“CLINICAL DETERMINANTS OF CORONARY

COLLATERALS AN ANGIOGRAPHY STUDY”

Dissertation submitted to
The Tamil Nadu Dr. M.G.R Medical University, Chennai
in partial fulfillment of the requirements for the degree of

DM Cardiology
Branch II
August 2013.

MADRAS MEDICAL COLLEGE

RAJIV GANDHI GOVERNMENT GENERAL HOSPITAL
CHENNAI 600 003

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

CHENNAI, INDIA

 
 CERTIFICATE

This is to certify that Dr. PREMANANTH .N, Post graduate

student [2010-2013] in the Department of Cardiology, Government

General Hospital, Chennai & Madras Medical College, Chennai-600003,

has done this Dissertation on “CLINICAL DETERMINANTS OF

CORONARY COLLATERALS AN ANGIOGRAPHY STUDY”

under my guidance and supervision in partial fulfilment of the regulations

laid down by The Tamil Nadu Dr. M.G.R Medical University, Chennai,

for DM Cardiology –Branch II examination to be held in August, 2013.

Prof. Dr.V.E.DHANDAPANI., MD.,DM.,

Prof. and Head
Department of Cardiology
Madras Medical College
Chennai– 03

Dr. V.KANAGASABAI, M.D.,

Dean
Madras Medical College
Rajiv Gandhi Government General Hospital
Chennai.
 DECLARATION

I hereby solemnly declare that the dissertation titled “CLINICAL

DETERMINANTS OF CORONARY COLLATERALS AN

ANGIOGRAPHY STUDY” was done by me at Department of

Cardiology, Madras Medical College and Rajiv Gandhi Government

General Hospital, Chennai-3 during 2012 under the guidance and

supervision of my unit Chief Prof. Dr.V.E.DHANDAPANI, MD,DM.

The dissertation is submitted to the Tamilnadu Dr. M.G.R. Medical

University towards the partial fulfillment of requirement for the award of

D.M. (Branch-2) in Cardiology.

Place: SIGNATURE OF THE CANDIDATE

Date :

( Dr. PREMANANTH .N)

 ACKNOWLEDGEMENT

I thank Prof. Dr.V.Kanagasabai , The Dean, Madras Medical

College, Chennai, for giving me the permission to do this study.

My warmest respects and sincere gratitude to our beloved teacher,

Prof.V.E.Dhandapani, Professor and Head of the Department of
Cardiology, Government General Hospital Chennai for his constant
guidance and encouragement to do this study.

My respectful thanks to Prof.M .S.Ravi , Prof. K.Meenakshi,

Prof. D.Muthukumar, Prof.N.Swaminathan, Prof.G.Gnanavelu and
Prof.G.Ravishankar for their guidance and advice.

I am grateful to Dr.S.Venkatesan., Registrar, Department of

cardiology for his help and guidance.

I thank Dr. G.Palaniswamy, Dr. C. Moorthy, Dr. C. Elangovan,

Dr.G. PratapKumar, Dr. Rajasekar Ramesh, Dr. S. Murugan,
Dr.G.Manohar, Assistant Professors of the Department of cardiology
for their personal help, involvement and advice for this study.

I thank Nurses and technicians for their help rendered through out
the period of study.

I also thank my fellow postgraduates for their love and affection.

Finally I wish to acknowledge my heartfelt thanks to all the patients for
their enthusiastic participation in this study.

 
 

“CLINICAL DETERMINANTS OF
CORONARY COLLATERALS”
AN ANGIOGRAPHIC STUDY
 CONTENTS

S. Title Page
No. No.
1. INTRODUCTION 1

2. AIMS AND OBJECTIVES 4

3. REVIEW OF LITERATURE 5

4. MATERIALS AND METHODS 14

5. OBSERVATION 19

6. RESULTS 46

7. DISCUSSION 50

8. SUMMARY 58

9. CONCLUSION 62

BIBLIOGRAPHY
ABBREVIATIONS
PROFORMA
MASTER CHART
ETHICAL COMMITTEE APPROVAL ORDER
CONSENT FORM
ANTI PLAGIARISM ORIGINALITY REPORT

 
 ABBREVIATIONS

ACS- Acute coronary syndrome

CSA- chronic stable angina

CAD- Coronary artery disease

DM- Diabetes mellitus

ECG- electrocardiogram

ECHO- echocardiogram

LAD- left anterior descending artery

LCX- left circumflex artery

OM –obtuse marginal branch

PDA- posterior descending artery

PLB- posterolateral branch

RCA- right coronary artery

SHT- Systemic hypertension

 INTRODUCTION

Coronary artery disease (CAD) is the leading cause of death in

developed countries and may become the most important reason for

mortality in the developing countries. Early interventions of these patients

with CAD by improving anginal symptoms, coronary blood flow with

anti-anginal medication, mechanical intervention as percutaneous

angioplasty and coronary stenting or coronary artery bypass grafting can

minimize the mortality and morbidity. The aim of the intervention is to

reduce cardiovascular mortality by reducing the myocardial infarction

size and to improve the left ventricular function. However, in extensive

CAD, 20–30% of patients may not be suitable for revascularization as

angioplasty or surgical bypass and carry a poor prognosis. Hence an

alternative treatment strategy for revascularization that improves

symptoms as well as the progression of CAD becomes essential.

In normal persons without significant CAD, myocardial blood flow

is by the major coronary arterial branches. Side branches originate from

the main branch and terminate as an extensive capillary network supply

different regions of the myocardium. When one of the major pathways is

severely obstructed by an atherosclerotic lesion, flow distal to the lesion

is compromised. Functional and structural capacity of myocardium

1
depends on the adequacy of flow through the alternate coronary pathways

or coronary collaterals.

Coronary collaterals are anastomotic connections without an

intervening capillary bed between branches of the same coronary artery

and between different coronary arteries (1). Collateral circulation has been

reported in literature to protect and preserve myocardium around the time

of coronary occlusion and improve residual myocardial contractility and

left ventricular function. Fukai et al found that well-developed coronary

collaterals may minimize the infarct size and increase the amount of

viablemyocardium.2 Sabia et al demonstrated that the myocardium may

remain viable in the presence of a good collateral circulation for a

prolonged period in patients with acute myocardial infarction with an

3
occluded infarct-related coronary artery . Fulton and Royen

demonstrated that in coronary artery obstruction, functional coronary

collaterals develop by enlargement of pre-existing coronary anastomotic

channels between side branches of two coronary arteries.4 Most

observers agree that more than 90% of occlusion of coronary artery is

necessary to bring changes in the new vessel formation. Current studies

have shown that vasculogenesis formation in fetus does not play a

significant role in adult collateralization. Angiogenesis and arteriogenesis

are the known mechanisms of coronary collateral development.

2
 There is lot of studies regarding the presence of collaterals, the

pathogenesis of collaterals, individual risk factors, But there is a paucity

in literature about the combined risk factors, correlation of clinical

presentation to the formation of collaterals. further there is scarcity of

studies for grading of collaterals in all the risk factors and clinical

presentations. Hence the knowledge of various variable and its

association with collateral formation and grade of collateral may provide

an insight in modifying the treatment modality.

This study is carried out to find the clinical determinants of

coronary collateral in patients with total or subtotal occlusion on coronary

angiography and to correlate with grading of collaterals. The information

obtained may add and cryatallize to the testimony of others to make it a

fruitful wisdom.

3
 AIMS AND OBJECTIVES

1. To study the impact of type of coronary artery disease in

coronary collateral development.

2. To study the role of conventional coronary risk factors in

the coronary collateral development.

3. To study the coronary collateral number, types and its

relationship with the coronary artery involved in total and

subtotal coronary artery occlusion.

4
 REVIEW OF LITERATURE

Coronary artery disease(CAD) is a commonly occurring disease

accounting for nearly 30% of all deaths worldwide6 .CAD has been

classified as acute coronary syndrome, sudden cardiac death, chronic

CAD. Acute coronary syndrome represents conditions which have a

common end result, acute coronary ischemia which is usually caused by

atherosclerotic plaque rupture, fissuring, erosion with or without

superimposed thrombus. This includes acute MI as STEMI [ ST elevation

MI ] or NSTEMI [non ST elevation MI] and unstable angina.

Conventional Risk Factors

There has been many conventional atherothrombosis risk factors

known which are associated with CAD, which includes smoking,

systemic hypertension, hyperlipidemia, insulin resistance and diabetes,

physical activity, and obesity. Novel atherothrombotic risk markers,

including high-sensitivity C-reactive protein (hsCRP) and other markers

of inflammation, as well as homocysteine and lipoprotein(a). 6

Coronary circulation

Coronary arteries are the major arterial supply to heart. Aortic

sinus gives off two major coronary arteries which subdivide on the
5
epicardial surface of heart. Left main coronary artery arises from left

aortic sinuses and right coronary artery arises from right aortic sinuses.

left main coronary artery after its origin, divides into anterior descending

and circumflex artery.7

Both coronary arteries gives off small, deeply penetrating branches

and an extensive network of intramural vasculature as arteries, arterioles

and capillaries (5). Small intramural collateral vessel connects the

coronary arteries which get enlarged after coronary obstruction. Venous

drainage of the Heart is via coronary sinus and thebesian veins.

The resting normal coronary blood flow is between 60 to 90

ml/min/100gm of myocardium and with a potential to augment flow

5 times rapidly during exercise. The coronary flow rate is mainly

determined by coronary perfusion pressure and vascular resistance within

and outside the coronary vascular bed. The control of coronary blood

flow can be metabolic [auto regulation],mechanical ,autonomic and

endothelial control .7

Coronary Collaterals:

Inspite of so much understanding about coronary circulation in

normal hearts, the knowledge about development of coronary collateral

6
circulation is still not clear. In any arterial occlusion, affected organ may

be less sensitive to episodes of ischemia if it is supplied with well

established collateral vessels. The potential of an individual to develop

coronary collateral is often neglected. Fukai et al found that a well

established coronary collaterals minimizes the ischemic area supplied by

occluded vessels2. In coronary artery occlusion, when original vessel fails

to provide sufficient blood supply, Coronary collaterals circulation forms

an important alternative source of blood supply. Coronary collaterals are

the communicating channels between the major coronary arteries and

their branches ().This anastomotic connections do not have an

intervening capillary bed between portions of the same coronary artery

and between different coronary arteries 1

History about literature on coronary collateral dates back to more

than 200 years ago, when Heberden astonishingly described a patient

who got nearly cured of his angina pectoris by sawing wood each day . 8

He described this phenomenon as warm up” or “first effort angina” and

ascribed this to coronary vasodilation mainly due to opening of coronary

collateral vessels to support the ischemic myocardium. More recent

literature reviews interpret this type of “walk through angina” as a

biochemical Ischemic preconditioning rather than due to collateral

7
recruitment . Both mechanisms may probably contribute to the described

phenomenon.

In 1956, Baroldi et al demonstrated the presence corkscrew-shaped

collaterals at birth in normal human hearts (while few other authors

demonstrated coronary collaterals in animals.9 Baroldi demonstrated

collateral diameter of 20 to 350 microns and lengths ranging from 1 to 5

cm in human, whereas schaper and others, demonstrated coronary

collaterals lumen greater than 50 microns in dog and less than 50

microns in pig. In dog the collaterals were found predominantly in

epicardial layer, whereas in pig the collaterals were demonstrated in

intramyocardial and subendocardial layers 10.

Development of coronary collaterals

Angiogenesis and Arteriogenesis are suggested as the mechanisms

of coronary collateral development.

Angiogenesis is a term formerly used to describe the formation of

new capillaries by sprouting out from preexisting postcapillary venules.

Arteriogenesis is the growth and development of the collateral

circulation in the form of the transformation of preexisting arterioles into

8
functional (muscular) collateral arteries concomitant with acquisition of

elastic and vasomotor properties.11

Current studies describes the process of angiogenesis and

arteriogenesis as newly differentiated vessels are due to endothelial cells

migration, differentiation and multiplication to form complex, mature

vascular network . 12

Further study shows that vasculogenesis, an initial step in blood

vessel formation in the fetus does not play a significant role in adult

collateralization.

Based on the histological structure, the coronary collaterals has

been classified into two categories:

• Capillary size collaterals without smooth muscle cells are

predominantly seen in subendocardium

• Large muscular collaterals located in epicardium develops from

preexisting arterioles. (uptodate coronary collateral circulation)13

Site of origin of collateral arteries

The collateral artery formed can orginate from different sites, as a

9
 • terminal extension of two coronary arteries,

• branching out from the side of the two arteries,

• branching from the same stenosed artery,

• or within the same artery through vasa vasorum.

These type of collaterals occurs most commonly in

• ventricular septum

• ventricular apex

• ventricular free septum,

• anterolateral left ventricular free wall,

• cardiac crux,

• atrial surfaces.

10
 • BL – bridging across
lesion

• AT – atrial

• SE - septal

• BR – branch to
branch in ventricular
free wall

Determinants of Coronary Collateral Circulation

Factors determining the formation of collaterals

1. Recurrent and severe myocardial ischemia:

Most important determinant of development of Coronary

collaterals is recurrent and severe myocardial ischemia 14. Takeshita et al

correlated intermittent myocardial ischemia with development of

coronary collaterals and preserved even at rest and becomes functional

when necessary.15

11
2. Duration of the ischaemia:

Herlitz et al compared patients with longer and short duration of

angina pectoris before acute MI and showed that longer the duration,

smaller the infarcts.16

3. Duration of ischaemia and collaterals

The coronary collaterals were increased in patients with longer

duration of disease. Longer the duration of the disease, larger is the

caliber of the vessel.

4. Timely enlargement of collaterals:

Enlargement of collaterals at the right time increases the period of

golden hours and avoid death and MI in symptomatic patients. Sabia et al

demonstrated that the myocardium in patients with acute MI may remain

viable for prolonged period, in the presence of collaterals.3

5. Myocardial sensitivity:

Studies suggest that biochemical signals stimulate the development

of coronary collaterals. These biochemical singals are the angiogenic

growth factors, vascular growth endothelial growth factor mRNA which

are released due to low oxygen levels. Buschmann & schaper suggested
12
that the growth of collaterals is not only dependent on ischemia, but also

depend on other factor like shear stress.17 Hypoxia induces angiogensis

whereas shear stress induces arteriogenesis.

6. Pressure gradient and stress:

Increase shear stress mechanically mediates the process of

arteriogenesis. Freedman SB et al stated that there exist a Pressure

gradient difference between the portion of artery distal to occlusion and

the collateral artery within 90s of occlusion, which provokes a

inflammatory response. The inflammatory response causes damage to the

internal elastic lamina and causes expansion of vessel. The maximal

functional capacity of the collateral vessel is achieved at period of 6

months through structural remodeling.

Grading of collaterals:

Rentrop and colleagues were the first to describe the coronary

angiographic method for collateral for spontaneously visible collaterals

without artificial vascular occlusion(8). But later it was modified and the

widely used method provides a score from 0–3 for recruitable collateral

vessels upon occlusion of the ipsilateral artery 18

13
 MATERIALS AND METHODS

The present study of “clinical determinants of coronary collaterals”

was carried out in the department of Cardiology, GGH, MMC, and

Chennai.

400 Consecutive coronary angiogram done over a period of six

months in the catheterization lab at GGH, MMC were observed. Among

them 50 patients who had total or subtotal occlusion in coronary

angiography were included in our study. Information regarding clinical

presentation, risk factors, previous CAD, family history was meticulously

recorded. This study was approved by the institute’s ethical committee.

Permission from the hospital administration and consent from the

patients was obtained for performing the study. Inclusion and exclusion

criteria mentioned in the protocol were strictly followed and adhered.

I INCLUSION CRITERIA:

1. Age > 18 years

2. Known CAD patients who had undergone conventional coronary

angiogram and had subtotal or total coronary artery occlusion on

coronary angiography were included.

14
II EXCLUSION CRITERIA:

1. Age < 18 years

2. Patients with relative contraindications for coronary angiography

which include active bleeding, coagulopathy, acute renal failure,

chronic renal failure, active infection, uncontrolled hypertension, and

severe anemia with Hb < 8gm, decompensated CCF were excluded.

III METHODS:

Patients with angiography showing subtotal or total coronary artery

occlusion were assessed for

1. Age group:

50 Patient who formed the study group were classified into

different age group

2. Risk factor:

A detailed history was elicited and documented for conventional

coronary risk factor. The patients were evaluated for conventional risk

factors like smoking, obesity, Diabetes mellitus, Systemic Hypertension,

Family history of CAD, prior CAD, and sedentary lifestyle. The risk

15
factor was correlated with development of coronary collaterals on

angiography as an isolated factor and as a multiple risk factor in patients

with multiple coronary risk factors.

3. Clinical Presentation:

The patients with coronary occlusion were assessed for the mode

of clinical presentation at the time of hospital admission prior to coronary

angiography. They were grouped into 5 categories as ST elevation

myocardial infarction(STEMI), non ST elevation myocardial

infarction(NSTEMI), unstable angina (USA), chronic stable angina

(CSA) and recurrent coronary artery disease(RECURRENT CAD).

4. Investigations:

Patients were investigated for hemoglobin, fasting and postprandial

estimation of blood sugar, blood urea, serum creatinine. Standard 12 lead

Electrocardiogram analyses were done in all patients. Echocardiographic

evaluation was done for analysis of regional wall motion abnormalities

and assessment of LV systolic function. A group of patients in our study

group in whom ECG stress test was already done prior to coronary

angiography were assessed for the correlation of stress test positivity and

development of coronary collateral. They were separated into three

16
groups based on stage of stress test positivity by Bruce protocol for

analysis of development of coronary collateral.

5. Coronary angiogram:

Detailed analysis of coronary angiograms of our study group was

done. The parameters assessed were

i. number of total/ subtotal occluded vessels,

ii. types and

iii. segments of coronary artery involvement,

iv. presence or absence of coronary collateral arteries.

6. The parameters for coronary collateral arteries were assessed for its

i. number,

ii. Types of collaterals whether from branches of same

coronary artery (homo collateral ) or from branches of

other coronary arteries (hetero collateral).

iii. Grading of collateral

17
 On coronary angiogram, grading of coronary collateral was done

by using Rentrop and cohen’s collateral classification. Rentrop and

cohen’s grading of coronary collateral classification defines

Grade 0: No collateral arteries are present.

Grade 1: Barely detectable coronary flow. Contrast medium passes

through collateral channels but fails to opacify the epicardial

vessels at any time.

Grade 2: Partial collateral flow. Contrast material enters but fails

to opacify the target epicardial vessel completely.

Grade 3: Complete perfusion. Contrast material enters and

completely opacifies the target epicardial vessel.

The grade of collaterals was correlated with the following

parameters

i. sex distribution

ii. age distribution

iii. risk factors

iv. clinical presentation

v. ECG stress test

vi. LV function
18
 OBSERVATION

In this present study of clinical determinants of coronary collaterals

400 consecutives coronary angiograms performed at Madras Medical

College were observed. Among the observed angiograms, patients with

total or subtotal occlusion of coronary artery formed the study group. The

following observation were made

1. Distribution of cases:

A total of 50 patients with total or subtotal coronary artery

occlusion formed the cases. The cases were categorized according to the

age group as follows:

19
 Table: I Distribution of cases

S/No. Age group (Yrs) No of cases

1. 18 – 30 0

2. 31 – 40 6

3. 41 – 50 14

4. 51 – 60 19

5. 61 - 70 9

>70 2

Total no of cases 50

20
2. Sex distribution

Among the observed patients with coronary occlusion, the

distribution of male and female patients were as follows:

21
 Table: II Sex distribution among cases

S/No. Age group (Yrs) No of cases

Male Female

1. 18 – 30 0 0

2. 31 – 40 4 2

3. 41 – 50 8 6

4. 51 – 60 16 3

5. 61 - 70 8 1

6. >70 2 0

Total no of cases 38 12

22
Chart II

23
3. Distribution of clinical presentation:

The patients in the study group with occlusion of coronary

angiogram were interviewed for condition at the time of admission, and

were cross checked with case records present at Madras Medical College,

the following clinical determinants were observed

Table III: Distribution of clinical presentation

S/ No. Clinical presentation No of cases

1. ST elevation MI 26

2. NON ST elevation 6

3. Unstable Angina 2

4. Chronic Stable Angina 10

5. Recurrent CAD 6

Total 50

24
 Chart III: Clinical presentation among cases

Table IV: Clinical presentation among Age groups

No. of Cases

Age in Recurrent
STEMI NSTEMI USA CSA Total
years CAD

31 - 40yrs 4 0 1 1 0 6

41 - 50yrs 7 3 1 2 1 14

51 - 60yrs 10 3 0 5 1 19

61 - 70yrs 5 0 0 1 3 9

> 70 0 0 0 1 1 2

Total 26 6 2 10 6 50

25
Chart IV: Clinical presentation among Male and Female

26
4. Risk factors:

The following conventional coronary risk factors in the patients

were recorded by interview of patients and by case records

Chart V: Distribution of risk factors among cases

27
5. Left ventricle function:

All the patients in the study group were subjected to Echo to

evaluate the left ventricle functional status. The patients were categorized

into mild, moderate and severe LV Dysfunction based on the standard

ECHO guidelines. The following information was recorded.

Table V: Distribution of cases according to LV function

Normal 18

Mild Dysfunction 20

Moderate Dysfunction 12

Severe Dysfunction No cases reported

28
 Chart VI: LV dysfunction in coronary artery occlusion

6. STRESS TEST:

Patients with who had undergone stress test prior to angiography

and found positive were graded according to standard BRUCE protocol.

29
Table VI: No of cases in different stage of STRESS +ve test

TMT +VE No Of Cases

STAGE I 4

STAGE II 4

STAGE III 2

Total 10

30
5. Description of coronary artery occlusion

The angiography of the study group patients were observed and

documented. The coronary artery occluded among the 50 angiograms

were classified into single artery occlusion and multiple artery occlusion,

the details are as follows:

Table VII: Type of coronary artery occlusion

Coronary artery No of cases

Male Female Total

Single artery

LAD 19 9 28

LCX 6 2 8

RCA 8 1 9

Multiple artery

LAD & RCA 3 0 3

LAD & LCX 2 0 2

TOTAL 50

31
Chart VII: Distribution of single artery and multiple artery occlusion

Chart VIII: Distribution of single coronary artery Occlusion

32
6. Site of occlusion of coronary artery

The site of occlusion of coronary artery was classified into

proximal, middle and distal.

Table VIII: Type and segment of coronary artery occlusion

Type of Coronary artery

Segment of
LAD LCX RCA
Coronary artery

Proximal 19 6 9

Middle 14 - 5

Distal 0 2 0

33
7. Coronary artery occlusion and grading of collateral

The angiography with occlusion of coronary artery showed

establishment of collaterals. The grading of collaterals was done

according to standard protocol. For each independent and dual artery

occluded, the artery from which the collaterals originated were studied

and following observation were made

Chart IX: Grading of collaterals among cases

Grade of collaterals among cases

0%
16%

46%
Grade 0
Grade 1
Grade 2
Grade 3

38%

34
 Table IX: LAD OCCLUSION AND COLLATERALS

Coronary Homo Hetero Both GRADING

artery

LCX RCA 0 1 2 3

Proximal 0 1 4 14 4 7 9 0

Middle 0 1 4 9 1 6 7 0

Distal No cases reported

Table X: LCX OCCLUSION AND COLLATERALS

Coronary
Homo Hetero Both GRADING
artery

LAD RCA 0 1 2 3

Proximal 0 3 0 3 1 2 3 0

Distal 0 0 0 2 0 1 1 0

35
 Table XI: RCA OCCLUSION AND COLLATERALS

Coronary
Homo Hetero Both GRADING
artery

LAD LCX 0 1 2 3

0
Proximal 0 4 0 5 2 3 4

Middle 1 3 0 1 0 2 3 0

Distal NO CASES REPORTED

36
8. Collaterals and Age factors:

The collaterals established were graded and correlated with age

groups

Table XII: AGE GROUP AND COLLATERALS

Age group
S/No. Collateral grading
(Yrs)

0 1 2 3

1. 18 – 30 0 0 0 0

2. 31 – 40 0 3 3 0

3. 41 – 50 1 4 9 0

4. 51 – 60 4 7 8 0

5. 61 - 70 3 3 3 0

6. >70 0 2 0 0

Total no of
8 19 23 0
cases

37
 Chart X: Age and collateral grading

9. Collaterals and clinical presentation:

The grading of collaterals formed were correlated with variety of

clinical presentation the patients presented with at the time of admission

38
 Table XIII: Clinical presentation and collaterals

S/ Clinical Total no of
No. presentation GRADE OF COLLATERAL Cases

0 I II III

1. ST elevation MI 4 12 10 0 26

2. NON ST elevation 1 3 2 0 6

3. Unstable Angina 1 1 0 0 2

Chronic Stable
4. Angina 1 2 7 0 10

5. Recurrent CAD 1 1 4 0 6

Total 8 19 23 0 50

39
Chart XI: clinical presentation and grade of collaterals

40
9. Risk factors and collaterals:The collaterals established were raded

and correlated with variety of risk factor of the patients presented with at

the time of admission

Table XIV: Risk factors and grade of collaters

Total
S/ GRADING OF
RISK FACTORS no of
No. COLLATERAL
cases
Isolated risk
factor
0 I II III
1 DM 3 6 1 0 10

2 SYSTEMIC HYPERTENSION 0 0 2 0 2

3 SMOKING 1 3 7 0 11

4 DYSLIPEDEMIA 0 0 0 0 0

5 PRIOR CAD 0 0 2 0 2

6 OBESITY 0

7 FAMILY HISTORY 0 0 1 0 1

8 SEDENTARY LIFESTYLE 0

9 NO RISK FACTOR 1 5 8 0 14
10 Multiple risk factors
3 5 2 10
8 19 23 0 50

41
Chart XII: Isolated risk factors and grade of collaterals

42
11. Collaterals and sex distribution

The variations in collaterals established were analysed among

different age group

Table XV: SEX DISTRIBUTION AND COLLATERALS

0 1 2 3

1. Male 6 14 18 0

2. Female 2 5 5 0

43
12. LV function:

Table XVI: LV function and collaterals

Total No
S/No. COLLATERAL GRADING
of Cases

LV FUNCTION 0 I II III

Normal 3 7 8 0 18

Mild LV
3 7 10 0 20
dysfunction

Moderate LV
2 5 5 0 12
dysfunction

Severe LV
No cases reported
dysfunction

Total 8 19 23 0 50

44
Patients who had undergone stress test were observed for collaterals.

Table XVII: Stress test and collaterals

TMT +VE No Of Cases GRADE OF COLLATERAL

0 I II III

STAGE I 4 1 1 2 0

STAGE II 4 0 1 3 0

STAGE III 2 0 0 2 0

Total 10 1 2 7 0

45
 RESULTS

In our study a total of 50 patients with angiography showing

total/subtotal occlusion formed the study group. Most of the patients

presented to the hospital were in the age group of 51- 60yrs, followed by

41-50yrs (Table I). Among the 50 patients studied, 38 were males and 12

were females (Table II). Male predominantly (66%) presented in the age

group >50 yrs whereas female presented early in life in the age group of

41- 50 years (chart I), but in all age group male were more in number

than females (chart II).

The patients presented to the hospital in different modes of clinical

presentation. Acute coronary syndrome accounted for 68% of the patients

(chart III). ACS occurred most commonly in the age group of 40-60yrs

(Table IV). Most common clinical presentation was STEMI (52%),

followed by chronic stable angina (20%), NSTEMI (12%), recurrent

CAD (12%) and unstable angina (4%) (chart III). Out of 26 patients with

STEMI, 17 patients were in the age group of 40-60yrs. 70% of the

Chronic stable angina occurred above the age group of 50yrs. Recurrent

CAD predominantly occurred in the age group of 60-70yrs (Table IV).

STEMI was a common clinical presentation both in males and females

46
(Chart IV). Unstable angina, CSA, recurrent CAD was more common in

males than in females of the same age group.

There were many associated risk factors observed among the

patients like smoking, diabetes mellitus, systemic hypertension, prior

CAD, dyslipidemia, obesity, and family history. There were 14 patients

(28%) without any known risk factors. 9 patients had two or more risk

factors. Most common risk factor observed was smoking, followed by

diabetes mellitus. Out of 38 males, 27 were smokers, with or without

other associated risk factors (Chart V).

On ECHO, the status of Left ventricular function was analyzed,

36% of the patients had normal LV function, 40% had mild LV

dysfunction, and 24% had moderate LV dysfunction (chart VI). Severe

LV dysfunction was not noted in our study (Table V).

Among the 10 patients who had undergone STRESS TEST, 4 were

in stage I, 2 patients were in stage II and 2 patients were in stage III

(Table VI), according to the standard Bruce protocol.

Angiography of the 50 patients under study revealed single

coronary or occlusion of both coronary arteries. 90% of the patients had

single coronary artery occlusion, whereas occlusion two coronary arteries

47
were found only in 10% of the patient (Chart VII). LAD was the most

common artery occluded both occurring in isolation or in association with

occlusion of other artery (Chart VIII). The other arteries occluded were

RCA AND LCX. In all the arteries occluded, proximal part of the artery

was the commonly involved segment (Table VI).

Among the 50 patients under study, grade II collaterals was found

in 46% of the patient, grade I collaterals was noted in 38% of the patients,

no collaterals were noticed in 16% of the patients (Chart IX). Grade III

collaterals were not noticed in any of our patients.

In both single artery occlusion and occlusion of two coronary

artery, the collaterals were from both homo and hetero type of collateral

(Table VII). LAD artery was the major contributor as collateral in both

LCX and RCA type of occlusion. In LAD artery occlusion, RCA was the

major contributor as collateral artery (Table VII, VIII, IX).

Grade 0 collateral was commonly observed in 50-70yrs of age. All

patients above 70yrs of age had Grade I collateral. Both male and female

patients had equal distribution of Grade of collateral (Table X).

Grade 0 collateral was found in 20% of patient with STEMI.

Majority of the patients had Grade II collaterals. Grade II collaterals were

48
observed in 70% of patients with CSA and 66% of patients with recurrent

CAD (Table XI).

Among 27 patients who were chronic smoker, 18 had grade II

collateral, Grade 0 collateral were present in 5 out of 24 patients with DM

mellitus. 50% of the patients with prior CAD had grade II collateral. Both

the patients with positive family history of CAD had grade II collaterals.

In patients with multiple risk factors, common collateral grade was Grade

0 and Grade1. Among 14 patients with no risk factors, 8 were found to

have Grade 2 collateral (Table XII). 6 males and 2 females had Grade 0

collaterals (Table XIII)

There was no significant variation in collateral grades among

normal and abnormal LV function (XIV).

Grade 0 collateral was noticed in 1patient among the 4 patients

who had stage 1 positive stress test. Among the 6 patients with stage 2 &

stage 3 positive stress test 5 patients had Grade 2 collaterals (XV).

49
 DISCUSSION

CAD forms one of commonly occurring disease with multiple

modes of presentation and risk factors, when detected early can reduce

the mortality and morbidity. Coronary Collaterals which form an alternate

source of blood supply forms vital as the presence of collaterals can delay

the golden period and decrease the morbidity and increase the viable

cardiac tissue.

Our study of clinical determinants of coronary collaterals was

undertaken to establish the relevance of different variables like clinical

presentation, Left ventricular systolic function, ECG stress

test,conventional risk factors, age and sex with coronary collateral

development.

In our study group of 50 patients with angiography showing total

or subtotal occlusion of coronary artery, 76% were males. Females

presented early around 40-50yrs of age, whereas males presented at a

later age of 50yrs and above.

The modes of clinical presentation with the patients presented to

hospital varied considerably. Two third of the patient presented with

acute coronary syndrome. The commonest mode of presentation was

50
STEMI. STEMI presented commonly in the age group of 40-60yrs of

age. Other modes of presentation in order of decreasing frequency in our

study were chronic stable angina, NSTEMI, recurrent CAD and unstable

angina. Chronic stable angina and recurrent CAD commonly presented

between the age group of 50-60yrs and 60-70yrs of age respectively.

The most common associated risk factor in our study was smoking.

Among male patients, 71% of them were smokers. 48% of the patients

had Diabetes mellitus. Dyslipidemia was present only in 24% of our

patients. 18% of the patients had multiple risk factors. History of prior

coronary artery disease was present in 28% of patients. Systemic

hypertension was seen in 22% of cases and a positive family history was

present in 4% of cases. Interestingly 28% of the patients had none of the

conventional coronary risk factors.

Piek JJ et al., observed angiographic study of single artery

occlusion, where 69% of patients had LAD artery occlusion and 25% had

right coronary artery occlusion19. In our study, 90% of the patients had

single artery occlusion, among the single artery occlusion, 62% of the

patients had LAD occlusion and 20% of the patients had RCA

involvement which is in concordance with Piek JJ et al. But our study

group had 18% of patient with LCX involvement which is double the

51
incidence of study of Piek JJ et al where only 6% of the patient had left

circumflex artery involvement. In Robert WC etal study revealed

proximal segment of the LAD and LCX are commonly involved

20
segments . In our study also proximal segment of the left coronary

system was most commonly involved were commonly affected . Cosby

RS etal ., study the proximal and mid portion of RCA was commonly

involved with least distal occlusion .21 In our study also proximal and mid

portion of RCA are the commonly involved and none of patients had

distal RCA occlusion.

Grading was done by Rentrop & cohen grading. In our study

grade 2 collateral was the commonest grade seen in 46% of patients .

Grade 2 collateral was more common in chronic CAD, recurrent CAD

patients. No collateral was seen in 16 % of patients with two third of

them occurred in diabetes mellitus patients.

Cosby RS etal. LAD occlusion had collaterals in majority of the cases

and collaterals originated from multiple collateral channels. The primary

source of inter coronary flow was from conus artery followed by

21
posterior descending artery (PDA) and posterolateral branches(PLB).

Collaterals from Septal and diagonals are less common.

52
In our study group with LAD occlusion , collateral were seen in 85% of

patients.Collaterals were separated as homocollateral ( from either

diagonal or septal branches) and heterocollateral from LCX( either from

obtuse marginal or distal LCX) or from RCA( conus branch, PDA,PLB).

The most common mode of collateral supply to LAD distal to occlusion

is supplied by both homo collateral and heterocollateral together in 66%

in proximal LAD and 65% in distal LAD occlusion. Only

Heterocollaterals supplied the distal portion in remainder of the patients.

none of the patients received only homocollaterals. RCA was the most

common artery supplying collateral to LAD. All our study findings

were in concordance with the corby RS etal.study.

In LCX occlusion , collaterals were formed in 7 out of 8 cases with grade

2 collateral in 50% of them. Both homo collateral and heterocollateral

together in 50% in proximal LCX and 100% of distal LCX occlusion .

Only Heterocollaterals supplied the distal portion in remainder of the

patients. LAD was the major source collateral supply to LCX .

In RCA occlusion, collaterals were found in 13 out of 14 patients.

Isolated Hetero-collaterals were commonly found in RCA occlusion than

LAD and LCX. Only one patient out of 50 patients had Homo-collateral,

53
which was present in RCA occlusion. Most of the collaterals for RCA

was from LAD.

Age and collateral:

In our study, Grade 0 (No collaterals) was observed in 25% of the

patients belonging to age group of 50 – 70yrs, and 36% had grade I

collaterals and rest with grade II collaterals. two patients were in the age

group above 70yrs and possessed grade I collaterals. Kurotobin et al.,

observed that the prevalence of collaterals decreases with advancing age

was in concurrence with our study.

Clinical presentation and collateral:

In patients with STEMI & NSTEMI presentation, 84%had

presence of collaterals. Grade 1 collaterals were the commonest type of

collaterals ,whereas in the total study group grade 2 collaterals were the

common collateral.

In patients with unstable angina, 50% of the patients had Grade I

and 50% had Grade 0 collateral.

Meir P et al. in a 10yr follow up study found that long term cardiac

mortality is decreased with patients with chronic stable angina due to

54
increased functional collaterals.23 Mills JD and others found in animal

studies that collaterals were well developed in chronic canine model.

Finding in our study patients with chronic stable angina was in

concurrence with above study. collaterals were found in 90% of the

patients. 70% had grade II collaterals. Recurrent CAD patients, 84% of

the patients had presence of collaterals. 66% of patients had grade II

collaterals, whereas total study group, 46% had grade II collaterals,

indicating that previous angina could trigger the formation of collaterals,

these findings are in concordance with Fujita M et al., found that

Collateral channels were present in two of 19 patients without angina

before infarction and nine of the 18 patients with angina before

infarction.24

Patients with acute coronary syndrome had predominantly grade I

collaterals, whereas recurrent CAD and chronic stable angina had

predominantly grade II collaterals

Risk factors and collaterals

In 90% of the patients with smokers had presence of collaterals,

60% had Grade II collaterals.

55
 Abaci et al, 1999, observed that there were more number of

diseased vessels in patients with diabetes mellitus and less number of

collaterals.25

In our study, patients with isolated risk factor as DM had 30% of

grade 0 collaterals and 60% of the patients had Grade I collaterals. 10%

of the patients with DM had grade II collaterals in comparison with 46%

of the total study population with grade II collaterals suggesting a poor

development of collaterals in diabetes patient in concordance with the

above study by Abaci et al.

Zenon S et al., studied that patient with systemic hypertension and

CAD had increased coronary collateral circulation in correlation with LV

wall thickness. In our study, two patients had systemic hypertension.

Both presented Grade II collaterals coincides with study of Zenon et al.

Only one patient had presented with isolated family history of

coronary heart disease. The patient presented as with STEMI possessed

grade II collaterals.

28% of our patients presented without any conventional risk

factors. 92% of the patients had coronary collaterals. 57% had grade II

collaterals.

56
 20% of our total study group had multiple risk factors. 30% of the

patients had grade 0 collaterals and 50% grade I collaterals. 20% had

grade II collaterals suggesting poorly developed collaterals.

There was no significant difference in grade of collaterals between

male and female.

LV function and collaterals:

Hansen JF (1989) and Nacolau JC et al.,(1997) analysed the

relationship between collateral flow and LV systolic function and found

26
improved LV function in patients with grade III collaterals. we could

not correlate between LV function as our patient did not present with

Grade III collaterals. Patients with Grade II and I collaterals did not have

much difference in LV function.

ECG stress test and collaterals

Akutsu Y et al., in their described that exercise reduce the blood

flow through collateral dependent area. In our study patients with stage I

positive stress test had grade 0, grade I, grade II collaterals, whereas

patients with stage II and III positive stress test had grade II collaterals,

suggesting that patients with grade II collaterals can have more tolerance

to exercise.
57
 SUMMARY

¾ This study was carried out at department of cardiology, Madras

Medical College, Chennai.

¾ Fifty patients with total/subtotal coronary artery occlusion on

coronary angiography formed the study group.

¾ Various variables like clinical presentation, Left ventricular

systolic function, ECG stress test, conventional risk factors, age

and sex were studied and correlated with coronary collateral

development.

¾ The collaterals were analyzed on coronary angiography.

¾ The grading of collaterals were correlated with variables

¾ The study group had more number of males than females

¾ The predominate age of presentation were in the age group of

40-60yrs of age

¾ The modes of clinical presentation was STEMI, NSTEMI,

Unstable angina, Chronic stable angina, and recurrent CAD.

58
¾ STEMI was the most common clinical presentation.

¾ Associated risk factors like smoking, DM, systemic Hypertension,

dyslipidemia, lifestyle, obesity, prior CAD, family history of CAD

was evaluated. The risk factors were categorized into isolated risk

factors and multiple risk factors. Most common associated risk

factor was smoking.

¾ On angiographic study, LAD was the most common artery

occluded, followed by LCX and RCA.

¾ Proximal segment of the coronary artery were the commonly

involved segment.

¾ Collaterals were graded according to Rentrop and cohen

classification on angiography.

¾ Grade II collateral was the commonest collateral observed

¾ Both homo and hetero collateral together were the mode of

collateral supply in LAD occlusion. Branches from RCA was most

the most common collateral in LAD occlusion.

59
¾ Both homo and hetero collateral together were the mode of

collateral supply in LCX occlusion, Branches from LAD was most

the most common collateral in LCX occlusion

¾ In RCA occlusion, hetero collaterals were the commonest mode of

supply. Isolated homo collateral was seen in RCA occlusion.

Branches from LAD was most the most common collateral in RCA

occlusion

¾ Grade II collateral was commonly seen in age groups below 70yrs

of age, and Grade I above 70yrs of age.

¾ In acute coronary syndrome, Grade I collaterals were the

commonest collateral.

¾ Most of the STEMI AND NSTEMI patients had coronary

collaterals and were predominantly grade I collaterals.

¾ In chronic stable angina, collaterals were found in majority of

patients, mostly Grade II collaterals.

¾ In Recurrent CAD, collaterals were found in majority of patients,

mostly Grade II collaterals

60
¾ In patients who were smokers, most of the patient had collaterals.

Grade II collaterals were commonly observed.

¾ Majority of the patients with isolated risk factor of DM had Grade

0 and Grade I collaterals.

¾ In patients with systemic hypertension, grade II collaterals were

commonly seen.

¾ Isolated family history, grade II collaterals was seen

¾ Majority of the patients with multiple risk factor of DM had Grade

0 and Grade I collaterals

¾ There was no correlation between LV function and grade of

collaterals.

No patients had Grade III collaterals

¾ In ECG Stress test, stage II & III positive patients had

predominantly grade II collaterals.

61
 CONCLUSION

¾ STEMI was the most common clinical presentation

¾ LAD is the most common artery occluded.

¾ Both homo and hetero collateral together were the

commonest mode of collateral supply.

¾ Collateral to LAD most commonly arise from RCA

¾ Collateral to RCA and LCX most commonly arise from

LAD

¾ The predominance of Grade II collaterals were observed in

patients with CSA, recurrent CAD, smokers, systemic

hypertension and patient with no conventional risk factors.

¾ Poorly formed collaterals (Grade 0 & Grade I) were

observed STEMI, NSTEMI, unstable angina, DM, multiple

risk factors, age > 50yrs.

62
 BIBLIOGRAPHY

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7. Joseph k.malouf, fuster , walsh HURST‘THE HEART 13 th edition
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vessel growth. Cardiovasc Res. 2001; 49: 507–52

13. wernerGS, ferrariM , etal. Collateral in chronic total occlusions,

circulation 2001;104;2074

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circulation. Circulation. 1992; 85: 1197–1204.
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of coronary collaterals during ergonovine-induced arterial spasm.
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prior to acute myocardial infarction and its relation to prognosis. Eur
Heart J. 1993; 14: 484–491

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Cardiovasc Res. 1999; 43: 835–837

18. Rentrop KP,cohen M etal changes in collateral channel filling after

coronary artery occlusion by an angiop[lasty balloon in human
subjects j am coll cardio 1885;5;587-592.

19. Piek JJ, van Liebergen RA, Koch KT, Peters RJ, David GK Clinical,
angiographic and hemodynamic predictors of recruitable collateral
flow assessed during balloon angioplasty coronary occlusion

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HR TI Collateral function in chronic total coronary occlusions is
related to regional myocardial function and duration of occlusion

21. Cosby RS, Giddings JA etal. Clinic arteriographic correlation in

angina with and without myocardial infarction
22. Kurotobi T, Sato H, Kinjo K, Nakatani D, Mizuno H, Shimizu M,
Imai K, Hirayama A, Kodama K, Hori M, OACIS Group Reduced
collateral circulation to the infarct-related artery in elderly patients
with acute myocardial infarction.

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year follow-up study in patients with stable coronary artery disease
undergoing quantitative collateral measurements Circulation.
2007;116(9):975

24. Fujita M, Sasayama S, Ohno A, Nakajima H, Asanoi H Importance of

angina for development of collateral circulation

25. Abaci A, Oğuzhan A, Kahraman S, Eryol NK, Unal S, ArinçH, Ergin

A Effect of diabetes mellitus on formation of coronary collateral
vessels

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SA The role of antegrade and collateral flow in relation to left
ventricular function post-thrombolysis.
 MASTER CHART

Ejection
Coronary artery COLLATERALS fraction
Risk factor
S. Clinical Angio (EF)
Name Age Sex
N. diagnosis NO.
LAD LCX RCA Type Origin Grade

36
Dm/smo/
1. Suryanarayanan 58 M STEMI 1706 + HETERO LAD &RCA 2
Prior
N
2. Haridas nil 53 M USA/ 1839 + nil 0

48
3. Swadesi Dm/Smo/Dys 40 M STEMI 1665 + Hetero RCA 2

42
DM/SHT/
4. Gopinath 57 M STEMI 1573 + Hetero RCA 1
Prior CAD
46
Pakkirisamy Both homo and
5. Nil 60 M STEMI 1515 + LCX/LAD 1
hetero
46
6. Savithra DM 38 F STEMI 1751 + Hetero RCA 1

48
7. Ganesan DM 55 M STEMI 1800 + Both hetero/homo LAD 2

49
Both homo and
8. Suman SMO 48 M NSEMI 1764 + RCA/LAD 2
hetero
55
Both homo and
9. chandrasekaran nil 45 M CSA/ tmt + 1812 + LCX/RCA 2
hetero
55
10. Kala SMO 38 F STEMI 1857 + heterocollateral LAD 1
 58
11. Ravi DM 45 M STEMI 1703 + + nil 0

38
12. Ruche SM/HT 65 F USA 1711 + heterocollateral RCA 2

36
13. Kumar DM 67 M CSA 1765 + Both hetero/homo LAD/RCA 2

46
14. Chitra NIL 62 F REC.CAD 1867 + Both hetero/homo RCA/LAD 1

48
15. Saravanan NIL 63 M STEMI 1550 + Both hetero/homo LAD 2

60
16. Ekambaram SMO 57 M STEMI 1729 + Both hetero/homo LAD 1

42
17. Sreenivas SMO 46 M CSA 1831 + nil 0

48
18. Gunasekarasn SMO/DM 48 M REC.CAD 1871 + heterocollateral RCA 2

56
19. Sundaram SMO/OBE 58 M STEMI 1864 + Both hetero/homo LAD 2

40
20. Narayanan SHT/DM 57 M CSA 1543 + + nil 0

48
21. Murugesan SMO/DM 53 M REC.CAD 1501 + Both hetero/homo LAD 1

50
22. Latha PRIOR CAD 69 F NIL 1509 + heterocollateral RCA 1

38
23. Hari SMO 37 M CSA 1753 + + Both hetero/homo LAD/LCX 2

56
24. Muniyammal DM/SHT 38 F STEMI 1821 + Both hetero/homo LAD 2
 55
25. Kamakchi SHT/DM 46 F NSTEMI 1859 + nil 0

42
26. Chandran SMO 42 M STEMI 1653 + Both hetero/homo LAD/LCX 1

38
27. Ambikapathi SMO/DM 57 M USA 1622 + Both hetero/homo LCX 2

52
28. Durai SMO/DM 55 M STEMI 1576 + + nil 0

50
29. Rajkumar SMO 67 M CSA 1669 + Both hetero/homo LAD 1

56
30. Visalakshi DM 63 F REC.CAD 1798 + Both hetero/homo LCX/RCA 2

58
Conus branch
31. Dayadharan OBE/SMO 55 M STEMI 1799 + homocollateral 2
RCA
46
32. Sreenivasan FAM H/O 70 M NSTEMI 1798 + heterocollateral LCX 1

48
33. Murugaraj SMO 75 M STEMI 1551 + heterocollateral RCA 1

58
34. Meenal DM/SHT 42 F CSA 1534 + nil 0

55
35. Nagaraj SMO/DM 57 M REC.CAD 1653 + heterocollateral LAD 2

42
36. Laksmi OBE/SMO 68 F STEMI 1789 + heterocollateral LCX/RCA 1

46
37. Balu DM/SMO 63 M STEMI 1834 + Both hetero/homo LAD/OM 1

40
DM/FAMH/O/S
38. Chinraj 48 M STEMI 1823 + nil 0
HT
39. Ragupathi SMO/SHT M 39 NSTEMI 1799 + heterocollateral 1 56

40. Laksman DM/SMO M 56 STEMI 1558 + nil 0 48

41. Beemn SMO M 48 CSA 1545 + Both hetero/homo 2 50

42. Kumuda DM F 68 STEMI 1826 + Both hetero/homo 2 46

PRIOR
43. Nagendrabau M 65 NSTEMI 1744 + heterocollateral 1 42
CAD/SMO

SMO/PRIOR
44. Veeraiya M 59 CSA 1894 + Both hetero/homo 1 50
CAD

45. Chinnasamy SMO M 51 STEMI 1508 + Heterocollateral; 2 56

46. Meenakshi DM F 49 REC.CAD 1503 + heterocollateral 2 55

47. Guru DM/SMO M 68 CSA 1590 + nil 0 42

48. Gopal DM M 52 STEMI 1578 + heterocollateral 1 40

49. Balu SMO M 47 NSTEMI 1540 + Both hetero/homo 2 46

REC.CAD
50. Rajui SMO/DM M 64 1644 + Both hetero/homo 2 48
ANGIOGRAPHIC PICTURES
ANGIOGRAPHIC PICTURES
 PROFORMA
NAME: AGE: yrs SEX: M / F

IP NO:

HT: WT: BMI:

ADDRESS:

ANGIO DATE & NO:

PRESENTATION:

1.STEMI

2. NSTEMI

3.USA

4. CSA

5.RECURRENT CAD

DURATION OF CAD:

RISK FACTORS :

1. IGT 2. DM 3. SHT

4. PRIOR CAD 5.SMOKING 6. DYSLIPEDEMIA

7. FAMILY H/O CAD 8.OBESITY

9. SEDENTARY LIFESTYLE

INVESTIGATIONS:

HB: BL.SUG: FS: PP[2HRS]:

HBA1C:

BL.UREA: Sr.CR:

TMT:
CORONARY ANGIOGRAM:

LMCA-

LAD-

LCX-

RCA-

NO.OF TOTALLY/SUBTOTALLY >95% OCCLUDED VESSELS:

ANGIOGRAPHIC DIAGNOSIS:

COLLATERALS:

NUMBER:

HOMOCOLLATERLS:

HETEROCOLLATERALS:

TYPESOF COLLATERALS:

GRADING OF COLLATERALS:
 Informed consent form
Title of the study -
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I,________(name of participant), have read the information in this form (or it has been read to
me). I was
free to ask any questions and they have been answered. I am over 18 years of age and,
exercising
my free power of choice, hereby give my consent to be included as a participant in ___ ” (title
of the study)
(1) I have read and understood this consent form and the information provided to me.
(2) I have had the consent document explained to me.
(3) I have been explained about the nature of the study.
(4) I have been explained about my rights and responsibilities by the investigator.
(5) I have informed the investigator of all the treatments I am taking or have taken in the past
______ months including any native (alternative) treatments.
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any reason and this will not affect my future treatment in the hospital.

(7) I hereby give permission to the investigators to release the information obtained from me
as result of participation in this study to the sponsors, regulatory authorities, Government
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I am aware, that if I have any questions during this study, I should contact the
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