LEUCOCYTE COUNT, ERYTHROCYTE SEDIMENTATION RATE …

A Dissertation on “A STUDY ON TOTAL LEUCOCYTE COUNT, ERYTHROCYTE

SEDIMENTATION RATE AND HIGH SENSITIVITY C-REACTIVE PROTEIN

AS PROGNOSTIC MARKERS IN ACUTE MYOCARDIAL INFARCTION”

Submitted to

THE TAMIL NADU DR.M.G.R.MEDICAL UNIVERSITY

CHENNAI - 600032

In partial fulfillment of the regulations for the award of the degree of

M.D. BRANCH – I (GENERAL MEDICINE)

DEPARTMENT OF GENERAL MEDICINE

GOVERNMENT STANLEY MEDICAL COLLEGE, CHENNAI.

THE TAMIL NADU DR. M.G.R.MEDICAL UNIVERSITY

TAMILNADU, INDIA

MAY 2020

CERTIFICATE BY INSTITUTION

This is to certify that this dissertation entitled “A STUDY ON TOTAL LEUCOCYTE

COUNT, ERYTHROCYTE SEDIMENTATION RATE AND HIGH SENSITIVITY

C-REACTIVE PROTEIN AS PROGNOSTIC MARKERS IN ACUTE

MYOCARDIAL INFARCTION” submitted by Dr. SURENDAR P B to the faculty of

General Medicine, The TamilNadu Dr. M.G.R Medical University, Chennai, Tamilnadu,

in partial fulfillment of the requirement for the award of M.D DEGREE BRANCH-I

(GENERAL MEDICINE) is a bonafide research work carried out by him under my direct

supervision and guidance.

Prof. Dr.T.B.UMADEVI M.D., Prof. Dr.C.HARIHARAN.M.D.,

Guide/ Professor of medicine, Head of the Department,

Department of Medicine, Department of Medicine,

Stanley Medical College and Hospital, Stanley Medical College and Hospital,

Chennai - 1. Chennai- 1.

PROF. DR.R.SHANTHIMALAR, M.D., D.A.,

DEAN

Government Stanley Medical College and Hospital, Chennai-1.

CERTIFICATE BY THE GUIDE

This is to certify that Dr.P.B.SURENDAR, Post Graduate student (May 2017 to April

2020) in the Department of General Medicine, Government Stanley Medical College and

Hospital,Chennai-1,has done this dissertation work titled “A STUDY ON TOTAL

LEUCOCYTE COUNT, ERYTHROCYTE SEDIMENTATION RATE AND HIGH

SENSITIVITY C-REACTIVE PROTEIN AS PROGNOSTIC MARKERS IN

ACUTE MYOCARDIAL INFARCTION” under my guidance and supervision in

partial fulfillment of the regulations laid down by The Tamilnadu Dr.M.G.R.Medical

University,Chennai for M.D.,(General Medicine),Degree examination to be held in May

2020.

Prof. Dr. T.B. UMADEVI M.D.,

Guide,

Professor of General Medicine,

Stanley Medical College and Hospital,

Chennai - 1.

CERTIFICATE - II

This is to certify that this dissertation work titled “A STUDY ON TOTAL

LEUCOCYTE COUNT, ERYTHROCYTE SEDIMENTATION RATE AND HIGH

SENSITIVITY C-REACTIVE PROTEIN AS PROGNOSTIC MARKERS IN

ACUTE MYOCARDIAL INFARCTION ”of the candidate Dr.Surendar.P.B. with

Registration Number 201711070 for the award of M.D., DEGREE in the branch of

BRANCH-I (GENERAL MEDICINE) was done under my guidance. 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 the result shows 9

percentage of plagiarism in the dissertation.

PROF DR.T.B.UMADEVI M.D.,

GUIDE

PROFESSOR OF GENERAL MEDICINE,

STANLEY MEDICAL COLLEGE,CHENNAI-1.

DECLARATION

I, Dr. SURENDAR P B, solemnly declare that the dissertation titled “A STUDY ON

TOTAL LEUCOCYTE COUNT, ERYTHROCYTE SEDIMENTATION RATE

AND HIGH SENSITIVITY C-REACTIVE PROTEIN AS PROGNOSTIC

MARKERS IN ACUTE MYOCARDIAL INFARCTION” is a bonafide work done by

me at Government Stanley Hospital, Chennai during June 2018 to November 2018 under

the guidance and supervision of Prof.Dr.T.B.UMADEVI.M.D., Professor of Medicine,

Government Stanley Hospital, Chennai. I also declare that this bonafide work or a part of

this work was not submitted by me or any other for award degree or diploma to any other

university, board either in India or abroad. This dissertation is submitted to the

Tamilnadu Dr. M.G.R Medical University, towards the partial fulfillment of requirement

for the award of M.D. Degree (Branch – I) in General Medicine.

Place: Chennai Signature of the candidate

Date: (Dr.SURENDAR P B )

SPECIAL ACKNOWLEDGEMENT

I gratefully acknowledge and thank

PROF. DR.R. SHANTHI MALAR M.D., D.A.,

DEAN

GOVERNMENT STANLEY MEDICAL COLLEGE AND HOSPITAL, CHENNAI.

For granting me permission to utilize the resources of this

Institution for my study

ACKNOWLEDGEMENT

At the outset I thank our Medical superintendent Prof.Dr.DHANASEKAR,

M.D., for permitting me to carry out this study in our hospital.

I express my profound thanks to my esteemed Professor and Teacher

Prof.Dr.C.HARIHARAN, M.D., Professor and HOD of Medicine, Stanley Medical

College Hospital, for encouraging and extending invaluable guidance to perform and

complete this dissertation.

I immensely thank my unit chief Prof.Dr. T.B. UMADEVI MD., and my former

Unit Chief Prof.Dr.NALINI KUMARAVELU MD., and Prof.Dr.KANNAN, MD,

DM., Head of the Department of Cardiology for their constant encouragement and

guidance throughout the study.

I wish to thank Dr. RSA Alexander MD., and Dr. Vijayalakshmi MD, Assistant

Professors of my unit, Department of Medicine, Stanley Medical College Hospital for

their valuable suggestions, encouragement and advice. I sincerely thank the members of

Institutional Ethical Committee, Stanley Medical College for approving my dissertation

topic.

I thank all my colleagues, House Surgeons, and Staff nurses and other para

medical workers for their support.

At this juncture I would also want to extend my heartfelt gratitude to my family

for their constant support and care.

I sincerely thank all those patients who participated in this study, for their co-

operation.

ABBREVIATIONS

CAD – Coronary Artery Disease

ACS – Acute Coronary Syndrome

MI – Myocardial Infarction

STEMI – ST segment Elevation Myocardial Infarction

NSTEMI – Non-ST segment Elevation Myocardial Infarction

UA – Unstable Angina

hs-CRP – high sensitivity C-Reactive Protein

ESR – Erythrocyte Sedimentation Rate

ESR-1 HR – Erythrocyte Sedimentation Rate at 1 Hour

LDL – Low Density Lipoprotein

HDL – High Density Lipoprotein

TC – Total Leucocyte count

WBC – White Blood Corpuscles

BMI – Body Mass Index

LAD – Left Anterior Descending artery

RCA – Right Coronary Artery

CK MB - Creatine Kinase-Myocardial Band

LBBB – Left Bundle Branch Block

PCI – Primary Coronary Intervention

ICH – Intra Cerebral Hemorrhage

LVEF – Left Ventricular Ejection Fraction

TABLE OF CONTENTS

S.No CHAPTERS PAGE NUMBER

1 INTRODUCTION 1

2 AIM AND OBJECTIVES OF THE STUDY 3

3 REVIEW OF LITERATURE 4

4 MATERIALS AND METHODS 45

5 OBSERVATION AND RESULTS 48

6 DISCUSSION 76

7 CONCLUSION 79

BIBLIOGRAPHY

PROFORMA

INFORMED CONSENT

ETHICAL COMMITTEE APPROVAL LETTER

PLAGIARISM CERTIFICATE

MASTER CHART

LIST OF TABLES

S.NO. TITLE PAGE NO.

1 Mean age in males and females 47

2 Age distribution in study population 48

3 Diabetes mellitus in study population 49

4 Smoking in study population 50

5 Frequency of distribution of type of MI 50

6 Comparison of total leucocyte count with LVEF at

admission

55

7 Comparison of total leucocyte count with arrhythmia 57

8 Comparison of total leucocyte count with cardiogenic

shock

58

9 Comparison of total leucocyte count with Severe LV

dysfunction at 1 week

59

10 Comparison of total leucocyte count with mortality 60

11 Comparison of hs-CRP with LVEF at admission 62

12 Comparison of hs-CRP with arrhythmia 63

13 Comparison of hs-CRP with cardiogenic shock 64

14 Comparison of hs-CRP with Severe LV dysfunction at 1

week

66

15 Comparison of hs-CRP with mortality 67

16 Comparison of ESR-1 hr with LVEF at admission 69

17 Comparison of ESR-1 hr with arrhythmia 70

18 Comparison of ESR-1 hr with cardiogenic shock 72

19 Comparison of ESR-1 hr with Severe LV dysfunction at 1

week

73

20 Comparison of ESR-1 hr with mortality 74

LIST OF FIGURES

S.NO TITLE PAGE NO.

1 Gender distribution in study population 47

2 Age distribution in study population 48

3 Systemic hypertension in study population 49

4 Type of Myocardial Infarction in study population 51

5 LV ejection fraction at admission 52

6 Cardiogenic shock in study population 52

7 Arrhythmia in study population 53

8 LV ejection fraction at 1 week 53

9 Mortality at 1 week 54

10 Total leucocyte count with LVEF at admission 55

11 Total leucocyte count with arrhythmia 56

12 Total leucocyte count with cardiogenic shock 57

13 Total leucocyte count with Severe LV dysfunction at 1 week 58

14 Total leucocyte count with mortality 60

15 hs-CRP with LVEF at admission 61

16 hs-CRP with arrhythmia 62

17 hs-CRP with cardiogenic shock 64

18 hs-CRP with Severe LV dysfunction at 1 week 65

19 hs-CRP with mortality 67

20 ESR-1 hr with LV systolic function at admission 68

21 ESR-1 hr with arrhythmia 70

22 ESR-1 hr with cardiogenic shock 71

23 ESR-1 hr with Severe LV dysfunction at 1 week 72

24 ESR-1 hr with mortality 74

1

INTRODUCTION:

Coronary artery disease (CAD) is the spectrum of diseases causing reduction in

the blood supply to myocardium of heart. CAD is one of the leading causes of death in

India and worldwide. It ranks first among the causes of death worldwide. CAD accounts

for around 8 million deaths in the year 2013 worldwide1

and its incidence is increasing

over recent decades especially in developed and developing countries. The rise in

incidence is mainly attributed to the dietary and lifestyle changes.

Coronary artery disease includes stable angina, unstable angina and myocardial

infarction(ST elevation MI and Non ST elevation MI). CAD can lead to dreadful

complications like heart failure and arrhythmias over time.

Acute coronary syndrome (ACS) includes new onset or worsening ischaemic

symptoms. ACS includes unstable angina, ST elevation Myocardial Infarction(STEMI)

and Non ST elevation Myocardial Infarction(NSTEMI). Among Acute coronary

syndromes, STEMI is more fatal and leading cause of death.

Acute myocardial infarction is a cardiac emergency causing substantial morbidity

and mortality worldwide. It continues to be the major health issue despite various

researches in diagnosis and treatment over last few decades

Diagnosis of myocardial infarction requires electrocardiographic, biochemical and

imaging modalities. Inflammation has an important role in the development of

atherosclerosis and ischemic heart disease. Acute myocardial infarction triggers an

2

inflammatory response to necrotic insult leading to rise in acute phase reactants. The

inflammatory process after infarction leads to change in morphology, size and thickness

of infarct area.

In patients with myocardial infarction, few biochemical markers like Total

leukocyte count, erythrocyte sedimentation rate, high sensitive C-reactive protein,

troponin-I, creatinine kinase-MB are useful in early risk assessment.

Among the biomarkers, total leukocyte count, Eythrocyte sedimentation rate and

high sensitive CRP are routinely available and these can be obtained with ease at bedside

in emergency department.

This study focuses the importance of routinely available biochemical tests in the

risk assessment in patients with acute ST segment elevation myocardial infarction.

3

AIM AND OBJECTIVES

To study the role of total leucocyte count, erythrocyte sedimentation rate

and high sensitivity C-Reactive Protein in the outcome of acute myocardial infarction in

terms of morbidity and mortality.

4

REVIEW OF LITERATURE :

ACUTE CORONARY SYNDROME:

Acute coronary syndrome (ACS) refers to set of clinical symptoms as a result of

myocardial ischemia. ACS includes the following clinical spectrum of conditions:

Non ST-segment elevation-ACS (NSTE-ACS)

o Unstable angina (UA)

o Non ST-segment elevation myocardial infarction (NSTEMI)

ST-segment elevation myocardial infarction (STEMI)

In united states, approximately 1.36 million cases of ACS are reported of which

0.81 million are for myocardial infarction and the remainder are for unstable

angina2

NON ST-SEGMENT ELEVATION –ACUTE CORONARY SYNDROMES :

NSTE-ACS results from imbalance between myocardial oxygen supply and

demand leading to myocardial ischemia. This results from one of the following 4

processes3 :

Unstable coronary plaque disruption secondary to plaque rupture or erosion

Coronary arterial vasoconstriction

Gradual coronary Intraluminal narrowing

5

Conditions producing increased myocardial oxygen demand

(thyrotoxicosis, fever, tachycardia) in the presence of fixed epicardial

coronary obstruction.

Non-ST elevation MI and Unstable angina are closely related conditions. They are

similar in their pathophysiology and clinical presentation but varies in severity.

UNSTABLE ANGINA :

The diagnosis of Unstable angina is made by following features:

Severe chest discomfort with one of the following three features:

o Occurring at rest or with minimal exertion, lasting >10 minutes

o Recent onset (within 2 weeks)

o Crescendo pattern (more severe, prolonged or frequent than prior

episodes)

Electrocardiography:

o New ST segment depression or

o New and Deep T-wave inversions (≥0.3 mV)

(These changes may be transient or persistent)

No evidence of myocardial necrosis(i.e., normal cardiac biomarkers) :

6

NON ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION (NSTEMI) :

The diagnosis of NSTEMI is made if the patient has chest discomfort and

electrocardiographic changes similar to unstable angina with evidence of myocardial

necrosis as evidenced by elevated biomarkers of myocardial necrosis such as

Cardiac Troponin I or T (highly specific and sensitive) or

MB isoform of Creatine kinase (CK-MB )

ST SEGMENT ELEVATION MYOCARDIAL INFARCTION :

ST segment elevation MI is the most acute clinical manifestation of coronary

artery disease. It is associated with increased morbidity and mortality. The incidence rises

sharply in both genders with increasing age. It is more common in black race compared

to white population.

The proportion of STEMI among ACS events has declined in the past decade. This

is due to the advent of more sensitive cardiac biomarkers of myocardial injury that

increases the number of NSTEMI cases relative to STEMI4

7

RISK FACTORS :

The risk factors for myocardial infarction are divided into modifiable and non-

modifiable risk factors.

MODIFIABLE RISK FACTORS:

o PHYSICAL INACTIVTY

o SMOKING

o ALCOHOL CONSUMPTION

o DYSLIPIDEMIA

o DIABETES MELLITUS

o SYSTEMIC HYPERTENSION

o OBESITY

o STRESS

NON-MODIFIABLE FACTORS:

o FAMILIAL

o AGE

o GENDER

8

PHYSICAL INACTIVITY :

Regular physical activity may reduce the risk of coronary artery disease by 20-30%5.

Inactive people with other multiple risk factors are more prone for developing MI.

Different types of physical activities have different effects on cardiovascular risk.

Activities like walking, climbing stairs and cycling provides protection against

cardiovascular disease. Intensive domestic activities does not offer protection against

cardiovascular disease.

SMOKING :

Cigarettes smoking is a strong risk factor for the development of premature

atherosclerosis, myocardial infarction and sudden cardiac death. Smoking is the

important cause for STEMI in otherwise healthy young individuals.

Smoking reduces serum HDL-cholesterol and increases serum LDL-cholesterol

and serum triglyceride levels and thus accelerating atherogenesis. Smoking also leads to

oxidised LDL-cholesterol accumulation within the arterial wall by promoting free radical

damage to LDL cholesterol.

Nicotine increases both heart rate and systolic blood pressure by activating

sympathetic system, thereby increasing the myocardial oxygen demand. Smoking

contributes to vascular inflammation which is reflected by higher levels of high sensitive

C-Reactive protein levels in smokers than in non-smokers.

9

Thus, cigarette smoking causes both increase in myocardial oxygen demand and

decreased myocardial oxygen supply by activating sympathetic nervous system and by

accelerating atherogenesis6.

Passive smoking is also associated with higher risk of cardiovascular disease in

non smoking individuals.

ALCOHOL CONSUMPTION :

Moderate consumption of alcohol is associated with lower risk of adverse

cardiovascular events. However, binge alcohol drinking is associated with higher

cardiovascular risk.7

Binge drinking is proven to increase Low density lipoproteins and it predisposes to

histological changes in myocardium and conducting system and it also reduces the

threshold for ventricular fibrillation by unknown mechanisms.8

The relationship between alcohol consumption and risk of myocardial infarction is

still controversial. Most of the researches showed that alcohol consumption can increase

LDL-cholesterol, serum triglyceride, heart rate and blood pressure and thus increasing the

risk of atherosclerosis and atrial fibrillation.

10

DYSLIPIDEMIA:

Dyslipidemia is a major risk factor of Cardiovascular disease. It is defined as total

cholesterol, LDL-cholesterol, apo B or Lp (a) levels above 90th

percentile or HDL-

cholesterol and apo A levels below 10th

percentile of general population.

Non fasting serum triglyceride level is a strong independent predictor of acute

myocardial infarction. High levels of total cholesterol, LDL-cholesterol and low levels of

HDL-cholesterol are the major risk factors for atherosclerosis.

Correction of dyslipidemia at the earliest by use of statins shown to reduce the risk

of myocardial infarction.9

DIABETES MELLITUS :

Type 2 Diabetes Mellitus (T2DM) shares several risk factors in common with

coronary artery disease. T2DM increases the risk of coronary artery disease by two to

four times.

The major cause of mortality in patients with type 2 diabetes mellitus is coronary

artery disease. CAD accounts for around 80% of all deaths in type 2 diabetic patients.

Atherosclerotic plaques are more vulnerable to rupture among diabetics. Myocardial

infarction is more fatal in diabetic patients compared with MI cases without diabetes.10

11

SYSTEMIC HYPERTENSION:

Prevalence of systemic hypertension is increasing across all races and age groups

worldwide. Almost 1 billion people have systemic hypertension worldwide.

Both systolic and diastolic hypertension increases the risk of acute myocardial

infarction. Higher the pressure, greater the risk of myocardial infarction11

. Around 69%

of people with first attack of myocardial infarction have blood pressure of 140/90 mm Hg

or higher.

Systemic hypertension accelerates atheroma formation, increases shear stress on

atheromatous plaques and impairs endothelial function. Strict control of blood pressure

by anti-hypertensive medications, dietary and lifestyle modifications reduces the risk of

myocardial infarction significantly.

OBESITY:

Increased BMI (overweight and obesity) is directly related to higher incidence of

acute myocardial infarction. Central obesity increases the risk of acute myocardial

infarction in both genders, all age groups and races.12

STRESS:

Chronic stress, anxiety and social isolation increases the risk of myocardial

infarction13

. Acute psychological stress may trigger the onset of myocardial infarction. It

12

increases the hemodynamic stress in coronary arteries and rupture of vulnerable

atheromatous plaque.

FAMILY HISTORY:

Several genetic variants are associated with increased risk of acute myocardial

infarction. Family history of myocardial infarction in first degree relatives doubles the

risk of myocardial infarction. There is a combined relative risk of 1.6 for future

cardiovascular events in people with first degree relative with coronary artery disease

compared with people without affected first degree relative. Presence of maternal or

paternal premature myocardial infarction increases the risk to 7 folds in children.

The persons with strong familial history of adverse cardiovascular events should

be counselled for dietary modification, physical activity, avoidance of alcohol, smoking

and tobacco.

AGE:

The risk of acute myocardial infarction increases with age. This is because of the

fact that the process of athereosclerosis increases with increasing age. Around 50% of the

adverse cardiovascular events occurs in individuals between 35 and 64 years old.

GENDER:

Males are more prone for acute myocardial infarction. In the United kingdom, 1 in

3 men and 1 in 4 women die from coronary artery disease.

13

PATHOPHYSIOLOGY OF ATHEROSCLEROSIS:

INITIATION OF ATHEROSCLEROSIS:

Atherosclerosis is a progressive inflammatory process of arterial wall. The process

of atherosclerosis begins as early in infancy in the form of fatty streak deposition and

continues lifelong. Atheromatous plaque formation primarily involves the intimal layer of

large sized arteries and medium sized arteries. Several risk factors like systemic

hypertension, diabetes, hypercholesterolemia and smoking leads to endothelial

dysfunction which plays an important role in the initiation of atherosclerosis14

.

PROGRESSION OF ATHEROSCLEROTIC PLAQUE : ROLE OF

INFLAMMATION:

Fatty streaks occur at the sites of endothelial injury (sites with shear stress) . These

develop when monocytes binds to endothelial receptors, migrate to intimal layer and they

take up oxidised low density lipoprotein to become “lipid laden macrophages or foam

cells”.

The lipid laden macrophages release chemoattractants and cytokines like

interleukin-1, tumour necrosis factor alpha and monocyte chemoattractant protein 1

accelerate the process by recruiting vascular smooth muscle cells and additional

macrophages. Macrophages also releases matrix metalloproteinases which digest

extracellular matrix leading to plaque disruption15

.

14

STABILITY OF ATHEROSCLEROTIC PLAQUE :

The smooth muscle cells to macrophages ratio plays a vital role in plaque

stabilisation. “High risk or vulnerable plaque” have a large lipid core, thin fibrous caps,

high density of macrophages with increased expression of matrix metalloproteinases and

T lymphocytes and low amount of smooth muscle cells16

. In contrast, “stable plaque”

have small lipid pool, thick fibrous cap, heavy calcification and plenty of collagen.

ATHEROSCLEROTIC PLAQUE DISRUPTION AND THROMBUS

FORMATION:

75 % of myocardial infarction deaths are caused by plaque rupture, whereas

remaining 25% is caused by superficial endothelial erosions17

. After plaque disruption,

the subendothelium rich in tissue factor is exposed to circulation leading to platelet

adhesion followed by activation and aggregation of platelets, ultimately leading to

thrombus formation.

Thrombi are of 2 types namely platelet rich thrombi and fibrin rich thrombi.

“Platelet rich thrombi” also known as white clot forms in the areas of high shear stress

and causes partial occlusion of artery. “Fibrin rich thrombi” also known as red clot is the

end process of activated coagulation cascade and decreased flow of blood in artery.

Fibrin rich clots frequently superimpose on platelet rich clots causing total occlusion.

15

PATHOGENESIS OF ATHEROSCLEROSIS

16

UNIVERSAL DEFINITIONS OF MYOCARDIAL INJURY AND MYOCARDIAL

INFARCTION:

CRITERIA FOR MYOCARDIAL INJURY:18

The term “Myocardial injury” should be used if there is an evidence of elevated

cardiac troponin values with at least one of the values above 99th

percentile upper limit.

The myocardial injury is considered to be acute if there is a rise and/or fall of cardiac

troponin values.

TYPES OF MYOCARDIAL INFARCTION:

TYPE 1 MYOCARDIAL INFARCTION:

Myocardial infarction caused by atherothrombotic coronary artery disease and

usually precipitated by rupture or erosion of atherosclerotic plaque.


Myocardial infarction secondary to imbalance between myocardial oxygen supply

and/or demand caused by conditions other than coronary artery disease. Caused by

conditions like coronary artery spasm, coronary embolism, coronary endothelial

dysfuntion, arrhythmias, anaemia, respiratory failure, hypotension, etc;

17


Death with symptoms suggestive of myocardial ischaemia with new ischaemic

changes or new LBBB on ECG but biomarker values are not available because of death

before collection blood samples or before cardiac biomarkers could rise.

TYPE 4a MYOCARDIAL INFARCTION:

Myocardial infarction related to percutaneous coronary intervention.

TYPE 4b MYOCARDIAL INFARCTION:

Myocardial infarction related to stent thrombosis.

TYPE 4c MYOCARDIAL INFARCTION:

Restenosis associated with percutaneous coronary intervention.


Myocardial infarction related to coronary artery bypass grafting.

18

CLINICAL FEATURES:

SYMPTOMS:

Chest pain – classical symptom

o precordial or retrosternal

o crushing, heaviness, tightness or burning type

o frequently radiating to neck, back, arms and sometimes epigastrium

o Maximum intensity over several minutes lasting >30 mins

o Associated with shortness of breath, nausea, diaphoresis and fear of

impending death.

Approximately 20% of myocardial infarction patients are asymptomatic or have atypical

symptoms. Painless MI occurs most commonly in diabetics, elderly and in postoperative

patients.

PHYSICAL EXAMINATION :

MI patients may have signs of acute left ventricular or right ventricular

dysfunction:

Signs of Left ventricular dysfunction:

Tachypnoea

Tachycardia

Features of shock – hypotension, cold extremities, decreased urine output

19

Pulmonary rales

Third heart sound

Signs of Right ventricular dysfunction: 19

Increased jugular venous pressure

Kussmaul sign

RV third heart sound

ELECTROCARDIOGRAPHY:20

Electrocardiography is the mainstay in the diagnosis of STEMI but ECG alone is

not sufficient for the diagnosis of STEMI.

ECG changes in MI gives information about acuteness and severity of MI and the

site of arterial blockade. It should be looked for conduction defects and arrhythmias.

The ECG changes evolve over time and are described as:

HYPER-ACUTE PHASE

EVOLVED PHASE

CHRONIC STABILISED PHASE

HYPER-ACUTE PHASE:

It occurs within few minutes to few hours after the onset of infarction indicating

ongoing myocardial injury. Characteristic ECG changes are:

20

Tall T waves

ST segment elevation

Increased ventricular activation time

TALL T WAVES:21

T waves exceeding the amplitude of R wave are considered tall or T waves ≥0.5

mV in limb leads and ≥1.0 mV in precordial leads. These T waves are symmetrical,

peaked and widened.

TALL T WAVES

21

ST SEGMENT ELEVATION:

New ST segment elevation in two anatomically contiguous leads of >0.1 mV in all

leads other than V2 and V3 leads

For V2 and V3 leads : ≥0.2 mV in males > 40 years, ≥0.25 mV in males <40

years and ≥0.15 mV in females in the absence of left ventricular hypertrophy or LBBB.

INCREASED VENTRICULAR ACTIVATION TIME:

Increase in the ventricular activation time(beginning of QRS complex to the apex

of R wave). Ventricular activation time >40 ms is significant.

EVOLVED PHASE:

ECG shows a combination of changes of injury, ischaemia and necrosis of

myocardium. Characterised by

Appearance of new q waves

ST segment elevation

T wave inversion

APPEARANCE OF NEW Q WAVES:22

Indicates infarct of myocardium

Q waves are considered pathological if >20 ms width in V1-V4 , >30 ms width in

other leads (except leads III and avR)

22

Q wave in lead III >40 ms width, Q wave in avF >20 ms width and or Q wave of

any duration in lead II is significant.

ST SEGMENT ELEVATION:

The convexity of ST segment elevation decreases in evolved phase but may appear

more convex upwards when accompanied with T wave inversion.

T WAVE INVERSION:

The tall peaked T waves of hyper acute phase decreases in amplitude and becomes

inverted. T wave inversion is deep and symmetrical. Amplitude of T wave inversion

varies and is proportional to the infarct size.

CHRONIC STABILIZED PHASE:

Occurs when the myocardium has totally infarcted or when the ischaemia has

totally been relieved. The changes are:

Changes in QRS complex

Changes in J point and ST segment

Changes in T wave

CHANGES IN QRS COMPLEX:

Q waves evolves maximally in proportion to infarct size. If there is early

restoration of blood flow and in smaller infarcts. R waves are smaller in infarct related

leads.

23

PATHOLOGICAL ‘Q’ WAVES

CHANGES IN ST SEGMENT:

ST segment returns to isoelectric baseline point. Persistent ST elevation denotes

ventricular aneurysm or persistent myocardial ischaemia.

CHANGES IN T WAVE:

Once the ischaemia gets relieved, T wave regains positivity. Persistent T wave

inversion signifies persistent ischaemia or aneursym.

24

CHANGES IN ECG FOLLOWING STEMI

25

LOCALISATION OF CULPRIT ARTERY BASED ON ECG:23,24

ST ELEVATION RECIPROCAL ST

DEPRESSION

INFARCT SITE AFFECTED

ARTERY

V1-V4, qRBBB II, III, aVF Antero-septal LAD before septal

branch, after

diagonal branch

I, aVL, V2-V4 ±V5, V6 Antero-lateral LAD before

diagonal branch,

after septal branch

V4-V6 aVL Antero-apical Distal LAD, after

diagonal and septal

branch

I, aVL, V1-V6 II, III, aVF Extensive anterior

wall

Proximal LAD,

before septal and

diagonal branch

I, aVL, ±V5, V6 II, III, aVF Lateral wall Ramus/ large

diagonal

I, aVL, V1-V6, aVR

> V1

II, III, aVF Extensive

anterolateral

Left main coronary

artery

II, III, aVF, V1,

V3R, V4R

I, Avl, ±V2, V3 Infero-posterior Proximal RCA

II, III, aVF I, aVL, ±V1-V3 Infero-posterior Distal RCA

II, III, aVF, V5, V6,

±I, aVL

V1-V3, aVR Infero-lateral Lateral circumflex

artery

V7-V9 V1-V3 Posterior Lateral circumflex

artery

26

LOCALISATION OF CULPRIT ARTERY IN STEMI

27

CARDIAC BIOMARKERS IN MYOCARDIAL INFARCTION:

Several proteins are released into the circulation by damaged cardiac myocytes.

Blood sampling for biomarker assay is done at admission, at 6-9 hours and at 12-24

hours25

. Some of the biomarkers are:

Cardiac Troponins

Creatine kinase-myocardial band (CK-MB)

Myoglobin

Aspartate transaminase

Lactate dehydrogenase

CARDIAC TROPONINS:

The cardiac troponins regulates the interaction between actin and myosin in the

cardiac myocytes. There are 2 isoforms namely cardiac troponin I and T. Their levels

starts to rise 3-12 hours after the onset of myocardial injury, peaks at 12-24 hours and

remains elevated for 8-21 days (troponin T) or 7-14 days (troponin I). High sensitivity

troponin assays are capable of detecting lower levels of troponin. Cardiac troponins are

vital in the diagnosis of myocardial infarction.

Currently these are the preferred biomarkers for myocardial injury because of high

specificity and sensitivity.26

28

CREATINE KINASE-MB:

The MB isoenzyme of creatine kinase is present in large concentration in

myocardium and small amounts (1-2%) is present in skeletal muscle. It appears in

circulation within 3 hours of onset of myocardial injury, peaking at 12-24 hours and

remains for 1-3 days27

. These are non specific for Myocardial infarction because it rises

with various conditions like cardioversion, cardiac surgery, myocarditis, pericarditis,

after PCI and in certain non cardiac conditions like hypothyroidism, crush injuries,

rhabdomyolysis, muscular dystrophy and in some neurovascular diseases.

CK-MB is used as an alternate for cardiac troponins. They are mainly useful in the

diagnosis of myocardial reinfarction because of its more early and disappearance in

circulation.

MYOGLOBIN:

Myoglobin levels rises within an hour of myocardial injury, reaches peak in 1-4

hours and remains elevated for 24 hours. It is non specific for myocardial injury and

hence not used in isolation for the diagnosis of myocardial infarction.

OTHERS:

Total Creatine Kinase, aspartate transaminase and lactate dehydrogenase are not

recommended as they are highly non specific.

29

PLASMA TEMPORAL PROFILE OF CARDIAC BIOMARKERS

CRITERIA FOR MYOCARDIAL INFARCTION TYPES 1, 2 AND 3 :28,29

The term “Acute myocardial infarction” should be used when there is acute

myocardial injury with clinical evidence of acute myocardial ischaemia and with

Detection of a rise and/or fall of cardiac troponin values with at least one value

above the 99th percentile upper reference limit and at least one of the following:

o Symptoms of myocardial ischaemia

o New ischaemic changes in ECG

o Development of pathological Q waves in ECG

o Imaging evidence of new loss of viable myocardium or new regional wall

motion abnormality

30

o Identification of a coronary thrombus by angiography or by autopsy (not

for type 2 or 3 MIs).

Demonstration of acute athero-thrombosis in the artery supplying the infarcted

myocardium by autopsy meets criteria for type 1 Myocardial infarction

Evidence of an imbalance between myocardial oxygen supply and demand

unrelated to acute athero-thrombosis meets criteria for type 2 Myocardial

infarction.

Cardiac death in patients with symptoms suggestive of myocardial ischaemia and

presumed new ischaemic ECG changes before cardiac troponin values becomes

available or abnormal meets criteria for type 3 Myocardial infarction.

CRITERIA FOR MYOCARDIAL INFARCTION TYPE 4a:30,31

Type 4a MI requires an elevation of cardiac troponin values greater than five times

the 99th percentile upper reference limit in patients with normal baseline value or rise in .

In addition, there should be evidence of new myocardial ischaemia, either from ECG

changes, imaging evidence, or from procedure related complications.

Other criteria regardless of cardiac troponin values is the development of new

pathological Q waves or autopsy evidence of recent procedure related thrombus in culprit

artery.

31

CRITERIA FOR MYOCARDIAL INFARCTION TYPE 4b:

Type 4b MI or stent thrombosis associated MI is detected by coronary angiogram

or by autopsy in the background of myocardial ischaemia with a rise and or fall in cardiac

biomarker values with atleast one value higher than 99th

percentile upper reference limit.

CRITERIA FOR MYOCARDIAL INFARCTION TYPE 5:32,33

Type 5 MI or CABG related MI is defined by elevation in cardiac biomarker

values more than 10 times the 99th

percentile upper reference limit in patients with

normal baseline value with any one of the following:

New pathological Q waves or new LBBB

Coronary angiography documented new graft occlusion

Imaging evidence of new region wall motion abnormality or new viable

myocardial loss.

CRITERIA FOR PREVIOUS MYOCARDIAL INFARCTION:34

Diagnosis of prior MI requires any one of the following:

Pathological Q waves in the absence of non-ischaemic causes

Imaging evidence of a region of viable myocardial loss in the absence of non-

ischaemic causes

Pathological findings of previous MI.

32

MANAGEMENT OF ST-ELEVATION MYOCARDIAL INFARCTION:

With the advances in the approach to reperfusion therapy from pharmacological

management to catheter based strategies, the case fatality rate for STEMI patients has

continued to decline. The management is broadly classified into:

PRE-HOSPITAL MANAGEMENT

IN-HOSPITAL MANAGEMENT

SECONDARY PREVENTION

PRE-HOSPITAL MANAGEMENT:

Any case of suspected Acute coronary syndrome should be hospitalised as soon as

possible and Reperfusion therapy should be started immediately in case of acute ST

elevation myocardial infarction.

The chain of survival for STEMI involves the following:

o Patient education about symptoms of myocardial infarction

o Early contact with hospital

o Practices to shorten door-to-reperfusion time

o Expeditious implementation of reperfusion strategy

PREHOSPITAL CARE:

Most of the STEMI deaths occurs in first hour of onset of symptoms. Therefore,

immediate resuscitation and rapid transportation of patient to hospital is very important.

The main components of the time from onset of symptoms to reperfusion includes the

following:

33

Time for the patient to identify the problem and seek medical attention

Pre-hospital evaluation, treatment and transportation

Time for diagnosis and treatment initiation in hospital(Door-to-Device / Door to

needle time)

Time from treatment initiation to coronary flow restoration.

IN-HOSPITAL MANAGEMENT:

A history of ischemic type chest discomfort and electrocardiography are the main

tools for screening the patients with possible myocardial infarction. ECG should be

obtained within 10 minutes of hospital arrival in suspected patients. All STEMI patients

should have bedside ECG monitoring and Intravenous access.

Presence of ST elevation in ECG with ischemic chest discomfort should be

followed by rapid assessment for initiating reperfusion strategy.

Critical factors for the selection of reperfusion strategy are:

Time elapsed since the onset of ischemic symptoms

Risk associated with STEMI

Risk related to fibrinolytic administration

Time required for the initiation of invasive strategy.

When the ECG is non-diagnostic but the patient’s history is suggestive of STEMI,

serial ECGs, evaluation of cardiac biomarkers, echocardiographic evaluation of

abnormalities in regional wall motion and myocardial perfusion imaging.

34

Door-to-needle time should preferably be less than 30 minutes and less for

fibrinolytic initiation. Door-to-device time should preferably be less than 90 minutes.

GENERAL MEASURES:

ASPIRIN:

162 to 325 mg of non-enteric coated Aspirin should be administered immediately

at initial medical contact.

CONTROL OF CARDIAC PAIN:

ANALGESICS:

Morphine 4 to 8 mg administered intravenously, followed by 2 to 8 mg repeatedly

at 5 to 15 minutes interval.

NITRATES:

Once hypotension is excluded, sublingual nitroglycerin tablet should be

administered and further doses should be administered while monitoring blood pressure

and heart rate of patient. Frequent BP monitoring is required when intravenous form is

used.

BETA-BLOCKERS:

Beta blockers aid in pain relief, reduce the analgesic need and reduce the infarct

size and reduce incidence of arrhythmias. They are contraindicated in patients with heart

failure, hypotension, bradycardia and Atrioventricular block.

35

OXYGEN:

Oxygen supplementation should be given for STEMI Patients with arterial

hypoxemia (Sao2 <90%)

MEASURES FOR LIMITATION OF INFARCT SIZE:

Early reperfusion

Reduction of myocardial energy demand

Prevention of reperfusion injuries

REPERFUSION THERAPY:

Reperfusion strategies available are:

Fibrinolytic therapy

Primary Percutaneous Coronary Intervention

Reperfusion strategy differs based on the availability of PCI availability in the

hospital.

REPERFUSION AT PCI-CAPABLE HOSPITAL:

RECOMMENDATIONS FOR PRIMARY PCI:

STEMI patients with ischemic symptoms of less than 12 hours.35

STEMI patients presenting in less than 12 hours with contra-indication to

fibrinolytic therapy irrespective of the time delay from first medical contact

STEMI patients with cardiogenic shock or acute severe heart failure, irrespective

of time delay from symptom onset

36

USE OF STENTS IN PRIMARY PCI:36

Stent placement (bare metal stent or drug eluting stent) is useful in primary PCI

for STEMI patients. Drug eluting stent placement decreases the rate of restenosis and

need for re-intervention. Drug eluting stents are contraindicated in patients who cannot

tolerate a prolonged course of dual antiplatelet therapy because of increased risk of

thrombosis in stent with premature discontinuation of one or both antiplatelet agents.

ADJUNCTIVE ANTI-THROMBOTIC THERAPY FOR PRIMARY PCI:

ANTI-PLATELET THERAPY:

Tablet aspirin 162-325 mg should be given before primary PCI. Aspirin should be

continued lifelong.37

P2Y12 receptor inhibitors (clopidogrel 600 mg or prasugrel 60 mg or ticagrelor

180 mg) should be given immediately or at the time of primary PCI to patients

with STEMI38

. Maintenance therapy for 1 year should be given for 10 year

following stent placement.

GP IIb/IIIa receptor antagonists – abciximab, tirofiban or eptifibatide at the time

of primary PCI is also a reasonable option.

ANTI-COAGULANT THERAPY:

Unfractioned heparin and bivalirudin are supportive anticoagulant regimens

recommended for STEMI patients undergoing primary PCI. Fondaparinux as a sole

anticoagulant is contraindicated because of the risk of stent thrombosis.39

37

REPERFUSION AT NON-PCI CAPABLE HOSPITAL:

FIBRINOLYTIC THERAPY:40

If there is no contraindications, fibrinolytic therapy should be given to all STEMI

patients presenting within 12 hours when PCI cannot be performed within 120 minutes of

first medical contact. No benefit has been established for fibrinolytic therapy after 12

hours.

FIBRINOLYTIC AGENT DOSE PATENCY RATE

Tenecteplase <60 kg – 3o mg IV

60-69 kg – 35 mg IV

70-79 kg – 40 mg IV

80-89 kg – 45 mg IV

>90 kg – 50 mg IV

85%

Reteplase 2 doses of 10 units IV bolus 30

minutes apart

84%

Alteplase 15 mg IV Bolus, 0.75 mg/kg

(maximum of 50 mg) for 30

minutes, then 0.5 mg/kg

(maximum of 35 mg) over next

60 minutes.

73-84%

Streptokinase (non fibrin

specific)

1.5 million units IV over 30-60

mins

60-68%

38

CONTRAINDICATIONS FOR FIBRINOLYTIC THERAPY:

ABSOLUTE:

Any prior ICH

Structural cerebral vascular lesion (eg., arteriovenous malformation)

Primary or metastatic intracranial neoplasm

Ischemic stroke within 3 months (except within 4.5 hours)

Suspected aortic dissection

Active bleeding or bleeding diathesis (excluding menses)

Closed head or facial trauma within 3 months

Intracranial or intraspinal surgery within 3 months

Uncontrolled severe systemic hypertension unresponsive to emergency therapy

For streptokinase, prior treatment within previous 6 months

RELATIVE:

History of chronic, severe, poorly controlled hypertension

SBP >180 mm hg or DBP >110 mm hg on presentation

History of prior ischemic stroke > 3 months

Dementia

Intracranial pathology not covered in absolute contraindications

Prolonged (>10 minutes) or traumatic Cardiopulmonary resuscitation

Major surgery (<3 weeks)

Recent (within 2 to 4 weeks) internal bleeding

39

Non-compressible vascular punctures

Pregnancy

Active peptic ulcer

Oral anticoagulant therapy

ASSESSMENT OF REPERFUSION AFTER FIBRINOLYSIS:41

Complete or near complete resolution of ST segment at 60 to 90 minutes after

fibrinolytic therapy is a marker of patent infarct artery. Lack of ST segment resolution by

atleast 50% in the worst lead at 60-90 minutes is a strong indication for proceeding with

coronary angiography immediately and rescue PCI.

INDICATIONS FOR TRANSFER FOR ANGIOGRAPHY AFTER

FIBRINOLYTIC THERAPY:42

Cardiogenic shock or severe acute heart failure irrespective of time delay from MI

onset

Failed reperfusion with fibrinolytics or re-occlusion

In stable patients after successful fibrinolysis (between 3-24 hours after

fibrinolysis)

40

CORONARY ARTERY BYPASS GRAFT SURGERY:43

INDICATIONS:

STEMI patients with coronary anatomy not amenable to PCI who have recurrent

or ongoing ischemia, severe heart failure or cardiogenic shock

STEMI patients without cardiogenic shock but not candidates for PCI or

fibrinolytic therapy

ROUTINE MEDICAL THERAPY:

Beta receptor antagonists

Angiotensin converting enzyme inhibitors or Angiotensin receptor blockers

Statins

Analgesics – morphine, nitroglycerine.

Oxygen

41

POST HOSPITALIZATION CARE:

Physical activity

Life style modifications:

o Smoking and alcohol cessation

o Diet/ nutrition

Management of comorbidities:

o Overweight/ obesity

o Systemic hypertension

o Diabetes

o Hypercholesterolemia

o Heart failure

o Arrhythmia

o Depression, stress and anxiety

Medications:

o Beta blockers

o ACE inhibitors / ARBs

o Aldosterone antagonists

o Statins

Provider follow up

Patient and family education.

42

ROLE OF INFLAMMATION IN MYOCARDIAL INFARCTION:

Inflammation plays a vital role in the development of atherosclerosis and

myocardial infarction. During myocardial ischaemia, there is a systemic pro-

inflammatory milieu leading to activation of leucocytes, platelets and other cells. Among

leucocytes, neutrophils plays a critical role in the acute phase of myocardial infarction.

Certain inflammatory markers are found to be associated with increased incidence

of complications and cardiac death in patients with myocardial infarction. Among these

biomarkers, some are found to be useful in the early risk assessment in patients with

myocardial infarction such as total leucocyte count, high sensitive CRP and cardiac

troponins.

Elevated leucocyte count indicates inflammation and it plays a key role in

atherogenesis, atherosclerotic plaque development, rupture and thrombosis. Some studies

have shown that leucocytes destabilize coronary artery plaque at the onset of myocardial

infarction and thus elevated leucocyte itself is considered as independent predictor of

complications and mortality following myocardial infarction.44

ROLE OF LEUCOCYTES IN MI:

Increase in leucocyte count is triggered by the necrotic insult and is considered the

control dogma of reparative process, leading to replacement of dead myocardium by

collagen. Several studies showed that greater the area of myocardial infarction, greater

would be the leucocyte response. A persistent and exaggerated inflammatory response

leads to widespread myocardial injury and tissue death by dysregulated and uncontrolled

release of proinflammatory mediators.

43

Increased cytokine activation leads to activation of nitric oxide synthase and

increased nitric oxide production causing inappropriate vasodilation. This leads to

reduction in systemic and coronary pressure and thus further increasing the myocardial

injury.

LEUCOCYTOSIS AND COMPLICATIONS OF MI:

Several studies demonstrated the strong correlation between the degree of

leucocytes and the extent of infarcted myocardium.

Elevated total leucocyte count has been associated with development of heart

failure in myocardial infarction patients. Release of pro-inflammatory mediators and

oxidative stress during myocardial ischemia contributes to heart failure.

Some of the mechanisms that are proposed as the basis of complications are as

follows:

Circulating leucocyte-platelet aggregates facilitate intravascular plugging leading

to infarct extension

Neutrophils accumulate in the reperfused myocardium and releases oxygen

derived free radicals which leads to further worsening of myocardial injury.

Degree of leucocytosis correlates positively with increased levels in coagulation

factors especially factor VII and factor VII.

LEUCOCYTOSIS AND PROGNOSIS:

Several studies confirms the positive association between leucocyte count and

adverse cardiovascular outcomes in myocardial infarction patients. Initial total leucocyte

count was found to be an independent predictor of 30 day mortality in patients with acute

44

myocardial infarction (both STEMI and NSTEMI). However, for unstable angina there

are varying results.

HIGH SENSITIVITY C-REACTIVE PROTEIN AND MYOCARDIAL

INFARCTION:45

High sensitivity C-Reactive protein is an acute phase reactant is a sensitive marker

of inflammation, tissue damage and infection. Plasma half-life of hs-CRP is 19 hours and

hence the plasma concentration is solely dependent on the synthesis rate. In healthy

asymptomatic individuals, elevated hs-CRP has been found to be a marker of adverse

cardiovascular events. In case of patients with myocardial infarction, elevated hs-CRP is

associated with increased incidence of complications and mortality.

45

MATERIALS AND METHODS

STUDY PARTICIPANTS:

Patients hospitalised at STANLEY MEDICAL COLLEGE AND HOSPITAL,

CHENNAI from June 2018 to November 2018.

DURATION OF STUDY:

6 months (June 2018 to November 2018)

PLACE OF STUDY:

Government Stanley medical college

SAMPLE SIZE:

150

STUDY DESIGN:

Descriptive study

PATIENT SELECTION:

Any patient coming with coronary ischemic symptoms diagnosed as ST elevation

MI. ST elevation MI is defined as new ST segment elevation in two anatomically

contiguous leads of >0.1 mV in all leads other than V2 and V3 leads. For V2 and V3

leads : ≥0.2 mV in males > 40 years, ≥0.25 mV in males <40 years and ≥0.15 mV in

females in the absence of left ventricular hypertrophy or LBBB, pathological Q waves, or

complete left bundle branch block of new onset with elevated troponin T (troponin I level

> 0.04 ng/mL).

46

EXCLUSION CRITERIA:

Hospital admission later than 24 hrs after the onset of symptoms

Lab tests later than 24 hrs after the onset of pain

Previous history of MI/ heart failure

Acute infection/ surgery in the previous 2 weeks

Malignancy

Liver Failure

Renal failure

METHODOLOGY:

All patients diagnosed as acute ST elevation myocardial infarction admitted in

intensive cardiac care unit between June 2018 to November 2018 were selected based on

inclusion and exclusion criteria. Relevant clinical history including comorbidities and

etiological history and complete clinical examination was done. ECG was done at

admission to establish diagnosis of STEMI. Blood samples were obtained at the time of

admission and analysed for total WBC count, ESR, hs-CRP and cardiac

enzymes(troponin I and CK-MB). Echocardiography was performed on the day of

admission and at end of one week. All patients were matched for variables such as age,

gender, diabetes mellitus, systemic hypertension and smoking. The patients are followed

for one week. The total WBC count, ESR and hs-CRP values obtained are then correlated

47

with LVEF at admission and at one week, occurrence of arrhythmia, cardiogenic shock

and death.

STATISTICAL ANALYSIS:

The collected data were analysed with IBM.SPSS statistics software 23.0 Version.

To describe about the data descriptive statistics frequency analysis, percentage

analysis were used for categorical variables and the mean & S.D were used for

continuous variables.

To find the significance in categorical data Chi-Square test was used similarly if

the expected cell frequency is less than 5 in 2×2 tables then the Fisher's Exact was

used.

In all the above statistical tools the probability value .05 is considered as

significant level.

48

OBSERVATION AND RESULTS:

POPULATION CHARACTERISTICS:

Figure 1: Gender distribution in study population

Out of the 150 patients, 97 were males and 53 were females. The incidence of acute

STEMI is twice in males than in females.

Table 1: Age and sex distribution

SEX N MEAN AGE

MALE 97 50.92

FEMALE 53 54.37

The mean age of occurrence of STEMI is 50.92 in males and 54.37 in females.

53

97

GENDER

Female Male

49

Table 2: Age distribution in the study population

AGE GROUP FREQUENCY PERCENTAGE

18 - 40 yrs 10 6.7

41 - 50 yrs 59 39.3

51 - 60 yrs 49 32.7

Above 60 yrs 32 21.3

Total 150 100.0

Most of the patients in the study are between 41 to 50 years. The overall mean age in the

study population is 52.14. only 10 patients are below 40 years. 59 were in 41-50 years

age group, 49 in 51-60 years age group and 32 were above 60 years of age.

Figure 2: Age distribution in study population

The above bar diagram shows that 39.3% of study population belongs to age group of 41-

50 years.

0.0

10.0

20.0

30.0

40.0

50.0

18 - 40 yrs 41 - 50 yrs 51 - 60 yrs Above 60 yrsPE

RC

EN

TA

GE

AGE DISTRIBUTION

18 - 40 yrs

41 - 50 yrs

51 - 60 yrs

Above 60 yrs

50

Figure 3: Systemic hypertension in study population

Out of 150 in the study population, 67 (44.7%) were known case of systemic

hypertension. The remaining 44.7 % cases were normotensive.

Table 3: Diabetes mellitus in study population

DIABETES FREQUENCY PERCENTAGE

YES 65 43.3

NO 85 56.7

TOTAL 150 100.0

65 out of 150 people were diabetic in the study population. 85 were non-diabetic.

55.3%

44.7%

SYSTEMIC HYPERTENSION

No Yes

51

Table 4: Smoking in the study population

SMOKING FREQUENCY PERCENTAGE

YES 64 42.7

NO 86 57.3

TOTAL 150 100.0

Out of 150 in the study population, 64 were smokers and 86 were non-smokers. All the

smokers were males.

Table 5: Frequency distribution of type of MI

TYPE OF MI FREQUENCY PERCENTAGE

ANTEROLATERAL MI 8 5.3

ANTEROSEPTAL MI 29 19.3

ANTERIOR WALL MI 47 31.3

INFEROPOSTERIOR MI 18 12.0

INFERIOR WALL MI 48 32.0

TOTAL 150 100.0

Out of 150 acute STEMI patients in the study population, 48 were diagnosed to have

inferior wall Myocardial infarction, 47 were diagnosed as anterior wall myocardial

52

infarction, 29 were diagnosed as anteroseptal MI, 18 were diagnosed as inferoposterior

wall MI and 8 were diagnosed as anterolateral wall MI.

Figure 4:Type of MI in study population

The above bar diagram shows that inferior wall MI (32%) is more common in the study

population followed by anterior wall MI (31.3%).

0.0

5.0

10.0

15.0

20.0

25.0

30.0

35.0

ALMI ASMI AWMI IPWMI IWMI

ALMI ASMI AWMI IPWMI IWMI

53

Figure 5: Left ventricular ejection fraction at admission

The above bar diagram shows that 46% of the study population had a left ventricular

ejection fraction between 40-49 % at the time of admission. 14.7% cases had normal

LVEF(50-70%). 30.7% cases had mild LV dysfunction(LVEF 30-39%). 8.7% had severe

LV dysfunction (LVEF <30%).

Figure 6: Cardiogenic shock in study population

Out of 150 patients, 16 went for cardiogenic shock during the study period of one week.

0.0

10.0

20.0

30.0

40.0

50.0

50-70% 40-49% 30-39% <30%

PE

RC

EN

TA

GE

LVEF AT ADMISSION

134

16

CARDIOGENIC SHOCK

No Yes

54

Figure 7: Arrhythmia in study population

Out of 150 patients in the study population, 20 patients had arrhythmias in the first week

of admission.

Figure 8: LV Ejection fraction at 1 week

130

20

Arrhythmia

No Yes

0.0

10.0

20.0

30.0

40.0

50.0

50-70% 40-49% 30-39% <30%

Pe

rce

nta

ge

LVEF AT 1 WEEK

55

The above figure shows left ventricular ejection fraction of the 137 patients who survived

at the end of one week. Out of 137 patients, 65 patients(47.4%) had mild left ventricular

dysfunction. 41(29.9%) had moderate LV dysfunction. Only 10(7.3%) had severe LV

dysfunction.

Figure 9: Mortality at 1 week

Out of 150 patients in our study, 13 patients(8.7%) expired within one week of

admission.

91.3%

8.7%

Death

No Yes

56

TOTAL LEUCOCYTE COUNT :

Figure 10 : Total leucocyte count with LVEF at admission

The above bar diagram shows that 84.6% patients with severe left ventricular dysfunction

had elevated total count whereas only 9.1% with normal LV function had elevated total

count.

Table 6: Comparison of Total leucocyte count with LVEF at admission

LVEF AT ADMISSION

Total

P-

value Normal Mild Moderate Severe

TC Normal Count 20 53 22 2 97

0.0005

% 90.9% 76.8% 47.8% 15.4% 64.7%

Elevated Count 2 16 24 11 53

% 9.1% 23.2% 52.2% 84.6% 35.3%

Total Count 22 69 46 13 150

0%

20%

40%

60%

80%

100%

Normal LVfunction

Mild LVdysfunction

Moderate LVdysfuntion

Severe LVdysfuntion

Pe

rce

nta

ge

TOTAL COUNT WITH LVEF AT ADMISSION

Normal Elevated

57

In the above chi-square test, elevated total count in relation to severity of LV dysfunction

is statistically highly significant (p value <0.0l)

Figure 11: Total leucocyte count with arrhythmia

The above bar diagram shows that 70% of cases with arrhythmias had elevated total

leucocyte count. Remaining 30 % cases had normal leucocyte count.

0%

20%

40%

60%

80%

100%

No Yes

Pe

rce

nta

ge

TC WITH ARRHYTHMIA

Normal Elevated

58

Table 7: Comparison of Total leucocyte count with arrythmia

ARRHYTHMIA

Total

χ 2

-

value

P-

value NO YES

TC Normal Count 91 6 97

12.138 0.0005

% 70.0% 30.0% 64.7%

Elevated Count 39 14 53

% 30.0% 70.0% 35.3%

Total Count 130 20 150

The above table shows that elevated total leucocyte count in comparison with occurrence

of arrhythmia is statistically highly significant.

Figure 12: Total leucocyte count with cardiogenic shock

The above bar diagram shows that 87.5% patients who went for cardiogenic shock had

elevated total leucocyte count.

0%

20%

40%

60%

80%

100%

No Yes

Pe

rce

nta

ge

TC WITH CARDIOGENIC SHOCK

Normal Elevated

59

Table 8: Comparison of total leucocyte count with cardiogenic shock

CARDIOGENIC

SHOCK Total

χ 2

–

value

P-

value

NO YES

TC

Normal

Count 95 2 97

21.332 0.0005

% 70.9% 12.5% 64.7%

Elevated

Count 39 14 53

% 29.1% 87.5% 35.3%


The above table shows that elevated total count in comparison with occurrence of

cardiogenic shock is statistically highly significant.

Figure 12: Total leucocyte count with Severe LV dysfunction at 1 week

0%

20%

40%

60%

80%

100%

No Yes

Pe

rce

nta

ge

TC WITH SEVERE LV DYSFUNTION AT

1 WEEK

Normal Elevated

60

The above bar diagram shows that among the patients who survived one week who had

severe LV dysfunction, all of them had elevated total leucocyte count. Among the

patients with normal LV function to moderate LV dysfunction, 74.8 % cases had normal

total count and only 25.2% cases had leucocytosis.

Table 9: Comparison of Total leucocyte count with Severe LV dysfunction at 1 week

SEVERE LV

DYSFUNCTION Total

χ 2-

value

P-

value

NO YES

TC

Normal

Count 95 0 95

24.4 0.0005

% 74.8% 0.0% 69.3%

Abnormal

Count 32 10 42

% 25.2% 100.0% 30.7%


The above table shows that elevated total count in relation with occurrence of severe LV

dysfunction at 1 week is statistically highly significant.

61

Figure 13: Total leucocyte count with mortality

The above bar diagram shows that 84.6% patients who died within 1 week of admission

had elevated total leucocyte count.

Table 10: Comparison of Total leucocyte count with mortality

DEATH

Total

χ 2-

value

P-

value NO YES

TC Normal Count 95 2 97

15.130 0.0005

% 69.3% 15.4% 64.7%

Abnormal Count 42 11 53

% 30.7% 84.6% 35.3%


The above table shows that elevated total leucocyte count in relation with mortality in

one week is statistically highly significant.

0%

20%

40%

60%

80%

100%

No Yes

Pe

rce

nta

ge

TC WITH MORTALITY

Normal Elevated

62

Figure 14: hs-CRP with LV function at admission

The above stacked bar diagram shows that 61.5% patients of severe LV dysfunction at

admission had elevated hs-CRP. 47.8% patients with moderate LV dysfunction had

elevated hs-CRP, 29% patients with mild LV dysfunction had elevated hs-CRP and %

patients with normal LV function had elevated hs-CRP levels.

0%10%20%30%40%50%60%70%80%90%

100%

Normal LVfunction

Mild LVdysfunction

Moderate LVdysfunction

Severe LVdysfunction

Pe

rce

nta

ge

hs CRP WITH LV FUNCTION AT ADMISSION

Normal Elevated

63

Table 11: Comparison of hs-CRP with LV systolic function at admission

LV FUNCTION AT ADMISSION

Total

P-

value

Normal

Mild

dysfunction

Moderate

dysfunction

Severe

dysfunction

hs

CRP

Normal Count 14 49 24 5 92

0.064

% 63.6% 71.0% 52.2% 38.5% 61.3%


% 36.4% 29.0% 47.8% 61.5% 38.7%

Total Count 22 69 46 13 150

The above table shows that hs-CRP in comparison with LV function at admission is not

statistically significant.

Figure 15: hs-CRP with arrhythmia

0%10%20%30%40%50%60%70%80%90%

100%

No Yes

Pe

rce

nta

ge

Groups

hs-CRP WITH ARRHYTHMIA

Normal Elevated

64

The above bar diagram shows that hS-CRP is elevated in 55% patients who had

arrhythmia and hS-CRP is elevated in only 36.2% patients without arrhythmia.

Table 12: Comparison of hs-CRP with arrhythmia

Comparison between hs CRP with Arrhythmia

ARRHYTHMIA

Total

χ2-

value

P-

value NO YES

hs

CRP

Normal Count 83 9 92

2.596 0.107

% 63.8% 45.0% 61.3%


% 36.2% 55.0% 38.7%


The hS-CRP is compared with occurrence of arrhythmia in above table. The association

between elevated hs-CRP and arrhythmia occurrence is not statistically significant.

65

Figure 16: hs-CRP with Cardiogenic shock

The above bar diagram shows that among 16 patients who went for cardiogenic shock, 10

patients(62.5%) had elevated hS-CRP.

Table 13: Comparison of hs-CRP with cardiogenic shock

CARDIOGENIC

SHOCK Total

χ2 -

value

P-

value

NO YES

hs

CRP

Normal

Count 86 6 92

4.29 0.038

% 64.2% 37.5% 61.3%

Elevated

Count 48 10 58

% 35.8% 62.5% 38.7%


The association between elevated hS-CRP and cardiogenic shock is statistically

significant.

0%

20%

40%

60%

80%

100%

No Yes

Pe

rce

nta

ge

hs CRP with Cardiogenic shock

Normal Elevated

66

Figure 17: hs-CRP with severe LV dysfunction at 1 week

The above bar diagram shows that hs-CRP is elevated in 70% of patients with severe LV

dysfunction at 1 week. hS-CRP is elevated only in 35.4% patients who had normal LV

function or mild to moderate LV dysfunction.

0%

20%

40%

60%

80%

100%

No Yes

Pe

rce

nta

ge

hs CRP with Severe LV dysfunction

Normal Elevated

67

Table 14: comparison between hS-CRP with severe LV dysfunction at 1 week

SEVERE LV

DYSFUNCTION Total

χ2 -

value

P-

value

NO YES

hs

CRP

Normal

Count 82 3 85

4.704 0.042

% 64.6% 30.0% 62.0%

Abnormal

Count 45 7 52

% 35.4% 70.0% 38.0%


The above table shows that the association between elevated hS-CRP and severe LV

dysfunction at 1 week is statistically significant.

68

Figure 18: hs-CRP with mortality

Out of 150 patients in the study, 13 expired in first week. Among 13, 7 patients had

elevated hS-CRP and 6 patients had normal hS-CRP levels.

Table 15: Comparison of hS-CRP with mortality

DEATH

Total

χ2 -

value

P-

value NO YES

hs

CRP


0.336 0.562

% 62.0% 53.8% 61.3%


% 38.0% 46.2% 38.7%


0%

20%

40%

60%

80%

100%

No Yes

Pe

rce

nta

ge

hs CRP WITH MORTALITY

Normal Elevated

69

The above table shows that the association between elevated hS-CRP levels and mortality

in first week is not statistically significant.

ERYTHROCYTE SEDIMENTATION RATE:

Figure 19: ESR at 1 hour with LV systolic function at admission

Out of 13 patients with severe LV dysfunction, 11(84.6%) had elevated ESR at 1 hour.

Among patient with moderate LV dysfunction, 78.3% had elevated ESR. 56.5% patients

with mild LV dysfunction had elevated ESR.

0%

20%

40%

60%

80%

100%

Normal LVfunction

Mild LVdysfunction

Moderate LVdysfunction

Severe LVdysfunction

Pe

rce

nta

ge

ESR-1 HR WITH LV FUNCTION AT

ADMISSION

Normal Elevated

70

Table 16: Comparison of ESR-1 hour with LV systolic function at admission

LV FUNCTION

Total

P-

value

Normal

LV

function

Mild LV

dysfunction

Moderate

LV

dysfunction

Severe LV

dysfunction

ESR

- 1

HR

Normal Count 13 30 10 2 55

0.004

% 59.1% 43.5% 21.7% 15.4% 36.7%


% 40.9% 56.5% 78.3% 84.6% 63.3%

Total Count 22 69 46 13 150

There is statistically highly significant association between elevated ESR at 1 hour and

severity of LV dysfunction at admission.

71

Figure 20: ESR-1hr with arrhythmia

Out of 150 patients, 20 had arrhythmia. Among these 20 patients, 13 patients(65%) had

elevated ESR and 7 patients(35%) had normal ESR. In the remaining 130 patients who

didn’t have arrhythmia, 63.1% had elevated ESR.

Table 17: comparison of ESR-1 Hour with arrhythmia

ARRHYTHMIA

Total

χ2 -

value

P-value

NO YES

ESR -

1 HR


0.028 0.868

% 36.9% 35.0% 36.7%


% 63.1% 65.0% 63.3%


0%

20%

40%

60%

80%

100%

No Yes

Pe

rce

nta

ge

ESR-1 HR with Arrhythmia

Normal Elevated

72

The above table shows that there is no statistically significant association between

increased ESR with occurrence of arrhythmia in the study population.

Figure 21: ESR – 1 hour with cardiogenic shock

The above stacked bar diagram shows that 87.5% patients with cardiogenic shock has

elevated ESR at 1 hour.

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

No Yes

Pe

rce

nta

ge

ESR-1 HR WITH CARDIOGENIC SHOCK

Normal Elevated

73

Table 18: comparison of ESR-1 hour with cardiogenic shock

CARDIOGENIC

SHOCK Total

χ2 -

value

P-value

NO YES

ESR -

1 HR

Normal

Count 53 2 55

4.504 0.042

% 39.6% 12.5% 36.7%

Elevated

Count 81 14 95

% 60.4% 87.5% 63.3%


On comparison with ESR at 1 hour with cardiogenic shock, there was a significant

association between the two (p<0.05)

Figure 22: ESR at 1 hour with Severe LV dysfunction at 1 week

0%

20%

40%

60%

80%

100%

No Yes

Pe

rce

nta

ge

ESR WITH SEVERE LV DYSFUNCTION AT 1

WEEK

Normal Elevated

74

The above stacked bar diagram shows that among 10 patients with severe LV dysfunction

at 1 week, 8 patients(80%) had elevated ESR and the remaining 2 patients had normal

ESR.

Table 19: comparison of ESR-1 hour with severe LV dysfunction at 1 week

SEVERE LV

DYSFUNCTION Total

χ2 -

value

P-value

NO YES

ESR -

1 HR

Normal

Count 51 2 53

1.588 0.316

% 40.2% 20.0% 38.7%

Elevated

Count 76 8 84

% 59.8% 80.0% 61.3%


The above table shows that association between ESR at 1 hour and severe LV

dysfunction at 1 week is not statistically significant.

75

Figure 23: ESR-1 hour with mortality

The above stacked bar diagram shows that ESR at 1 hour is elevated in 11(84.6%) out of

13 expired patients. Amount the patients who survived 1 week, 61.3% had elevated ESR

at 1 hour.

Table 20: Comparison of ESR-1 hour with mortality

DEATH

Total

χ2 –

value

P-value

NO YES

ESR -

1 HR


2.776 0.096

% 38.7% 15.4% 36.7%

Abnormal Count 84 11 95

% 61.3% 84.6% 63.3%


The above table shows that the association between elevated ESR at 1 hour and mortality

is not statistically significant.

0%

50%

100%

No Yes

Pe

rce

nta

ge

ESR-1 HOUR WITH MORTALITY

Normal Elevated

76

DISCUSSION:

Of the total 150 cases in this study, who were selected as per inclusion and

exclusion criteria, 137 patients survived and 13 patients expired during the period of one

week.

There were 97 males(64.7%) and 53 females(35.3%) in the study. The mean age

of occurrence of STEMI in this study is 50.9 years in males and that of females is 54.37

years in our study.

Among 150 cases in the study, 67 cases(44.7%) were known case of diabetes

mellitus and 65 cases(43.3%) were known case of systemic hypertension. 27 cases had

both diabetes mellitus and systemic hypertension. 46 cases were neither diabetic nor

hypertensive.

In this study, 64 cases(42.7%) were smokers and the remaining 84 cases(57.3%)

were non-smokers. All the smokers were males. Among smokers, 26 cases were

hypertensive and 21 cases were diabetic.

The most common type of myocardial infarction in the study population is inferior

wall myocardial infarction(48 cases) followed by anterior wall myocardial infarction

(47 cases).

Out of 150 cases in the study, 22 cases (14.7%) had normal left ventricular

function at admission. 69 cases (46%) had mild left ventricular dysfunction, 46 cases

(30.7%) had moderate LV dysfunction and 13 cases (8.7%) had severe LV dysfunction at

admission.

77

Total leucocyte count is elevated in 53 patients (35.3%) and normal in 97 patients

(64.7%). The mean total leucocyte count of the study population is 9966 per cubic mm.

13 cases (84.6%) of severe LV dysfunction at admission had elevated Total leucocyte

count. 14 cases (70%) of arrhythmia had leucocytosis. 87.5% of cases who went for

cardiogenic shock had elevated Total count. Out of 137 survivors at the end of one week,

10 cases had severe LV dysfunction and all of them had elevated total count.

In our study, strong association was found between leucocytosis and occurrence of

arrhythmia, cardiogenic shock, LV dysfunction and mortality in one week.

According to Grzybowski et al46

, elevated total count is associated with

complications such as LV failure, cardiogenic shock and in-hospital mortality, and is an

important predictive factor for in-hospital complications. A study by Menon et al

47 also

shows association between increased baseline total leucocyte count and cardiac

complications after acute myocardial infarction.

13 cases expired during the study period and 11(84.6%) of them had elevated

total count. A study by cannon et al48

also shows higher mortality rate in cases of acute

myocardial infarction with elevated total leucocyte count.

Out of 150 cases in the study, high sensitivity CRP is elevated in 58 cases

(38.7%)and it is within normal limits in 92 cases (61.3%). Mean hs-CRP in the study

population is 2.8 mg/L. 61.5% cases who had severe LV dysfunction at admission had

elevated hs-CRP. 11 cases (55%) who had arrhythmia during the study period had

elevated hs-CRP. Among the cases who went for cardiogenic shock, 62.5% had elevated

78

hs-CRP. Out of 10 cases who had severe LV dysfunction, 7 cases had elevated hs-CRP.

46.2% cases who expired during the study period had elevated hs-CRP.

In our study, elevated hs-CRP levels are associated with severe LV dysfunction at

1 week and occurrence of cardiogenic shock but association with mortality is not

statistically significant.

In a study conducted by Roubin et al.49

, higher levels of hs-CRP is associated

with increased incidence of in-hospital cardiac events in patients with acute myocardial

infarction.

In our study, out of 150 cases, 95 cases (63.3%) had elevated ESR at 1 hour. The

mean ESR at 1 hour is 20.1 mm. ESR was elevated in 11 cases (84.6%) in patients with

severe LV dysfunction. 65% (13 cases) who had arrhythmia during study period had

elevated ESR. ESR is elevated in 14 cases (87.5%) of patients who developed

cardiogenic shock. 8 out of 10 cases with severe LV dysfunction at one week had

elevated ESR.

In our study, significant association was found between elevated ESR and

occurrence of cardiogenic shock but no significant association with LV dysfunction or

arrhythmias.

11 cases(84.6%) who expired within one week had elevated ESR. In a study by

timmer et al.50

, in 346 patients of Acute myocardial infarction, significant association was

found between elevated ESR and short-term cardiovascular mortality. But in our study,

no statistically significant association was found between ESR and mortality in one week.

79

CONCLUSION:

Majority of the patients are males. The mean age of occurrence is earlier in this

study when compared to the current trend. The most common type of MI is

inferior wall Myocardial Infarction.

Most of the patients are either diabetic or hypertensive. The occurrence is most

common among smokers.

The mean total WBC count is higher. Higher the levels of Total WBC count,

higher the occurrence of in-hospital cardiovascular complications and

cardiovascular deaths in first week after acute myocardial infarction.

Elevated hs-CRP levels are strongly associated with severe LV dysfunction at 1

week and cardiogenic shock.

High ESR values are associated with occurrence of cardiogenic shock.

Among the inflammatory markers, Total leucocyte count has a strong association

with short-term complications and mortality after acute myocardial infarction.

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PROFORMA

NAME :

AGE/SEX : DATE OF ADMISSION :

IP NO : DATE OF DISCHCARGE :

ADDRESS :

CONTACT NO :

COMPLAINTS:

H/O CHEST PAIN

DURATION : RADIATION:

SITE : ASSOCIATED SYMPTOMS :

TYPE :

H/O BREATHLESSNESS/SYNCOPE/PALPITATION

PAST HISTORY :

H/O DM/SHT/CAD/CKD/CLD.

PERSONAL HISTORY : SMOKER/ALCOHOLIC

PHYSICAL EXAMINATION :

Built and nourishment

Hydration

Anaemia

Peripheral edema

JVP

Pulse: BP: RR:

CVS-

RS-

P/A-

CNS-

INVESTIGATIONS:

ECG :

CARDIAC BIOMARKERS : TROPONIN I –

CK-MB-

TOTAL LEUCOCYTE COUNT:

ERYTHROCYTE SEDIMENTATION RATE :

HIGH SENSITIVITY C-REACTIVE PROTEIN :

ECHO AT ADMISSION:

ECHO AT 1 WEEK:

OUTCOMES:

ARRHYTHMIA – YES/NO

CARDIOGENIC SHOCK - YES/NO

DEATH - YES/NO

INFORMED CONSENT

“A STUDY ON TOTAL LEUCOCYTE COUNT, ERYTHROCYTE



Place of study: Govt. Stanley medical college, Chennai

I …………………………………….……………………. have been informed about the

details of the study in my own language.

I have completely understood the details of the study.

I am aware of the possible risks and benefits, while taking part in the study.

I agree to collect samples of blood/saliva/urine/tissue if study needs.

I understand that I can withdraw from the study at any point of time and even then, I can

receive the medical treatment as usual.

I understand that I will not get any money for taking part in the study.

I will not object if the results of this study are getting published in any medical journal,

provided my personal identity is not revealed.

I know what I am supposed to do by taking part in this study and I assure that I would

extend my full cooperation for this study.

Volunteer: Witness:

Name and address Name and address

Signature/thumb impression: Signature/thumb impression

INFORMED CONSENT

“A STUDY ON TOTAL LEUCOCYTE COUNT, ERYTHROCYTE



CERTIFICATE BY INSTITUTIONAL ETHICS COMMITTEE

PLAGIARISM CERTIFICATE

MA

ST

ER

CH

AR

T

S N

AG

E SEX

SHT

DM

SMO

KI

NG

D

IAG

NO

SIS TC

h

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3

5

N

N

N

N

9

51

M

Y

Y N

IW

MI

10

,30

0 2

.6 2

0

0.2

5 8

.1 4

5

44

N

N

N

N

10

5

5

M

N

N

Y A

WM

I 8

,90

0 1

.8 1

8

0.0

6 6

.8 4

5

48

N

N

N

N

11

6

2

F Y

Y N

A

WM

I 1

1,3

00

3.8

16

0

.24

8.5

35

2

8

N

N

Y N

12

5

6

M

Y N

Y

IPW

MI

12

,60

0 2

.2 1

0

0.2

9.6

30

Y N

Y

13

6

0

F N

N

N

A

LMI

9,8

00

3.5

17

0

.11

7.5

42

4

5

N

N

N

N

14

5

8

M

Y Y

Y A

SMI

14

,50

0 2

.6 3

0

0.2

11

.5 2

6

N

Y

Y

15

6

1

M

N

N

Y IW

MI

12

,70

0 2

.7 2

6

0.1

8 9

.7 3

4

38

N

N

N

N

16

4

3

M

Y N

N

A

WM

I 9

,90

0 2

.4 1

2

0.0

9 7

.5 4

5

45

N

N

N

N

17

6

8

M

Y Y

Y IP

WM

I 1

4,7

00

3.8

18

0

.35

11

.8 3

2

35

Y

N

N

N

18

6

0

M

N

N

Y A

SMI

12

,40

0 3

.7 1

6

0.1

8 1

0.4

28

N

Y

Y

19

3

5

M

N

N

Y IW

MI

9,7

00

3.5

8

0.1

2 8

.9 3

5

36

N

N

N

N

20

4

6

F Y

Y N

A

WM

I 1

2,3

00

2.9

26

0

.26

10

.5 3

5

35

N

N

N

N

21

5

3

M

N

N

N

IWM

I 7

,30

0 2

.2 3

2

0.1

3 7

.5 3

4

35

Y

N

N

N

22

5

8

M

N

Y Y

ASM

I 9

,90

0 1

.8 3

0

0.1

6 7

.2 3

8

38

N

N

N

N

23

5

4

F N

N

N

IP

WM

I 1

1,3

00

2.6

36

0

.24

10

.2 4

0

42

N

N

N

N

24

7

1

F Y

N

N

ASM

I 6

,60

0 1

.9 2

8

0.1

6.9

33

3

2

N

N

N

N

25

3

9

M

Y N

Y

AW

MI

8,9

00

1.8

22

0

.07

7.2

38

3

8

N

N

N

N

26

3

6

M

N

Y Y

IWM

I 1

0,3

00

2.8

25

0

.25

8.5

46

4

5

N

N

N

N

27

5

8

F Y

Y N

A

WM

I 1

6,4

00

3.5

32

0

.3 1

1

25

2

5

Y N

Y

N

28

6

1

M

N

N

Y IW

MI

9,5

00

2.6

18

0

.06

10

.5 4

5

45

N

N

N

N

29

4

7

M

Y N

Y

IPW

MI

5,1

00

1.9

22

0

.1 6

.8 3

7

38

N

N

N

N

30

6

6

M

N

Y N

A

WM

I 1

0,3

00

3.6

20

0

.22

9.4

40

4

2

N

N

N

N

31

5

9

F Y

N

N

IWM

I 1

2,8

00

3.4

34

0

.28

8.5

40

Y Y

Y

32

3

2

M

N

N

Y IW

MI

6,9

00

2.2

23

0

.14

6.8

55

5

5

N

N

N

N

33

6

3

M

N

Y N

A

SMI

5,9

00

2.3

18

0

.12

7.1

48

4

8

N

N

N

N

34

6

2

M

Y Y

N

AW

MI

11

,00

0 3

3

0

0.2

6 1

0.2

37

N

N

Y

35

4

8

F Y

N

N

IWM

I 1

0,6

00

3.3

28

0

.19

11

.8 3

8

38

N

N

N

N

36

4

4

M

N

N

N

AW

MI

9,5

00

2.2

12

0

.21

9.5

45

4

5

N

N

N

N

37

4

9

F N

Y

N

IPW

MI

8,3

00

2.9

25

0

.15

8.2

50

5

0

N

N

N

N

38

5

5

M

Y Y

Y A

WM

I 9

,80

0 1

.9 1

4

0.0

6 8

.8 3

8

36

N

N

N

N

39

5

7

M

Y N

Y

AW

MI

12

,80

0 3

.6 3

4

0.2

2 1

0.5

30

3

2

N

Y N

N

40

4

8

M

N

N

N

ASM

I 1

4,6

00

3.5

30

0

.3 1

1.1

32

Y Y

Y

41

5

8

F N

N

N

A

WM

I 9

,60

0 2

.9 2

4

0.1

5 7

.2 5

0

52

N

N

N

N

42

6

6

M

N

N

Y IW

MI

9,8

00

2.5

22

0

.19

8.1

56

5

6

N

N

N

N

43

6

2

M

Y N

N

IW

MI

6,7

00

2.9

9

0.1

6 6

.8 4

8

49

N

N

N

N

44

5

8

F N

N

N

IP

WM

I 1

0,7

00

3.5

22

0

.21

10

.2 4

0

40

N

N

N

N

45

4

6

M

Y N

Y

IWM

I 1

3,7

00

3.7

25

0

.24

11

.4 3

5

30

N

Y

N

N

46

4

1

M

Y N

N

IW

MI

12

,20

0 2

.8 1

8

0.3

4 1

0.1

28

2

8

N

N

Y N

47

5

3

M

N

N

N

ASM

I 4

,50

0 3

.8 2

0

0.0

9 8

.5 3

5

35

N

N

N

N

48

4

9

M

N

Y Y

AW

MI

3,9

00

2.1

17

0

.07

7

48

4

8

N

N

N

N

49

5

2

F N

N

N

A

WM

I 1

1,4

00

2.5

22

0

.12

10

.8 4

0

40

N

N

N

N

50

6

3

F Y

N

N

ASM

I 2

0,1

00

3.8

32

0

.15

12

.1 2

5

N

Y

Y

51

6

1

M

N

N

Y IW

MI

9,5

00

2.4

18

0

.08

8.2

42

4

2

Y N

N

N

52

5

4

F Y

Y N

IW

MI

8,3

00

2.6

18

0

.1 7

.3 4

5

42

N

N

N

N

53

6

5

M

N

N

N

AW

MI

13

,60

0 3

.6 2

4

0.1

2 1

0.5

32

2

8

N

N

Y N

54

6

3

M

N

Y Y

AW

MI

11

,50

0 3

.4 3

0

0.2

11

.2 2

8

26

N

N

Y

N

55

4

7

M

Y Y

Y A

SMI

7,5

00

2.4

22

0

.09

10

.1 5

0

50

N

N

N

N

56

4

9

F N

Y

N

IPW

MI

4,3

00

2.3

19

0

.07

9.5

52

5

0

N

N

N

N

57

5

1

F Y

N

N

AW

MI

9,8

00

1.8

8

0.1

2 8

.9 4

5

42

N

N

N

N

58

5

8

M

N

N

Y A

SMI

11

,20

0 3

.6 3

2

0.2

3 1

0.8

40

4

0

N

N

N

N

59

6

3

M

Y N

N

IW

MI

3,9

00

2.1

14

0

.08

6.8

45

4

5

N

N

N

N

60

6

5

M

Y N

Y

IPW

MI

18

,20

0 2

.5 3

0

0.2

4 8

.6 3

0

32

N

N

N

N

61

5

2

M

N

Y N

A

WM

I 6

,70

0 2

.6 2

5

0.1

4 7

.1 4

5

45

N

N

N

N

62

4

7

F N

Y

N

ASM

I 7

,50

0 2

.6 2

2

0.1

8 8

.2 4

8

48

N

N

N

N

63

5

6

F Y

Y N

IW

MI

12

,60

0 3

.2 3

3

0.3

9.5

33

3

5

N

N

N

N

64

4

5

M

N

N

Y A

WM

I 6

,30

0 3

.5 1

4

0.0

8 7

5

0

50

N

N

N

N

65

4

7

M

N

Y N

A

WM

I 1

1,0

00

2.9

29

0

.18

10

.2 3

4

35

N

N

N

N

66

6

5

F Y

Y N

A

SMI

13

,30

0 3

.6 2

8

0.2

4 1

0.5

26

N

N

Y

67

3

6

M

N

N

Y IP

WM

I 1

1,4

00

2.6

25

0

.27

9.8

32

3

0

Y N

N

N

68

4

7

M

Y N

Y

IWM

I 8

,90

0 3

1

0

0.1

2 7

.2 4

8

48

N

N

N

N

69

4

3

M

Y Y

N

ASM

I 1

0,2

00

2.6

20

0

.25

9.7

34

3

5

N

N

N

N

70

5

5

M

Y Y

Y A

LMI

5,7

00

2.6

24

0

.12

8.2

46

4

6

N

N

N

N

71

6

4

M

Y Y

N

AW

MI

11

,40

0 3

.5 3

0

0.1

5 1

1

40

4

0

N

N

N

N

72

4

3

F Y

N

N

IWM

I 6

,70

0 3

.1 1

8

0.1

2 7

.5 5

2

52

N

N

N

N

73

4

8

M

N

Y Y

IPW

MI

8,6

00

2.6

14

0

.08

7.8

42

4

4

N

N

N

N

74

6

3

F N

Y

N

IWM

I 7

,40

0 2

.9 9

0

.07

8.2

46

4

6

N

N

N

N

75

4

8

M

Y Y

Y A

WM

I 1

6,7

00

2.7

40

0

.24

13

.8 2

8

28

N

N

Y

N

76

7

1

F N

N

N

A

WM

I 6

,90

0 3

.4 2

5

0.0

8 8

.8 4

5

45

N

N

N

N

77

5

3

M

N

Y N

A

SMI

9,0

00

3.5

21

0

.09

7.5

38

3

8

N

N

N

N

78

5

8

M

Y Y

N

IPW

MI

8,5

00

2.6

16

0

.1 6

.8 4

5

45

N

N

N

N

79

4

9

M

N

Y Y

AW

MI

12

,30

0 3

.5 3

5

0.2

1 1

2.5

33

3

5

N

N

N

N

80

5

4

M

Y N

Y

IWM

I 9

,00

0 3

.6 2

6

0.0

8 1

0.1

54

5

5

N

N

N

N

81

4

9

F N

N

N

A

LMI

5,7

00

2.8

14

0

.07

9.5

50

5

0

N

N

N

N

82

6

1

F N

Y

N

ASM

I 1

1,4

00

2.9

38

0

.13

12

.5 4

0

42

N

N

N

N

83

4

2

M

Y N

Y

AW

MI

4,8

00

3.5

7

0.0

7 9

.5 4

6

46

N

N

N

N

84

5

1

M

N

Y N

IW

MI

10

,30

0 2

.5 1

0

0.2

9.9

35

3

2

N

N

N

N

85

7

0

M

N

Y N

IW

MI

8,2

00

2.4

4

0.1

2 8

.6 5

4

55

N

N

N

N

86

4

5

F Y

N

N

AW

MI

7,4

00

1.8

9

0.1

4 7

.8 5

2

52

N

N

N

N

87

5

1

M

N

N

Y A

SMI

9,2

00

3.1

12

0

.18

8.5

48

4

8

N

N

N

N

88

4

6

M

N

N

Y A

WM

I 1

1,9

00

3.5

22

0

.29

13

.5 3

8

35

Y

Y N

N

89

4

9

F N

N

N

IW

MI

7,5

00

2.5

16

0

.2 8

.5 4

5

45

N

N

N

N

90

5

6

F Y

Y N

IP

WM

I 9

,40

0 2

.7 2

3

0.2

5 7

.6 4

6

48

N

N

N

N

91

5

2

M

Y N

Y

ALM

I 5

,60

0 1

.8 1

5

0.1

7.2

43

4

5

N

N

N

N

92

5

9

F N

Y

N

AW

MI

13

,90

0 3

.2 2

6

0.1

2 1

3.4

34

2

8

N

N

Y N

93

6

1

M

N

Y N

IW

MI

17

,00

0 3

.8 2

8

0.2

5 1

4.6

30

3

0

Y N

N

N

94

4

6

M

Y N

Y

IWM

I 8

,30

0 2

.1 1

0

0.0

8 1

0.5

48

4

5

N

Y N

N

95

6

3

F N

Y

Y A

SMI

10

,70

0 2

.6 1

4

0.1

5 8

.5 3

5

35

N

N

N

N

96

5

8

M

Y Y

N

AW

MI

7,8

00

2.2

9

0.0

8 1

0.1

42

4

2

N

N

N

N

97

5

2

F N

Y

N

ASM

I 1

2,2

00

3.7

16

0

.22

12

.5 2

8

28

Y

N

Y N

98

4

9

F N

N

N

A

WM

I 1

0,4

00

3.6

28

0

.2 1

1.5

38

3

5

N

N

N

N

99

5

0

M

Y Y

Y IP

WM

I 6

,90

0 1

.8 1

5

0.1

2 1

0.6

45

4

5

N

N

N

N

10

0 4

7

F Y

Y N

A

SMI

7,3

00

2.7

4

0.1

9.5

48

4

8

N

N

N

N

10

1 6

3

F N

Y

N

AW

MI

6,8

00

1.9

22

0

.11

8.6

42

4

5

N

N

N

N

10

2 4

2

M

N

N

Y A

LMI

12

,90

0 2

.9 1

6

0.1

8 1

3.5

30

N

Y

Y

10

3 5

1

M

Y N

Y

AW

MI

9,3

00

2

25

0

.08

7.6

46

4

5

N

N

N

N

10

4 4

7

M

Y Y

N

AW

MI

6,8

00

2.1

6

0.0

6 8

.2 4

8

48

N

N

N

N

10

5 3

7

M

N

Y Y

IWM

I 5

,90

0 2

.2 1

1

0.0

7 8

.5 5

2

52

N

N

N

N

10

6 4

0

M

N

Y N

IW

MI

11

,70

0 3

.1 2

8

0.1

8 1

2.6

45

4

2

Y N

N

N

10

7 6

3

M

Y N

Y

ASM

I 8

,00

0 2

.2 1

4

0.1

4 8

.5 4

5

45

N

N

N

N

10

8 5

3

F N

Y

N

AW

MI

10

,70

0 3

.2 2

6

0.2

2 1

0.5

40

3

8

N

N

N

N

10

9 4

2

M

N

N

Y A

WM

I 7

,00

0 2

.5 1

2

0.1

5 7

.6 4

2

45

N

N

N

N

11

0 4

5

F N

N

N

IW

MI

7,9

00

2.6

26

0

.09

6.9

47

4

8

N

N

N

N

11

1 3

3

M

N

N

Y A

SMI

14

,60

0 3

.7 2

4

0.2

12

.6 3

6

35

N

N

N

N

11

2 4

5

M

Y Y

Y IW

MI

10

,50

0 3

.6 1

2

0.1

8 1

1.5

46

4

6

N

N

N

N

11

3 4

8

F Y

N

N

AW

MI

8,6

00

2.5

7

0.1

2 9

.2 5

2

52

Y

N

N

N

11

4 6

2

F N

Y

N

IWM

I 7

,50

0 2

.6 1

8

0.1

1 8

.5 5

0

50

N

N

N

N

11

5 4

6

M

N

N

Y IW

MI

12

,80

0 3

.4 2

0

0.1

9 1

2.5

45

4

4

Y N

N

N

11

6 5

3

M

N

N

Y A

SMI

13

,70

0 3

.9 1

8

0.1

8 1

1.9

30

2

8

N

Y Y

N

11

7 5

0

F Y

N

N

ASM

I 8

,90

0 3

.3 2

0

0.0

8 8

.5 5

2

52

N

N

N

N

11

8 5

2

F Y

N

N

ALM

I 1

0,4

00

4.2

22

0

.12

11

4

5

45

N

N

N

N

11

9 4

5

M

N

Y Y

AW

MI

7,4

00

3.2

16

0

.08

7.5

50

5

0

N

N

N

N

12

0 4

3

M

N

Y N

IP

WM

I 1

0,3

00

3.6

15

0

.14

11

.5 4

8

48

N

N

N

N

12

1 5

1

M

Y N

Y

IWM

I 8

,30

0 2

.9 8

0

.07

9.5

46

4

5

N

N

N

N

12

2 4

9

M

N

Y N

IP

WM

I 1

0,6

00

3.5

22

0

.14

10

.5 2

8

30

N

N

N

N

12

3 4

2

M

N

N

Y A

WM

I 4

,90

0 2

.2 1

6

0.0

8 7

.2 4

8

52

N

N

N

N

12

4 5

0

M

Y N

Y

AW

MI

13

,80

0 3

.3 2

2

0.2

13

.2 2

4

N

Y

Y

12

5 4

7

M

Y Y

N

IWM

I 1

0,6

00

4.2

20

0

.19

11

.2 3

8

40

N

N

N

N

12

6 5

9

F N

N

N

A

SMI

12

,70

0 2

.6 2

4

0.2

2 1

1.6

40

3

8

N

N

N

N

12

7 4

2

M

N

N

N

IWM

I 8

,90

0 2

.1 1

5

0.1

2 7

.6 4

5

45

Y

N

N

N

12

8 5

1

F Y

Y N

IP

WM

I 7

,80

0 2

1

4

0.1

7.2

48

4

5

N

N

N

N

12

9 4

3

M

N

N

Y IW

MI

12

,90

0 3

.3 1

6

0.2

2 1

0.5

40

4

0

N

N

N

N

13

0 4

9

M

Y N

Y

IWM

I 1

1,6

00

3.1

6

0.2

11

.8 3

6

38

N

N

N

N

13

1 5

0

F Y

N

N

AW

MI

7,4

00

2.5

26

0

.08

7

42

4

0

N

N

N

N

13

2 5

8

F N

Y

N

ASM

I 9

,40

0 2

.6 2

2

0.1

1 8

.2 4

5

45

N

N

N

N

13

3 3

8

M

N

N

Y IW

MI

6,3

00

2.7

8

0.1

7.2

48

4

5

N

N

N

N

13

4 4

2

M

N

Y Y

AW

MI

10

,40

0 2

.9 1

0

0.1

4 1

0.1

36

3

5

Y N

N

N

13

5 4

8

F Y

N

N

ALM

I 6

,90

0 2

.4 2

5

0.0

8 9

.5 4

3

45

N

N

N

N

13

6 5

1

M

N

N

N

IWM

I 1

3,6

00

3.6

9

0.1

6 9

.2 4

0

35

N

N

N

N

13

7 4

7

F N

N

N

A

WM

I 1

0,3

00

3.2

14

0

.2 1

2.6

32

3

5

N

N

N

N

13

8 4

5

M

N

Y Y

IWM

I 9

,50

0 2

.8 1

5

0.0

9 1

0.8

46

4

6

N

N

N

N

13

9 6

5

M

Y Y

Y IW

MI

11

,40

0 2

.9 2

5

0.1

5 1

2.6

40

3

5

N

N

N

N

14

0 4

9

F Y

N

N

IPW

MI

5,8

00

2.3

20

0

.08

9.5

55

Y Y

Y

14

1 5

6

F Y

Y N

A

WM

I 1

1,6

00

2.6

22

0

.22

11

.8 3

8

40

Y

N

N

N

14

2 5

3

M

N

N

Y A

SMI

13

,60

0 1

.8 2

5

0.1

9 1

3.5

32

3

0

N

N

N

N

14

3 4

3

M

Y N

Y

IWM

I 1

0,3

00

2.5

30

0

.24

14

.2 3

5

35

N

N

N

N

14

4 5

7

M

Y N

N

A

WM

I 8

,90

0 3

.2 1

6

0.0

8 8

.5 4

5

46

N

N

N

N

14

5 6

2

F N

Y

N

IWM

I 1

1,5

00

3.4

18

0

.14

9.8

52

5

0

Y N

N

N

14

6 4

9

M

N

N

Y IW

MI

13

,90

0 4

.2 2

5

0.1

9 1

0.5

40

3

8

N

N

N

N

14

7 4

7

M

N

N

Y A

SMI

16

,90

0 2

2

4

0.2

3 1

4.5

32

N

Y

Y

14

8 5

6

F N

Y

N

ASM

I 1

1,6

00

2.2

28

0

.2 1

3.5

24

2

5

N

N

Y N

14

9 6

1

M

Y N

N

A

WM

I 1

0,5

00

2.4

30

0

.16

12

.8 3

6

35

N

N

N

N

15

0 5

8

F Y

Y N

IW

MI

9,5

00

3.1

18

0

.09

9.5

50

5

0

N

N

N

N

Y- Y

ES

N-N

O

Documents

LEUCOCYTE COUNT, ERYTHROCYTE SEDIMENTATION RATE …