2-V3.

 In leads V2-V3 - >2mm(.2mv) in men > 40 years of age.

>2.5mm(.25mv) in men <40 years of age.

>1.5mm(.15mv) in women.
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 In the setting of an old LBBB, acute myocardial infarction is

diagnosed by Sgarbossa criteria

1. ST-segment elevation >1mm and concordant with

QRS complex-5 points.

2. ST-segment depression >1mm in lead V1,V2,V3 -3

points.

3. ST-segment elevation >5mm and discordant with QRS

complex-2points.

 Score more than 3 has specificity of 98% for acute myocardial

infarction.
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 ECG CRITERIA FOR DIAGNOSIS OF NSTEMI

1. New ST- segment depression ( downsloping or horizontal )

>0.05mv in two contiguous leads.

2. T-wave inversion >.1mv in two contiguous leads with prominent R

wave

or with R/S ratio >1

LOCALISATION OF MI.
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EXTENSIVE ANTERIOR WALL MI.

ACUTE LATERAL WALL MI

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ACUTE INFERIOR WALL MI

NSTEMI OF ANTERIOR WALL

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LEFT BUNDLE BRANCH BLOCK.

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 Posterior myocardial infarction is an entity that is often

unrecognized, it should be suspected in the patients with inferior of

lateral wall myocardial infarction.

 The “reverse mirror test” is useful to identify posterior wall

myovardial infarction, ST segment depression in leads V1to V3 is

actually a ST elevation in posterior wall. The prominent R wave is

actually represent posterior Q wave.

 Inferoposterior or inferolateral myocardial infarction involves the

right coronary artery(RCA) or left circumflex obtuse marginal

branch.

 There are condition that mimic electrocardiographic changes of

myocardial infarction, it is termed as “pseudoinfarction”. They are

1. Ventricular hypertrophy.

2. Preexitation syndrome.

3. Primary myocardial disease.

4. Pneumothorax, Pulmonary embolism.

5. Primary and metastatic tumors of heart.

6. Amyloid disease, cardiac sarcoidisis.

7. Intracranial hemorrhage.

8. Hyperkalemia.

9. Pericarditis.
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IMAGING

CHEST RADIOGRAPHY:

 A standard chest radiography ( CXR ) should be included in

initial evaluation. Pulmonary edema in CXR us important

prognostic and therapeutic implications. prominent vascular

markings in CXR reflects elevated LV end diastolic pressure.

ECHOCARDIOGRAPHY:

 The evaluation of a patient with a non diagnostic ECG, Finding

of echocardiography such as regional wall motion abnormality

can support the diagnosis of myocardial infarction. It also useful

in localising the territory at risk.

 LV function assessed in echocardiography correlates well with

measurements in angiography are useful in establishing

prognosis in myocardial infarction.

 Echocardiography can help in detecting in mechanical

complication of MI such as mitral regurgitation, ventricular

septal rupture, cardiac tamponade.

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CARDIAC BIOMARKERS

Markers of myocardial necrosis:

Myocardial injury can be detected by presence of circulating

proteins in serum which is released by damaged myocardium. Most

commonly used serum markers are cardiac specific troponin and creatine

kinase MB.

Cardiac specific troponins:

The preferred marker to detect myocardial injury is cardiac

troponin which consists of three subunits that regulate calcium mediated

contractile process of striated muscle. Troponin I binds to actin and

inhibits interaction of actin-myosin. Troponin T binds to tropomysin

thereby attaching the troponin complex to thin filaments. Only cardiac

specific isoforms of troponin T(cTnT) and troponin I(cTnI) are

exclusively expressed in cardiac myocyte.

In myocardial infarction, cardiac specific troponin T and I begin to

rise 3 hours after onset of chest discomfort. It may persist for 7 to 10 days

in myocardial infarction patients because of continuous proteolysis of

contractile apparatus in necrotic myocardium.

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Other causes of elevated troponin are myocarditis, pericarditis,

cardiac contusion/trauma, aortic dissection, endocarditis, post cardiac

arrest, pulmonary embolism, cardiac arrhythmia, sepsis, renal failure.

Creatine kinase MB:

Creatine kinase MB can be used as a alternative assay in the

absence of cardiac troponin assay. Even improve test system for

quantitative determination of creatine kinase MB based on

immunological determination did not substantially increase the sensitivity

for detection of minor myocardial injury.

Other biomarkers:

C-reactive proteins and BNP assay can be used for risk

stratification but there is no clear guidance available for specific

therapeutic maneuvers in the setting of myocardial infarction in response

to these biomarkers.

Other laboratory investigations:

Serum lipid profile should be done in all patients with acute

myocardial infarction within 24hours of symptoms. Ratio of total

cholesterol to HDL cholesterol is no longer used for risk assessment.

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Elevation in WBC count usually occurs after 2 hours of chest pain,

reaches the peak 2 to 4 days after infarct and returns to normal range in 7

days. increased risk of adverse outcome are seen in patients with higher

WBC count in patients with acute MI. The haemoglobin value at time of

admission with myocardial infarction independently predicts major

cardiovascular events.
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RISK STRATIFICATION :

Whereas risk factors for the development of atherothrombosis

provides in insights into disease mechanism and the opportunity for

primary and secondary prevention therapy, analysis of risk for adverse

outcome after presentation is important in guiding management and

therapeutic decisions.

Analysis usually uses a combination of various clinical, ECG and

biochemical parameter. Five simple baseline parameter can be used to

predict 30-day mortality more than 90% of patients:

1. Age.

2. Systolic blood pressure.

3. Killip class.

4. Heart rate.

5. Localisation of infarct.
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KILLIP CLASSIFICATION

KILLIP class was proposed by Thomas killip III and John Kimball

in 1967 involved bedside stratification. This risk stratification was based

on bedside clinical examination in patients with acute myocardial

infarction and it is used to identify who are at highest risk of death and

potential benefits of specialised care in intensive coronary care unit.20

 Killip I: with no clinical signs of heart failure.

 Killip II: with rales in the lungs, third heart sound (S3), and

elevated jugular venous pressure

 Killip III: with acute pulmonary edema (APE).

 Killip IV: with cardiogenic shock or arterial hypotension

(measured as systolic blood pressure < 90 mmHg), and evidence of

peripheral vasoconstriction (oliguria, cyanosis, and diaphoresis).

The 30 day mortality rate of killip class are

Killip I: 6% of mortality.

Killip II: 17% of mortality.

Killip III: 38% of mortality.

Killip IV: 81% of mortality.20

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The other classification used in acute myocardial infarction are

 Simplified forrester & Diamond hemodynamic

classification(STEMI).

 The GRACE risk score for Acute Coronary syndrome (not

STEMI alone).

 TIMI(The Thrombolysis In Myocardial Infarction) score.

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SIMPLIFIED FORRESTER CLASSIFICATION

TIMI SCORE.
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The Grace risk score for ACS:

GRACE score calcultes mortality rate in hospital and 6 month in

acute coronary syndrome.

It uses data like

 Enzyme elevation.

 Pci done/ not.

 Serum creatinine.

 Killip class.

 ST depression.
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INFARCT LOCATION

 Prognosis of myocardial infarction is also related to extent of

myocardium at risk and also site of coronary occlusion.the ECG

reflects the infarct location( TABLE 2). Patients with left main

stem occlusion rarely reaches the hospital for reperfusion therapy.

 Occlusion of proximal left anterior descending artery proximal to

first septal branch is assocated with high early and late mortality (

window- maker).

 Large inferior wall myocardial infarction result of dominant right

coronary artey occlusion are also a high risk especially when right

ventricle is involved.

 Other location such as apical due to distal left anterior descending

artery, lateral myocardial infarction due to diagonal branch

occlusion or small inferior wall infarction due to distal right or

circumflex occlusion have better outcome.

 Strictly posterior wall myocardial infarction may escape routine

ECG leads or evident only by st depression in V1- V4 usually have

a good outcome.
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TREATMENT

Treatment of STEMI:
PRE HOSPITAL CARE:

In STEMI, pre hospital care has a very important role because

many deaths occur within one hour of onset that usually results from

ventricular fibrilliation. So immediate of resuscitative action and quick

transportation to hospital is very important. Emergency medical service

system should have three components: emergency medical dispatch, first

response and EMS ambulance service. The EMS should have expanded

capability to record a pre hospital 12- lead ECG.

GENERAL TREATMENT:
Aspirin:

Aspirin is very effective in all acute coronary syndrome. It is initial

management strategy for all patients with suspected STEMI. In order to

achieve therapeutic blood level,162 to 325 mg tablet should be chewed to

increase buccal absorption.

 46

Pain management:

Most commonly used analgesics in myocardial infarction are

morphine, pentazocine, mepiridine. The ideal dose of morphine in

STEMI is 4 to 8mg in intravenous route repeated at interval of 5 to 15

minutes. It also has beneficial effect in acute pulmonary edema because

of peripheral arterial and venous dilatation.

Nitrates:

Their ability to enhance blood flow of coronaries and to decrease

preload by venodilation, sublingual nitrates are indicated in acute

coronary syndrome once hypotension and right ventricular infarct were

ruled out.

Beta blockers:

This drug reduces the pain, prevent life threatening arrhythmia, and

also reduces infarct size. Beta blockers are contraindicated in patients

with hypotension, bradycardia or patients with significant heart block.

Metoprolol is common drug used in this category.

 47

Oxygen:

Hypoxemia is common in STEMI due to ventilation-perfusion

abnormality as a sequelae of left ventricular failure. So patients should be

treated with oxygen for a period of 24 to 48 hours. Patients with severe

pulmonary edema may need endotracheal intubation and mechanical

ventilation in order to correct hypoxemia.

 48

Reperfusion therapy:

Fibrinolysis:

It recanalizes the coronary artery thrombotic occlusion, thereby it

resore the coronary flow and reduces infarct size. Fibrinolysis improves

both short term and long term survival.

Assessment of reperfusion done by TIMI flow grade, TIMI frame

count, electrocardiogram, echocardiography.

TIMI flow grade-when assessed after 60 to 90 minutes after

fibrinolytic therapy TIMI grade 3 has lowest mortality and grade 0 and 1

has highest mortality.

In ECG, resolution of ST segment is a strong predictor of positive

outcome.
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CONTRAINDICATION FOR FIBRINOLYTICS

Absolute contraindication are

 Previous intracranial hemorrhage (ICH).

 History of structural cerebral vascular lesion.

 History of intracranial malignancy.

 Ischemic stroke within 3 month of period.

 Suspicion of aortic dissection.

 Active hemorrhage or bleeding diathesis (excluding menses).

 History of head injury or facial injury within 3 months.

 Recent Intracranial, intraspinal surgery within 2 months.

 Severe uncontrolled hypertension ,not responding to

emergency management.

 For streptokinase, prior treatment in previous 6 months.

Relative contraindication are

 History of intracranial pathology.

 Previous ischaemic stroke > 3 months.

 Recent history of trauma.

 Prolonged CPR more than 10 minutes.

 Major surgery < 3 weeks.

 Active peptic ulcer disease.

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 Recent internal bleeding within 2 to 4 weeks.

 Systolic BP >180, Diastolic > 110mm Hg.

 History of severe or poorly controlled blood pressure.

 Dementia.

 History of non compressible vascular puncture such as IJV and

subclavian lines.
 51

Percutaneous coronary intervention(PCI):

Current recommendations according to ACC/AHA guidelines in STEMI:

Primary PCI

 symptoms of STEMI within 12 hours.

 Severe heart failure and cardiogenic shock

 Contraindications for thrombolysis with symptoms of STEMI

Delayed PCI:

 Fibrinolytic failure

 Hemodynamically stable stenosis after 24 hours of symptoms.

 52

Treatment of NSTEMI:
 53

Complications of myocardial infarction:

Complication of acute myocardial infarction include mechanical,

ischemic, arrhythmic, embolic and inflammatory.

Circulatory failure, one of the mechanical complications is the mos

common cause of death in acute myocardial infarction.

Mechanical complications:

 Cardiac failure.

 Cardiogenic shock.

 Mitral valve regurgitation.

 Papillary muscle dysfunction.

 Ventricular septal rupture.

 Free wall rupture.

Ischemic:

 Angina.

 Reinfarction.

 Extension of infarct.
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Arrhythmic complication:

 Atrial and ventricular arrhythmia .

 Sino nodal or AV nodal dysfunction.

Embolic complication:

 Peripheral and central nervous system embolism.

Inflammatory:

 Pericarditis.

 Dressler’s syndrome.
 55

SERUM URIC ACID IN ACUTE MYOCARDIAL

INFARCTION

Uric acid-production and metabolism:

 Uric acid production and metabolism is a complex processes

involving various factors that regulate hepatic production, as well

as renal and gut excretion of this compound.

 Uric acid is the end product of exogenous and endogenous purine

metabolism.19

 The exogenous pool varies significantly with diet, and animal

proteins contribute significantly to purine pool

 The endogenous production of uric acid is mainly produced from

the liver, intestines and other tissues like muscles,kidneys and the

vascular endothelium.

 The chemical formula of Uric acid is C5H4N4O3 (7,9-dihydro-

1H-purine-2,6,8(3H)-trione)

 Molecular weight of uric acid is 168 Da.19

 Various enzymes are involved in the conversion of the two purine

nucleic acids, adenine and guanine, to uric acid.

 First step, adenosinemonophosphate (AMP) is converted to inosine

by two different mechanisms; either by removal of an amino group

 56

by deaminase to form inosine monophosphate (IMP) then

followed by dephosphorylation with nucleotidase to form inosine,

or by removal of a phosphate group by nucleotidase to form

adenosine then followed by deamination to form inosine.

 Guanine monophosphate (GMP) is converted to guanosine by the

enzyme nucleotidase.

 The nucleosides, inosine and guanosine, then converted to purine

base hypoxanthine and guanine, respectively by enzyme purine

nucleoside phosphorylase (PNP).

 Hypoxanthine is then oxidized to form xanthine by enzyme

xanthine-oxidase(XO), and guanine is deaminated to form xanthine

by the enzyme guanine deaminase.

 Xanthine is again oxidized by xanthine oxidase to form the final

product, uric acid.

 57

 At physiologic pH, uric acid is a weak acid with pKα of 5.8. Uric

acid exists majorly as urate, which is the salt of uric acid. When

urate concentration increases in blood, uric acid crystal formation

increases.

 The normal value of uric acid in human blood is 1.5 to 6.0mg/dL in

women and 2.5 to 7.0 mg/dL in men.

 The solubility of uric acid in water is low, and in humans, the

average concentration of uric acid in blood is close to the solubility

limit (6.8 mg/dL). When the level of uric acid is higher than 6.8

mg/dL, crystals of uric acid form as monosodium urate (MSU).19

 Uric acid concentration can be measured in serum, plasma, urine

and also in exhaled breath condensate.

 Various methods are

1. phosphotungistic acidmethods (PTA).

2. Uricase methods.

3. High-performance liquid chromatography methods.

4. Dry chemistry systems and biosensor methods.

 The production and catabolism of purines are relatively constant

between 300 and 400 mg per day. Two third of uric acid is excreted

by kidney and remaining one third is excreted by gastrointestinal

tract.
 58

URIC ACID AND CARDIOVASCULAR DISEASE

An association between high uric acid and cardiovascular disease

has been reported in the 19th century itself. Since then number of studies

have been conducted and supported this relationship and considered uric

acid as an independent risk factor for cardiovascular events, such as

coronary vascular disease, cerebrovascular disease, and congestive heart

failure in high risk population (subjects with diabetes mellitus,

hypertension, hyperlipidemia) However, the importance of a link between

high uric acid and cardiovascular events in the general population still

remains to be clarified.

Chen JH, Chuang SY, Chen HJ, Yeh WT, Pan WH et al repored a

study involving a large group of patients with hypertension and/or

diabetes, a serum uric acid level more than 7 mg/dl was associated with

increased cardiovascular mortality12.

Hyperuricemia is also significantly correlated with an increased

mortality rate in patients with congestive heart failure in some studies.11

 59

URIC ACID IN ACUTE MYOCARDIAL INFARCTION:

Many studies were conducted in various places to prove the

association of uric acid in acute myocardial infarction in predicting

mortality and severity. Some studies have shown close relationship

between serum uric acid and killip class in acute myocardial infarction.

1. C.-W. Liu et al. / International Journal of Cardiology 226 (2017)

Relationship of serum uric acid and Killip class on mortality after

acute ST-segment elevation myocardial infarction and primary

percutaneous coronary intervention.Hyperuricemia increased the1-

year mortalityof STEMI patients in Killip class I, but not of

patients in Killip classes II–IV. An interaction of hyperuricemia and

Killip class significantly affects the mortality of STEMI patient.

2. Study of serum uric acid level in patients of acute myocardial

infarction 1Dr.Anil Katdare, 2 Dr.A.L.Kakrani, 3Dr.Sridevi, 4

Dr.Vivek Vilas Manade. This hospital based case study was

performed in the parent institute. A total of 75cases of Acute MI

were studied. Mean SUA for discharged patients was 4.67 ±1.95

/dl and it was 7.1±1.45 mg/dl for the patients who died in the

hospital. There was correlation between serum uric acid level after

acute myocardial infarction and age and body mass index.

 60

The causes of increased serum uric acid level in acute myocardial

infarction:

 Uric acid are produced in endothelium by rapid degradation of

adenosine which is synthesized in vascular smooth muscle, then

undergo rapid efflux to the vascular lumen due to low intracellular

pH and negative membrane potential.

 The activity of xanthine oxidase and production of uric acid is

increased in ischaemic condition hence elevated uric acid can be

used as a marker of tissue ischaemia.10

 Hyperuricaemia is also associated with some harmful effects on

endothelial dysfunction, oxidative metabolism, platelet
adhesiveness, haemorheology, and aggregation.

 Some study suggest that uric acid may also have a negative effect
on cardiovascular disease by causing inflammation, which is
clearly involved in the pathogenesis of cardiovascular disease.

 Uric acid, as a general marker of cell death and hyperuricemia is

associated with obesity, dyslipidemia, hypertension, insulin
resistance, male gender, aging, menopause, excessive alcohol
intake and diuretic use.

 Elevated Uric acid level reflects increased xanthine oxidase

pathway activity, which has the ability to contribute in the
progression of left ventricular dysfunction by interfering with
myocardial energetics and myofilament calcium sensitivity.
 61

SUMMARY

Acute myocardial infarction is life threatening condition. Prompt

action is essential as it has very high mortality in hospital and long term

mortality and morbidity. So risk stratification forms the crux of

management protocol since physicians has to know which patients are

likely to develop serious and life threatening complications.

Killip class is a bed side assessment test which is useful in

predicting mortality in acute myocardial infarction. Hyperuricemia is

associated in increased cardiovascular mortality in high risk patients.

There are few studies which states the association between killip class

and uric acid level.So our goal is to find out the any quantal relationship

between killip class and serum uric acid in acute myocardial infarction in

our population.
 62

MATERIALS AND METHODS

STUDY DESIGN:

Cross sectional study (Descriptive)

STUDY PERIOD:

Data collection done for a period of 6 months between april 2017

to september 2017

PLACE OF STUDY:

Govt.Kilpauk Medical College and hospital, Chennai-10.

STUDY POPULATION:

Patients >18 years of age with STEMI or non-ST segment

elevation MI (NSTEMI) on the basis of history, clinical examination,

electrocardiographical changes and biochemical markers.

SAMPLE SIZE : 70
 63

INCLUSION CRITERIA :

Patients >18 years of age with -STEMI or non-ST segment

elevation MI (NSTEMI) on the basis of history, clinical examination,

electrocardiographical changes and biochemical markers.

1. History ( resting chest pain lasting more than30 min)

2. Electrocardiographical changes

 New or presumed new significant ST-segment T-wave (ST-

T) changes or new left bundle branch block

(LBBB),Development of pathologic Q waves in the

electrocardiogram(ECG)

3. Imaging evidence of new loss of viable myocardium or new

regional wall motion abnormality

4. Biochemical markers:

 Rise of serum cardiac enzymes concentration (CK-MB and

Troponins).
 64

EXCLUSION CRITERIA :

 Patients with a condition known to elevate SUA level (eg,

chronic kidney disease, gout, hematological malignancy,

hypothyroidism, hyperparathyroidism)

 Patients taking drugs that increase SUA

salicylates [>2 g/day], ethambutol, amiloride, bumetanide,

chlorthalidone, cisplatin, cyclophosphamide, cyclosporine,

ethacrynic acid, thiazide diuretics, furosemide, indapamide,

isotretinoin, ketoconazole, levodopa, metolazone,

pentamidine, phencyclidine, pyrazinamide, theophylline,

vincristine or vitamin C.
 65

METHODOLOGY

 Patients more than 18 years of age diagnosed to have acute MI

who presented to hospital within 24 hours of onset of symptoms

were included in the Study.

 Patient with increased myocardial enzyme concentrations with

typical chest pain persisting more than 30 minutes with

1. electrocardiographic changes (including ischemic ST-

segment depression, ST-segment elevation or pathologic Q

waves).

2. Increased enzyme concentrations were defined as ( Creatine

kinase,Troponin) peak level more than 2 times upper limit of

normal.

 Complete history taking and physical examinations was done,

patient with exclusion criteria was identified and excluded in the

study.After getting informed consent from the patient, they were

included in study.

 The data of each patient will be collected in a special

proforma,which includes patient’s name, age, sex,demographic

details and presenting complaints.

 66

 Blood pressure,random sugar,urea,creatinine will be taken

immediately after admission,killip classification applied at the time

of admissions.

 Baseline Serum Uric acid level will be done by withdrawing 4ml of

blood.uric acid level in serum is measured by uricase method with

COBRA INTEGRA/COBAS C SYSTEM.

 Cardiac enzyme assay were done in patients with NSTEMI.

 Reference level for uric acid

Male -3.1-7.0 mg/dl

Female- 2.5 to 5.6 mg/dl

 The data of each patient will be collected in specific

proforma(ANNEXURE 2) which includes patient’s name, age, sex,

demographic details, presenting complaints, risk factors and all

clinical data.

 All the relevant data and values are then entered in master chart in

Microsoft excel format an then analyzed statiscially.

 67

STATISTICAL ANALYSIS

The data was collected in the master chart obtained in the

Microsoft excel format.

The collected was analysed with SPSS 16.0 version. To

describe about the data descriptive statistics frequency analysis,

percentage analysis were used for categorical variable and the mean

were used for continuous variable. To find the significant of two

variables by unpaired t test. To find the correlation between the two

variables kruskal wallis test were used with p value less than .05 is

considered as significant.
 68

RESULTS

The total patients recruited in our study were 70. The following

charts depicit frequency distributions.

These are the frequency distributions of various variable used in

our study.

GENDER:

In a total of 70 patients participated in our study 44 patients were

male and 26 patients were females. This distribution shows the

predominance of males in acute myocardial infarction.

GENDER

Frequency Percent

F 26 37.1

M 44 62.9

Total 70 100.0
 69

GENDER DISTRIBUTION

FEMALE 38%

MALE 62%
 70

ASSOCIATION BETWEEN SERUM URIC ACID AND GENDER:

Mean Uric Acid

5.59

6.0000
4.60

5.0000
Mean Uric Acid

4.0000

3.0000

2.0000

1.0000

0.0000
Male Female

Mean uric acid levels was more among males (5.59) and less

among females (4.6). This difference is statistically significant by

unpaired t test.(p=0.004)
 71

AGE DISTRIBUTION:

N Minimum Maximum Mean Std.

Deviation

AGE 70 35 69 53.77 8.054

Valid N
70
(listwise)

The mean age of the patients in our study is 54years. The minimum

age of patient is 35years in our study.

 72

DISTRIBUTION OF DIABETES:

In a total of 70 patients,46 patients were diabetes and 24 were non

diabetic. It clearly shows acute myocardial infarction are common in

diabetes patients.

Frequency Percent Valid Cumulative

Percent Percent

N 24 34.3 34.3 34.3

Y 46 65.7 65.7 100.0

Total 70 100.0 100.0

DIABETES DISTRIBUTION
DIABETES NON DIABETES

34%

66%
 73

DISTRIBUTION OF HYPERTENSION:

In total of 70 patients included in our study 49 patients were

hypertensive ant the remaining 21 patients were not hypertensive.

HYPERTENSION

Frequency Percent Valid Percent Cumulative

Percent

NO 21 30.0 30.0 30.0

YES 49 70.0 70.0 100.0

Total 70 100.0 100.0

HYPERTENSION DISTRIBUTION

30%

HYPERTENSION

NON
HYPERTENSIVE
70%
 74

Association between serum uric acid hypertension / diabetes

Kruskal-Wallis Test

Variable Mean serum Std. Mean P value

uric acid Deviation Rank

Both diabetes and

5.546429 1.5469162 39.07
hypertension present

Either diabetes or 0.485

5.030769 1.3442184 33.05
hypertension present

No hypertension /
4.766667 .4163332 34.00
diabetes

Total 5.225714 1.4173547

No significant association was found between mean serum uric

acid levels and presence of diabetes or hypertension by kruskal wallis test
(p=0.485)
 75

SMOKING DISTRIBUTION:

Out of 70 patients in our study,37 patients had smoking habits and

remaining 33 were non smokers. Out of 44 male patients 37 were

smokers.

SMOKING
Frequency Percent Valid Cumulative Percent
Percent

N 37
52.9 52.9 52.9

Y 33
47.1 47.1 100.0

Total 70
100.0 100.0

SMOKING
SMOKERS
NON SMOKERS
33; 47%
37; 53%
 76

ACUTE MYOCARDIAL INFARCTION TYPES:

AWMI: Anterior wall myocardial infarction.

LWMI: Lateral wall myocardial infarction.

IWMI: Inferior wall myocardial infarction.

NSTEMI: Non ST elevation myocardial infarction.

NSTEMI

IWMI

NO OF PATIENTS

AWMI/LWMI

AWMI

0 5 10 15 20 25 30 35
 77

Out of 70 patients, 33 patients had AWMI,8 patients were both

AWMI/LWMI, 24 patients were IWMI,5 patients had NSTEMI.

AWMI/IWMI/LWMI/NSTEMI

Frequency Percent Valid Cumulative

Percent Percent

AWMI 33 47.1 47.1 47.1

AWMI/LWMI 8 11.4 11.4 58.6

Vali
IWMI 24 34.3 34.3 92.9
d

NSTEMI 5 7.1 7.1 100.0

Total 70 100.0 100.0

 78

KILLIP CLASSIFICATION:

KILLIP CLASS

Frequency Percent Valid Percent Cumulative

Percent

CLASS I 41 58.6 58.6 58.6

CLASS II 15 21.4 21.4 80.0

CLASS III 8 11.4 11.4 91.4

CLASS IV 6 8.6 8.6 100.0

Total 70 100.0 100.0

KILLIP CLASS
CLASS IV
CLASS III 9%
11%

CLASS I
CLASS II CLASS I CLASS II
21% 59% CLASS III
CLASS IV
 79

Out of 70 patients in our study killip class I and II was around

80%, killip class III and IV was around 20%

Association between serum Uric Acid levels and Killip classification:

Killip class Mean Mean Rank P value

I 4.475 25.06 0.000

II 5.253 38.33

III 7.250 62.06

IV 7.583 64.33

KILLIP IV

KILLIP III

KILLIP II

KILLIP I

0 1 2 3 4 5 6 7 8
 80

Kruskal-Wallis Test

Ranks

Killip class N Mean Mean P value

coded Rank

1.00 41 4.475610 25.06

2.00 15 5.253333 38.33 0.000

SERUM URIC
3.00 8 7.250000 62.06
ACID
4.00 6 7.583333 64.33

Total 70 5.225714

Uric acid level was significantly higher among patients in class IV

(7.58), in class III(7.25) than patients class II (5.25) and class I (4.47).

Mean difference was statistically significant by kruskal wallis test

(p=0.000).
 81

DISCUSSION

Acute myocardial infarction is a spectrum of disorder which

include ST elevation myocardial infarction (STEMI) and non ST

elevation myocardial infarction( NSTEMI).STEMI is usually associated

with short term and as well long term mortality. The diagnosis of STEMI

and NSTEMI is done by clinical features and characteristic ECG changes

such as new onset or presumed new changes in ST segment and new

onset LBBB and elevation of cardiac biomarkers such as troponin I and

T, creatine kinase MB.

Acute myocardial infarction is associated with high death rate

within 24 hours. And most of the death occur within one hour of onset of

symptoms. So risk stratification has a important role in the management

of acute myocardial infarction. Blood pressure, localisation of infarct,

killip class, TIMI score are some methods useful in risk stratification and

estimation of mortality in intensive coronary unit.

Killip classification is bedside evaluation test to predict the

mortality in acute coronary syndrome. It has 4 class in which class III and

IV has a higher mortality than the class I and II. The mortality rate of

killip class IV is 81%. The other scores such as TIMI( Thrombolysis In

Myocardial Infarction) was used to predict mortality in only in STEMI. 20

 82

Serum uric acid is a product of purine metabolism and

hyperuricemia is also a independent risk factor for cardiovascular disease

in high risk population such as diabetes, hypertension, dyslipidemia.13

Some studies shows that uric acid level more than 7gm/dl are associated

with the high mortality rate in cardiac failure.11 In Japan, study conducted

on STEMI patients reported that hyperuricemia increases 1-year mortality

rate in killip class IV.22 Our study is conducted to assess the relationship

between serum uric acid level and killip class in acute myocardial

infarction.

In our study total of 70 patients were included, who were admitted

in ICCU. All patients were included in study after getting consent, detail

history and physical examination and after ruling out the exclusion

criteria. Out of 70 patients 44 patients were male and 26 patients were

females. This distribution shows the predominance of males in acute

myocardial infarction. This results are similar to other study regarding

male predominance in acute myocardial infarction.

Uric acid of male patients is significantly higher than the female

patient, which is similar to other studies. In our study the risk factors such

as diabetes, hypertension, smoking were taken into consideration. Out of

70 patients 49 patients were hypertensive and 46 patients has diabetes, 37

patients had smoking habits, smoking is common in males in our

 83

population. Out of 70 patients in our study 33 patients had AWMI,8

patients were both AWMI/LWMI, 24 patients were IWMI,5 patients had

NSTEMI.

Out of 70 patients in our study, 80% of the patients were under

killip class I and II at the time of admission, 20% of the patients were on

killip class III and IV at the time of admission. Uric acid level was

significantly higher among patients in class IV (7.58), in class III (7.25)

than patients class II (5.25) and class I (4.47). Mean difference was

statistically significant by kruskal wallis test (p=0.000). The results in our

study shows that serum uric acid level are high in killip class III and IV in

acute myocardial infarction patients. Combination of serum acid and

killip classification will be useful in assessing the prognosis in acute

myocardial infarction patients.

 84

CONCLUSION

In general, serum uric acid level is significantly higher in male

patients than the female patients.

Diabetes and hypertension remains the major risk factors for acute

myocardial infarction.

Hyperuricemia is associated with killip class III and IV in Acute

myocardial infarction patients.

Further study on combination of killip class and serum uric acid

level in predicting mortality will be informative and useful.

 85

BIBILOGRAPHY

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and cardiovascular disease: recent developments, and where do

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Behar S. Serum uric acid for risk stratification of patients with

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Cardiovasc Pharmacol. 1995;25:119-25.

11. Ochiai ME, Barretto AC, Oliveira MT. Uric acid renal excretion

and renal insufficiency in decompensated severe heart failure. Eur

J Heart Fail. 2005;7:468-74.

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Yamagishi M, et al. Prognostic usefulness of serum uric acid after

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 89

PROFORMA

Name Age: Sex

Educational status: Occupation:

Address:

Ht in cms

Wt in kgs:

BMI [kg/m2]:

Clinical presentation on admission:

Time of onset of symptoms:

 Chest pain Typical/Atypical

 Syncope.

 Palpitation.

 Shortness of breath.

 Cerebral symptoms.

• PAST HISTORY: yes no

• Diabetes
 90

• Hypertension

• Myocardal infarction

• Angina pectoris

• Cerebrovascular diseases

• Drug intake

• PERSONAL HISTORY:

• Diet: vegetarian/non vegetarian:

• Smoking/ Alcohol /Tobacco chewing:

• Sedentary habits:

• Menstrual and Obstetric History:

• GENERAL EXAMINATION
• VITALS PR: BP: JVP :
• Anemia:
• Jaundice
• Cyanosis:
• Clubbing:
• EDEMA
EXAMINATION OF CARDIOVASCULAR SYSTEM

• EXAMINATION OF RESPIRATORY SYSTEM:

• ABDOMEN EXAMINATION

• CENTRAL NERVOUS SYSTEM

91
 92

INVESTIGATIONS
• ECG: ECHO

• CBC:

• CARDIAC ENZYMES:

• RFT:

• LFT:

• SERUM URIC ACID LEVEL:

93
 94

S.NO NAME AGE SEX HT DM SMOKING AWMI/IWMI/LWMI/NSTEMI KILLIP CLASS SERUM URIC ACID
1 SIVAKUMAR 48 M N Y Y AWMI CLASS I 4.9
2 ABRAHAM 58 M Y Y N IWMI CLASS I 4.6
3 SRIDHAR 45 M N N Y IWMI CLASS I 4.3
4 ABDUL RAHIM 35 M Y Y Y IWMI CLASS I 3.3
5 AROKIAMARY 69 F Y N N IWMI CLASS I 5.6
6 RAVIKUMAR 52 M N Y N AWMI CLASS I 4.1
7 MURUGAN 55 M Y Y Y AWMI/LWMI CLASS II 6.2
8 SARASWATHI 61 F Y Y N AWMI CLASS II 3.4
9 PRAKASH 35 M N N Y AWMI CLASS I 4.9
10 SUBBAIYA 49 M Y Y N IWMI CLASS I 4
11 TAMILARASI 52 F Y Y N AWMI CLASS I 4
12 KANNAN 51 M Y N Y AWMI CLASS I 4.1
13 LATHA 60 F Y Y N AWMI/LWMI CLASS II 6.2
14 DURAISAMY 55 M N Y Y AWMI CLASS I 4.3
15 ILAYARAJA 52 M Y N Y AWMI CLASS I 6.6
16 VENKATESAN 61 M Y Y N AWMI/LWMI CLASS IV 7.6
17 KUMARESAN 54 M Y Y Y AWMI CLASS II 6.1
18 RAJAMMAL 58 F Y Y N IWMI CLASS I 5.8
19 CHELLAYA 51 M N Y Y NSTEMI CLASS I 4.4
20 SHANMUGAM 48 M Y Y Y IWMI CLASS I 4.2
21 RAJASEKAR 62 M Y N Y AWMI/LWMI CLASS II 5.8
22 KUMAR 48 M N N Y IWMI CLASS I 5.1
23 LOGANATHAN 62 M Y N Y AWMI CLASS I 4.8
24 LAKSHMI 56 F Y N N IWMI CLASS I 3.9
25 PERUMAL 60 M Y N Y IWMI CLASS I 4
 95

26 SEETHALAKSHMI 68 F Y Y N AWMI CLASS I 4.2

27 KALAISELVI 55 F N Y N AWMI CLASS I 3.4
28 NANDHAGOPAL 63 M Y Y Y AWMI CLASS III 6.8
29 GANGAIAMMAL 51 F Y Y N AWMI/LWMI CLASS III 7.8
30 KUMAR 35 M N Y Y AWMI CLASS I 6.9
31 KAMALAMMAL 54 F Y Y N IWMI CLASS II 3.8
32 GOMATHI 66 F Y Y N AWMI CLASS I 3.4
33 PARAMESHWARAN 51 M Y Y Y AWMI/LWMI CLASS II 4.8
34 LAKSHMINARAYAN 68 M Y N Y AWMI CLASS IV 8.1
35 PUSPHALATHA 51 F Y N N IWMI CLASS I 4.2
36 CHELLAPPAN 60 M Y N Y AWMI CLASS II 4.3
37 ANBALAGAN 54 M Y Y N AWMI CLASS II 4.8
38 VALLI 49 F N Y N IWMI CLASS I 2.8
39 NAGARAJ 54 M Y N Y AWMI CLASS I 4.1
40 MOHAMED JINNA 58 M Y N Y IWMI CLASS I 4.8
41 VASUKI 59 F Y Y N AWMI CLASS I 3.8
42 DHARMARAJ 40 M Y N Y AWMI CLASS I 4.3
43 GOVUNDRAJ 49 M Y Y Y AWMI/LWMI CLASS IV 7.2
44 RANI 54 F Y N N IWMI CLASS II 5.1
45 KAUVERI 66 F N Y N IWMI CLASS I 5
46 DURAISAMY 50 M Y Y Y AWMI CLASS II 5.5
47 KOMALA 49 F N Y N IWMI CLASS I 4
48 RAJESHWARI 60 F Y N N NSTEMI CLASS I 3.4
49 GOPI 54 M Y Y Y AWMI/LWMI CLASS IV 7.8
50 KATHIRVEL 38 M N Y Y AWMI CLASS I 4.8
51 BHAVANI 65 F Y N N NSTEMI CLASS I 3.2
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52 GUNASEKAR 55 M Y Y N AWMI CLASS II 5.2

53 SENTHIKUMAR 48 M N Y Y IWMI CLASS II 5.5
54 MAHADEVAN 53 M Y Y N AWMI CLASS III 6.5
55 JAGATHAMBAL 61 F Y Y N AWMI CLASS I 6
56 ESWARI 56 F Y N N IWMI CLASS IV 6.4
57 SHANTHI 50 F N Y N IWMI CLASS I 4.2
58 KANNAN 39 M N Y Y IWMI CLASS I 4
59 MEENAKSHI 56 F N Y N AWMI CLASS I 3.8
60 DEVARAJ 57 M Y Y Y AWMI CLASS III 7.5
61 GOPAL 47 M Y N Y AWMI CLASS III 7
62 SARSWATHI 58 F Y Y N NSTEMI CLASS I 6.4
63 SRINIVASAN 62 M Y Y N IWMI CLASS IV 8.4
64 RAVI 40 M N Y Y AWMI CLASS III 7.8
65 RAMACHANDRAN 51 M Y N N AWMI CLASS II 6.1
66 AMBIKA 55 F N Y N IWMI CLASS I 5.1
67 MANICKAM 53 M N Y N AWMI CLASS III 6.8
68 VEERAMANI 61 M Y N N IWMI CLASS II 6
69 JOSEPH 40 M N Y Y AWMI CLASS III 7.8
70 ANTHONIAMMAL 64 F Y N N NSTEMI CLASS I 4.8

HT-HYPERTENSION
DM- DIABETES MELLITUS
Y-YES
N-NO
AWMI-ANTERIOR WALL MYOCARDIAL INFARCTION
IWMI-INFERIOR WALL MYOCARDIAL INFARCTION
LWMI- LATERAL WALL MYOCARDIAL INFARCTION
NSTEMI-NON ST ELEVATION MYOCARDIAL INFARCTION
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PATIENT CONSENT FORM

Study detail: “correlation between Serum Uric acid level and killip
class in acute myocardial infarction ”
Study centre : KILPAUK MEDICAL COLLEGE, CHENNAI
Patients Name :
Patients Age :
Identification Number :
Patient may check ( ) these boxes
I confirm that I have understood the purpose of procedure for the above study. I have
the opportunity to ask question and all my questions and doubts have been answered
to my complete satisfaction.

I understand that my participation in the study is voluntary and that I am free to

withdraw at any time without giving reason, without my legal rights being affected.

I understand that sponsor of the clinical study, others working on the sponsor’s behalf,
the ethical committee and the regulatory authorities will not need my permission to
look at my health records, both in respect of current study and any further research
that may be conducted in relation to it, even if I withdraw from the study I agree to
this access. However, I understand that my identity will not be revealed in any
information released to third parties or published, unless as required under the law. I
agree not to restrict the use of any data or results that arise from this study.

I agree to take part in the above study and to comply with the instructions given
during the study and faithfully cooperate with the study team and to immediately
inform the study staff if I suffer from any deterioration in my health or well-being or
any unexpected or unusual symptoms.

I hereby consent to participate in this study.

I hereby give permission to undergo complete clinical examination and diagnostic

tests including hematological, biochemical, radiological tests.

Signature/thumb impression:

Patients Name and Address: place date

Signature of investigator :

Study investigator’s Name : place date

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