1

ABSTRACT
OBJECTIVE
To evaluate the technical success of percutaneous
coronary intervention of chronic total occlusion.

STUDY DESIGN
Observational study.

SETTING
Cardiology Department, Punjab Institute of
Cardiology, Lahore.

DURATION OF STUDY
Six months after approval of synopsis.

METHODS:
70 Patients fulfilling inclusion and exclusion criteria
were included after taking informed consent on a consent
form (Appendix I). A proforma (Appendix II) was used for
data Collection included parameters of study.
The study was conducted at Punjab Institute of Cardiology,
Lahore.
Duration of occlusion was defined as the elapsed
time, in months, from the onset of symptoms (acute
myocardial infarction or change of anginal pattern) or on
coronary angiography.
All patients received a loading dose of 300 mg of
clopidogrel and then 75 mg/d for 9 months in addition to
150 mg/d aspirin. All the PCIs of CTOs were performed by
experienced cardiologist. Local anesthesia was given at the
site of arterial puncture that was radial or femoral. A
fluoroscopy time of 30 minutes was

allocated to wire the

lesion. If the angioplasty guide wire failed to progress, or

complications

occurred

such

as

coronary

dissection,

perforation or hemodynamic instability the procedure was

abandoned

and

declared

unsuccessful.

Selection

of

angioplasty guide wires and supporting balloons was at the

discretion of PCI operators. Operators progressed from soft
to stiff wires. Balloon pre-dilatation was mandated before
stent placement. Stent assignment was blinded to both the
physician and the patient. Bare metal and drug eluting
stents were used of available lengths 8-18 mm lengths and
2.5, 3.0, and 3.5 mm diameters. They were identical in
appearance.
angiographic

Post

dilation

deployment.

was
During

done

to

the

optimize
procedure,

intravenous heparin boluses were administered.

The procedure was concluded on achievement of the
primary end point or any of the Secondary end points.

RESULTS:
Mean age of patients was 52.79.9, mean height was
167.22 6.4 cm and mean weight was 76.39 kg.
Out of 70 patients 57 (81.4%) were male 13 (18.6) were
female. Regarding coronary artery risk factors 22 (31.4%)
were

Diabetic,

39

(55.7%)

hypertensive,

34(48.6%)

smokers, 17(24.3%) with family history of ischemic heart

disease and 13(13%) had previous history of ischemic
heart disease.
Diseased artery was LAD in 32 (45.7%), LCX in 9(12.9%)
and RCA in 29 (41.4%).
Regarding lesion characteristics of CTO Distal vessels
visualized in 56 (80%), Antegrade Flow was found in
45(64.3%) ,Retrograde Flow

25(35.7%), and

Calcification found in 9(12.9%).

Regarding Procedural characteristics JR Guider was used in
42(41.4%)

and XB-3 Guider was used 41(58.6%). Wire crossed with

balloon support 54(77%). TIMI III flow achieved
54(77%) and Technical success was 54(77%),
Residual stenosis was fonund >30%

16(22.9%)

Predictors of successful PCI Stump shape was Tapering in

46(65.7%) and Flat in 24(34.3%).
Collaterals were found in 36(51.4%), Bridging collaterals
were in 13(18.6%), Side branch collatrals were in
42(60%)
Length of leison was <10mm in 4(5.7%), 10-20mm in
30(42.9%), >20mm in 36 (51.4%).

CONCLUSION

KEY WORDS

INTRODUCTION
Percutaneous coronary intervention (PCI) of chronic total
occlusion

(CTO)

is

one

of

the

major

challenges

in

interventional cardiology.1 The true prevalence of CTO in the

general population is unknown because a certain proportion of
patients with CTO are either asymptomatic or minimally
symptomatic and never undergoes Coronary angiogram. 1
Chronic total coronary occlusion (CTO) is a common problem
seen in 10-30% of patients undergoing PCI. 2

The currently

accepted indication for re-canalization of a chronic coronary

occlusion is ischemic symptoms or inducible ischemia related
to the occluded vessel.

The re-canalization of a chronic total

coronary occlusion leads to relief of angina and to recovery of

left ventricular function with a favorable effect on survival 3.
Primary success rate is relatively low, as re-canalization of CTO
is a complex procedure due to inability to cross the occlusion
with the guide wire. Moreover, the overall procedure and
fluoroscopy time is longer and equipment use is higher than
PCI of non-occluded Vessels and with a high recurrence rate. 45

Percutaneous transluminal coronary angioplasty (PTCA)

of chronic coronary occlusions can be performed with a
success rate of 88.990.8%, but with a higher rate of
restenosis than after angioplasty of non-occluded vessels. 7
This study is designed to evaluate the outcome of PCI
of CTO in terms of technical success.
Furthermore to identify factors leading to successful
PCI i.e. tapered stump, smaller missing segment.
The study will clarify our understanding of PCI to CTO
in terms of patient selection who will be benefited most
from intervention and in whom intervention should not be
performed. Successful PCI for CTO has been shown to
alleviate

anginal

symptoms,

improve

left

ventricular

ejection fraction, decrease the need for coronary bypass

graft surgery, and prolong life.

REVIEW OF LITERATURE

HISTORICAL BACKGROUND
Over the past two centuries, the Industrial and
Technological Revolutions and their associated economic
and social transformations have resulted in dramatic shifts
in

the

diseases

responsible

for

illness

and

death.

Cardiovascular disease (CVD) has emerged as the dominant

chronic disease in many parts of the world, and early in the
21st century it is predicted to become the main cause of
disability and death worldwide.8
At the beginning of the 21st century, CVD accounts for
nearly half of all deaths in the developed world and 25
percent in the developing world. By 2020, it is predicted
that CVD will claim 25 million lives annually and that
coronary heart disease (CHD) will surpass infectious disease
as the worlds number one cause of death and disability.9-10

10

The global rise in CVD is the result of a dramatic shift

in the health status of individuals around the world during
the course of the 20th century. Equally important, there has
been an unprecedented transformation in the dominant
disease profile, or the distribution of diseases responsible
for the majority of cases of death and debility. Before,
1900, infectious diseases and malnutrition were the most
common causes of death. These have been gradually
supplanted in some (mostly developed) countries by chronic
diseases such as CVD and cancer. As this trend spreads to
and continues in developing countries, CVD will dominate as
the major cause of death by 2020, accounting for at least
one in every three deaths.11

11

Coronary angiography
Coronary angiography remains the gold standard for
identifying the presence or absence of arterial narrowing
related to atherosclerotic coronary artery disease.12 The
first selective coronary angiogram was performed in 1958
by Dr. F. Mason Sones, Jr., a cardiologist at The Cleveland
Clinical

Foundation.13

Quite

accidentally,

the

catheter

positioned in the aorta for an angiogram to assess aortic

insufficiency dove into the RCA, and an image was obtained
before it was fully realized what had occurred.
When Dr. Sones and Dr. Earl K Shirey published their
results of more than 1,000 procedures in 1962, interest in
coronary
important

angiography
role

in

the

surged.

Radiologists

development

of

played

an

catheterization

techniques in the early 1960s. New preformed catheter

designs, such as those by Dr. Melvin Judkins and Dr. Kurt
Amplatz, enabled selective angiography to be performed
with greater ease than was previously possible with the
Sones catheters. Additionally, percutaneous approaches
were also now possible, and arterial cut-downs were no

12

longer required.

Improvements in radiographic imaging

concomitantly led to better image quality.13

Percutaneous coronary intervention

Percutaneous

coronary

intervention

(PCI),

traditionally known as percutaneous transluminal coronary

angioplasty (PTCA) or simply coronary angioplasty, has
emerged, predominantly as balloon angioplasty, in its first
20 years as the most common major medical intervention.
Coronary balloon angioplasty is an offspring of transluminal
angioplasty of peripheral arteries initiated by Dotter and
Judkins in 1964.14
Their method of dilating stenoses by successively
introducing a coaxial double catheter with a diameter of 8Fr
(2.7 mm) and 12 Fr (3.7 mm), respectively, was crude. It
required an access hole with a diameter equal to the target
lumen.

In Germany, angiology, an important subspecialty

of internal medicine, provided fertile soil for development of

new techniques.14

13

Gruentzig had introduced the Dotter method at the

University Hospital in Zurich in 1971, inspired by Zeilter
from Germany. For several years, he experimented with
different balloon types. 15 In 1974, he performed the first
balloon angioplasty in a peripheral artery in Zurich. 16 In
1975,

Gruentzig

presented

the

double-lumen

balloon

catheter, which was introduced over a guidewire. 17 In 1976,

he presented a poster at the American Heart Association
(AHA) meeting in Miami demonstrating the feasibility of
coronary balloon angioplasty in dogs.
On September 16, 1977, in Zurich, Dr. Andreas
Gruentzig, managed a 38 years-old patient with a single
discrete stenosis of left anterior descending coronary artery
(LAD) percutaneously for the first time, when he advanced
a fixed-wire, distensible balloon across a coronary stenosis
and briefly inflated it to 6atm.18-19 This procedure was
termed as percutaneous transluminal coronary angioplasty
(PTCA). The procedure was initially limited to less than 10
percent of patients with symptomatic CAD who had focal
non-calcified lesion of a single, proximal coronary vessel,

14

where it was used as an alternative to coronary artery

bypass grafting (CABG).
Despite

these

improvements,

two

major

complications limited the widespread use of balloon PTCA.

The first was abrupt closure of the treated vessel, which
occurred in 5 to 8 percent of cases and required emergency
CABG in 3 to 5 percent of the cases. The second
complication was the development of symptom recurrence
because of restenosis of the treated segment in 15 to 30
percent of patients within 6 to 9 months after the initial
procedure.19
The concept of a temporary endoluminal splint to
scaffold an occluded peripheral vessel was introduced by
Charles Dotter nearly 40 years ago but was not practiced
until the first human coronary implantation was performed
in 1986.19 In 1986, the Monorail principle facilitated the use
of guidewire.20 After the first clinical use of a coronary stent
on March 28, 1986, by Paul in Toulouse, the pattern of PCI
changed.20

15

Self expanding wire mesh stents were initially used

but never attained broad clinical use because of high
thrombosis rate. In contrast, a series of balloon expandable
stents has been available in United States since 1994. 19
Initially bare metal stent (BMS) were used which are
expandable, balloon mounted, stainless steel, flexible,
laser-cut and polished, slotted tubes. Compared to PTCA
alone, stents reduce restenosis by approximately 30 % in
patients of CAD.21
Although stent implantation itself has been shown to
reduce restenosis but in-stent restenosis still occurs in 1040 % of the patients. A large body of evidence has heen
accumulated to understand the processes involved in
restenosis.

It

was

evident

that

following

mechanical

dilatation and stent implantation, neointimal formation,

which, when excessive, may re-narrow the vessel lumen
(restenosis). Utilizing the stent itself as the plateform for
local drug delivery is an appealing approach. The local
agent should be one that inhibits the complex cascade of
events that leads to neointimal formation after stent
implantation.

16

Sirolimus eluting stents are available for clinical use in

Europe, Asia and South America since 2002 and in United
States since 2003. Sirolimus (Rapamycin), is a naturally
occurring

macrocyclic

lactone

with

potent

immunosuppressive action used in renal transplantation

recipients since 1999, approved by United States Food and
Drug Administration (FDA).
Polymer coated paclitaxel eluting stents have been
commercialized in Europe, Asia and South America since
2003 and in United States since 2004. Paclitaxel was
originally

isolated

from

the

bark

of

Pacific

Yew,

an

antiplatelet agent, currently used to treat breast and

ovarian cancer.
As equipment design and operator experience evolved
rapidly over the last two decade, PCI is expanded to a
broader

spectrum

of

patients,

such

as

those

with

multivessel disease, more challenging anatomy, reduced

left

ventricular

function,

medical conditions.19

and

other

serious

comorbid

17

RISK FACTORS for Coronary artery disease

The global variation in CVD rates is related to
temporal and regional variations in known risk behaviors
and factors. Ecological analyses of major CVD risk factors
and

mortality

demonstrate

high

correlations

between

expected and observed mortality rates for the three main

risk factors; smoking, serum cholesterol and hypertension
and suggest that many of the regional variations are based
on differences in conventional risk factors.22-23
1

Increasing age: Over 83 percent of people who die of

coronary heart disease are of 65 years or older. At
older ages, women who have heart attacks are more
likely than men, are to die from them within a few
weeks.

Male sex (gender): Men have a greater risk of heart

attack than women do, and they have attacks earlier
in life. Even after menopause, when women's death
rate from heart disease increases, it's not as great as
men's.

18

Heredity including Race: Children of parents with

heart

disease

are

more

likely

to

develop

it

themselves. Most people with a strong family history

of heart disease have one or more other risk factors.
Just as one can't control age, sex and race, one can't
control family history. Therefore, it's even more
important to treat and control any other risk factor
one has.
4

Tobacco smoke: Smokers risk of developing coronary

heart disease is 24 times that of nonsmokers.
Cigarette smoking is a powerful independent risk
factor for sudden cardiac death in patients with
coronary heart disease; smokers have about twice
the risk of nonsmokers. Cigarette smoking also acts
with other risk factors to greatly increase the risk for
coronary heart disease. People who smoke cigars or
pipes seem to have a higher risk of death from
coronary heart disease (and possibly stroke) but their
risk isn't as great as cigarette smokers'. Exposure to
other people's smoke increases the risk of heart
disease even for nonsmokers.

19

Drinking

alcohol:

It

can

indirectly

contribute

to

coronary artery disease. Drinking too much alcohol

can raise blood pressure, cause heart failure and lead
to stroke. It can contribute to high triglycerides,
cancer and other diseases, and produce irregular
heartbeats. It contributes to obesity, alcoholism,
suicide and accidents.
6

High blood pressure: High blood pressure increases

the heart's workload, causing the heart to thicken and
become stiffer. It also increases risk of stroke, heart
attack, kidney failure and congestive heart failure.
When

high

blood

pressure

exists

with

obesity,

smoking, high blood cholesterol levels or diabetes,

the risk of heart attack or stroke increases several
times.24-25
7

High blood cholesterol: As blood cholesterol rises, so

does risk of coronary heart disease. When other risk
factors (such as high blood pressure and tobacco
smoke) are present, this risk increases even more. A
person's cholesterol level is also affected by age, sex,

20

heredity and diet.26

8

Physical inactivity: An inactive lifestyle is a risk factor

for coronary heart disease. Regular, moderate-tovigorous physical activity helps prevent heart and
blood vessel disease. The more vigorous the activity,
the

greater

are

the

benefits.

However,

even

moderate-intensity activities help if done regularly

and long term. Physical activity can help control blood
cholesterol, diabetes and obesity, as well as help
lower blood pressure in some people.27-28
9

Obesity and overweight: People who have excess

body fat, especially if a lot of it is at the waist, are
more likely to develop heart disease and stroke even
if they have no other risk factors. Excess weight
increases the heart's work. It also raises blood
pressure and blood cholesterol and triglyceride levels,
and lowers HDL cholesterol levels. It can also make
diabetes more likely to develop. Many obese and
overweight people may have difficulty losing weight.
But by losing even as few as 10 pounds, one can

21

lower his heart disease risk.29

10

Diabetes mellitus: Diabetes seriously increases the risk

of developing cardiovascular disease. Even when
glucose (blood sugar)

levels

are

under

control,

diabetes increases the risk of heart disease and

stroke, but the risks are even greater if blood sugar is
not well controlled. About three-quarters of people
with diabetes die of some form of heart or blood
vessel

disease.

If

someone

has

diabetes,

it's

extremely important to work with healthcare provider

to manage it and control any other risk factors that
one has.30-31

22

ANATOMY
ARTERIAL SUPPLY OF THE HEART

The arterial supply of the heart is provided by the right and

left coronary arteries, which arise from the ascending aorta.
They supply the myocardium, including papillary muscles
and conducting tissue. The coronary arteries and its
branches are distributed over the surface of the heart, lying
within the subepicardial connective tissue.32

23

Fig.1: Coronary arteries anterior view

Source: www.houstonheartcenter.com/Coronary_Arteries

24

RIGHT CORONARY ARTERY (RCA)

The right coronary artery arises from the anterior aortic
sinus of the ascending aorta and run forward between the
pulmonary trunk and the right auricle. It descends almost
vertically in the right atrioventricular groove, and at the
inferior border of the heart it continues posteriorly along
the atrioventricular groove to anastomose with the left
coronary artery in the posterior interventricular groove. The
following branches of right coronary artery (RCA) supply
the right atrium, right ventricle and parts of left atrium, left
ventricle and the atrioventricular septum.33
BRANCHES OF RCA
Right conus artery supplies the anterior surface of
the pulmonary conus (infundibulum of the right ventricle)
and the upper part of the anterior wall of the right ventricle.
Anterior ventricular branches are two or three in
number, and supply the anterior surface of the right
ventricle.

25

The marginal branch is the largest and runs along

the lower margin of the costal surface to reach the apex.
The posterior ventricular branches are usually two
in number and supply the diaphragmatic surface of the
right ventricle.
Atrial branches supply the anterior and lateral
surface of the right atrium. One branch supplies the
posterior surface of the both the right and left atria.
The artery of sinuatrial node supplies the node and
the right and left atria; in 35% of the individuals it arises
from the left coronary artery.32
Posterior interventricular (descending) artery
runs toward the apex in the posterior interventricular
groove. It gives off branches to the right and left ventricle,
including its inferior wall. It supplies branches to the
posterior part of the ventricular septum but not to the
apical part, which receives its supply from the anterior
interventricular branch of the left coronary artery. A large
septal branch supplies the atrioventricular node. In 10% of

26

individual the posterior interventricular artery is replaced by

a branch from the left coronary artery.

27

Fig.2: Coronary arteries posterior view

Source: www.houstonheartcenter.com/Coronary_Arteries

28

LEFT CORONARY ARTERY (LCA)

The left coronary artery is usually larger than the
right coronary artery, supplies the major part of the heart,
including the greater part of left atrium, left ventricle, and
ventricular septum. Left main stem (LMS) or left main
coronary artery arises from the left posterior aortic sinus of
the ascending aorta and passes forward between the
pulmonary trunk and left auricle.
Left

main

atrioventricular

coronary

groove

and

artery

then

divides

into

enters
left

the

anterior

descending (LAD) branch and left circumflex branch (LCX).

LAD: Left anterior descending branch runs downward in the
anterior interventricular groove to the apex of the heart.
LAD gives rise to septal perforating branches to supply the
interventricular septum and diagonal branches that supply
antero- lateral wall. It then bifurcates distally and tapers
out as a whales tail at the cardiac apex, although
sometimes it wraps around the apex to supply part of the
inferior wall.

29

LCX: Left circumflex branch (LCX) courses along the left

atrioventricular groove and provides small atrial branches to
the left atrium and marginal branches that supply the
lateral wall of the left ventricle. The marginal branches are
sometimes referred to as lateral branches, with the first
marginal branch called the high lateral and subsequent
lateral branches referred to as lateral or posterolateral
branches. Occasionally, LMS trifurcates to give rise also to a
ramus intermedius branch that supplies the high lateral wall
of left ventricle.32

30

PHYSIOLOGY OF THE CORONARY BLOOD

FLOW
Coronary flow is a function of driving pressure and
resistance, it can be stated in the equation Q=P/R where Q
is coronary flow, P is the driving pressure across the
coronary

vascular

bed

and

is

the

total

coronary

resistance. Resistance can be in three forms, R1=Viscous

resistance,

R2=Autoregulatory

resistance

and

R3=Compressive resistance.
1) VISCOUS RESISTANCE (R1):
It is the impedance to flow offered by the entire coronary
vascular bed during diastole when fully dilated and can be
considered to be relatively static.
2) AUTOREGULATORY RESISTANCE (R2):
It is four to five times greater than R1, is the major
component of resistance and is thought to result from tonic
contraction of vascular smooth muscle at the arteriolar
level.55 It has three mechanisms, metabolic, neurohumoral
and myogenic which adjust arteriolar tone.

31

In metabolic regulators of coronary resistance, the role of

adenosine is pivotal. With the onset of myocardial hypoxia,
adenosine is formed as 5-adenine monophosphate (5AMP)
and released into the interstitial space where it produces
vasodilation by an unexplained action on resistance vessels.
Adenosine is removed by
1) Conversion into inosine and hypoxanthine in red cells
and vascular endothelium.
2) Transport across the sarcolemma into the myocyte
3) Intravascular transport. Adenosine is found in very
small concentrations in myocardial perfusates, tissue
homegenates and coronary sinus blood.
Other investigators believe that adenosine is not the
primary metabolic controller of coronary resistance and that
this is a role of prostaglandins.34
Coronary

vascular

smooth

muscle

is

known

to

be

responsive to neurohumoral stimuli including adrenergic

constrictor and dilator mechanisms. A vagal mechanism has
also been described.

32

3) COMPRESSIVE RESISTANCE (R3):

It

arises

from

compression

of

vascular

channels

by

intramyocardial pressure as it varies through the cycle.

There is an intramyocardial systolic pressure gradient that
varies through the cycle. This intramyocardiac systolic
pressure gradient varies from 20-40 mm Hg in the outer
third of myocardium to 100 mm Hg in the inner third.
Diastolic intramyocardial pressures have been measured at
4-20 mm Hg without a transmural gradient. In the empty
beating

(on

cardiopulmonary

hypertrophic heart,

by

pass)

normal

or

the gradient in myocardial tissue

pressure persists. Ventricular fibrillation is associated with a

continuous gradient across the ventricular wall and a
subendocardial pressure of 50mm Hg in the normal heart
and 67mm Hg in the hypertrophic heart.
The transmural gradient in intramyocardial pressure during
systole is primarily responsible for the normal phasic
coronary flow in which 70-80% of flow occurs during
diastole. Thus, little or no flow reaches the middle and deep
myocardium during systole when flow is limited to more

33

superficial

layers

compensate

for

of

the

this

myocardium.
systolic

In

order

to

maldistribution

correspondingly greater proportion of diastolic flow must be

delivered to the inner myocardium. This is accomplished by
reduction of autoregulatory tone in the deeper myocardium
so that resistance is lower than in the more superficial
myocardium permitting greater subendocardial perfusion.35

MYOCARIAL OXYGEN CONSUMPTION

Heart provides blood for the circulatory needs of the body;
similarly it also supplies its own metabolic requirements
through

the

coronary

circulation.

Because

of

limited

capacity for anaerobic metabolism to support cardiac work,

its metabolism can be considered essentially aerobic. A
unique feature of the coronary circulation is the high degree
of oxygen extraction under basal conditions so that the
heart can adjust to changing oxygen needs by only a small
increment

in

oxygen

extraction.

Increasing

oxygen

requirements must be met by proportionate increases in

coronary flow.36

34

Animal studies have delineated factors that govern oxygen

requirements

of

the

myocardium.

Although

mean

myocardial oxygen consumption (MVO2) is difficult to

measure,

clinical

studies

have

been

consistent

with

laboratory data. The normal heart has sufficient reserve to

meet myocardial oxygen needs.
Oxygen consumption correlated with the tension time index
only until the peak systolic pressure had been attained at
which 91% of oxygen consumption per beat had occurred. 37
Thus myocardial oxygen consumption is not a uniform
function of duration of systole (tension time index) because
it is insensitive to the duration of pressure maintenance
between peak systolic pressure and the end of relaxation.
Wall stress is more fundamentally related to MVO2 then is
pressure development.38
Myocardial contractility or inotropic state is the second
major

determinant

of

MVO2.

Inotropic

interventions

(norepinephrine, calcium or paired electrical stimulation)

that increase Vmax by 50% result in a 40% increase in

35

MVO2. Myocardial contractility is as important as pressure

development as a determinant of MVO2.39
The fairly direct relationship between heart rate and
myocardial oxygen consumption is well known. When
oxygen consumption per beat is measured, it did not
exceed that which could be accounted for on the basis of
the concomitant increase in the velocity of the contractile
element. Basal oxygen requirement of the potassium-plegic
heart is about 20% of the oxygen consumption of the
working heart. The oxygen cost of electrical activation of
the heart has been determined to be less than 1% of the
oxygen need of the normal working heart.

36

PATHOLOGY
Almost all myocardial infarctions result from coronary
atherosclerosis,

generally

with

superimposed

coronary

thrombosis. Prior to the fibrinolytic era, clinicians typically

divided patients with myocardiacl infarction into those
suffering a Q-wave and those suffering a non-Q-wave
infarct, based on the evolution of the pattern on the ECG
over

several

days.

The

term

Q-wave

infarction

was

frequently considered to be virtually synonymous with

transmural infarction, whereas non-Q-wave infarctions were
often referred to as subendocardial infarctions. Phibbs

40

summarized the arguments that previous distinctions were

based on erroneous interpretation of pathological data and
should not serve as the basis for designing therapy. A more
suitable framework based on pathophysiology is referred to
as the acute coronary syndromes.

37

Atherosclerotic plaque
Slowly occurring high-grade stenoses of epicardial
coronary arteries can progress to complete occlusion but do
not usually precipitate STEMI, probably because of the
development

of

rich

collateral

network

over

time.

However, during the natural evolution of atherosclerotic

plaques, especially those that are lipid-laden, an abrupt and
catastrophic transition can occur, characterized by plaque
disruption. Some patients have a systemic predisposition to
plaque disruption that is independent of traditional risk
factors.41-43
After
substances

plaque
that

disruption,
promote

there
platelet

is

exposure

activation

of
and

aggregation, thrombin generation, and ultimately thrombus

formation.44-45 The resultant thrombus that is formed
interrupts blood flow and leads to an imbalance between
oxygen supply and demand and, if this imbalance is severe
and persistent, to myocardial necrosis (Fig.3).

38

Composition of Plaques
At autopsy, the atherosclerotic plaque of patients who
died of STEMI is composed primarily of fibrous tissue of
varying

density

and

cellularity

with

superimposed

thrombus. Calcium, lipid-laden foam cells, and extracellular

lipid each constitutes 5 to 10 percent of the remaining area.
The

atherosclerotic

plaques

that

are

associated

with

thrombosis and a total occlusion, located in infarct-related

vessels, are generally more complex and irregular than
those in vessels not associated with STEMI. Histological
studies of these lesions often reveal plaque rupture or
erosion. Coronary arterial thrombi responsible for STEMI
are approximately 1 cm in length in most cases, adhere to
the luminal surface of an artery, and are composed of
platelets,

fibrin,

erythrocytes,

and

leukocytes.

The

composition of the thrombus may vary at different levels: a

white thrombus is composed of platelets, fibrin, or both,
and a red thrombus is composed of erythrocytes, fibrin,
platelets and leukocytes.43 Early thrombi are usually small
and non-occlusive and are composed predominantly of
platelets.

39

Fig.3: Plaque formation and nomenclature of acute

coronary syndrome
Antman EM, Braundwald E. ST-elevation myocardial
infarction: pathology, pathophysiology, and clinical features.
In: Zipes DP, Libby P, Bonow RO, Braunwald E, eds.
Braunwalds heart disease: a textbook of cardiovascular
medicine. 7th Ed. Piladelphia: Saunders, 2005; 1143

40

Plaque Fissuring and Disruption

In atherosclerotic plaques prone to disruption, there
is an increased rate of formation of metalloproteinase
enzymes such as collagenase, gelatinase, and stromelysin
that degrade components of the protective interstitial
matrix.44 These proteinases can be elaborated by activated
macrophages and mast cells that have been shown to
accumulate

in

high

concentration

at

the

site

of

atheromatous erosions and plaque disruption in patients

who died of STEMI.44 Examination of specimens from
atherectomy reveals a much higher content of macrophages
and tissue factor in patients with unstable angina or STEMI
compared with patients with chronic stable angina. 46 In
addition to these structural aspects of vulnerable or highrisk plaques, stresses induced by intraluminal pressure,
coronary vasomotor tone, tachycardia (cyclic stretching and
compression), and disruption of nutrient vessels, all these
combine to produce plaque disruption at the margin of the
fibrous cap near an adjacent plaque-free segment of the
coronary artery wall (shoulder region of plaque). 44 A

41

number of key physiological parameters such as systolic

blood pressure, heart rate, blood viscosity, endogenous
tissue plasminogen activator (t-PA) acitivity, plasminogen
activator inhibitor-1 (PAI-1) levels, plasma cortisol levels,
and plasma epinephrine levels that exhibit circadian and
seasonal variations are increased at times of stress. They
act in concert to produce a heightened propensity to plaque
disruption and coronary thrombosis, yielding the clustering
of STEMI in the early morning hours, and especially in the
winter and after natural disasters.47

42

Acute Coronary Syndromes

When plaque disruption occurs, a sufficient quantity of
thrombogenic substances is exposed, and the coronary
artery lumen may become obstructed by a combination of
platelet aggregates, fibrin, and red blood cells. An adequate
collateral network that prevents necrosis from occurring can
result in clinically silent episodes of coronary occlusion.
Disruption of plaques is now considered to be the common
pathophysiological
syndromes

(ACS).

substrate

of

the

Characteristically,

acute
such

coronary
completely

occlusive thrombi lead to a large zone of necrosis involving

the full or nearly full thickness of the ventricular wall in the
myocardial bed subtended by the affected coronary artery
and typically produce ST elevation on the ECG. The
infarction process alters the sequence of deporalization
ultimately reflected as changes in the surface of QRS. The
most characteristic changes in the QRS that develops in
about 75 percent of patients initially presenting with ST
elevation is the evolution of Q waves in the leads overlying
the infarct zone, leading to the term Q-wave infarction. In

43

about 25 percent of patients presenting with ST elevation,

no Q-waves develop,48 but other abnormalities of the QRS
complex are frequently seen such as diminution in R wave
height and notching or splintering of the QRS. Patients
presenting without ST elevation are initially diagnosed as
suffering

either

from

non-ST-elevation

myocardial

infarction (NSTEMI) or unstable angina (Fig.3).

The ACS spectrum concept, organized around a
common

pathophysiological

substrate,

is

useful

framework for developing therapeutic strategies.49 Patients

presenting

with

persistent

ST-segment

elevation

are

candidates for reperfusion therapy (either pharmacological

or catheter-based) to restore flow in the occluded epicardial
infarct-related artery.
ACS patients presenting without ST segment elevation are
not candidates for pharmacological reperfusion but should
receive anti-ischemic

therapy, often

followed by PCI.

Antithrombin therapy and antiplatelet therapy should be

administered to all patients with ACS regardless of the
presence or absence of ST-segment elevation. Thus, the

44

12-lead ECG remains at the center of the decision pathway

for management of patients with ACS to distinguish
between presentations with ST elevation and without ST
elevation.50

The

ECG

lacks

sufficient

sensitivity

and

specificity to permit reliable distinction of transmural from

subendocardial infarcts. Categorization of patients into
those with Q-wave and those with non Q-wave infarction
pattern is best conceived of as only a crude guide to the
extent of ventricular damage, and prognostic considerations
must take into account other important factors, such as
whether the ECG abnormality is due to a first infarct versus
subsequent infarct, the location of infarction (anterior
versus inferior), infarct size, and demographic factors such
as patient age.

45

LABORATORY FINDINGS
Serum Markers of Cardiac Damage

The classic World Health Organization (WHO) criteria

for the diagnosis of Mi requires that at least two of the
following three elements be present: a history of ischemictype chest discomfort, evolutionary changes on serially
obtained ECG tracing, and a rise and fall in serum cardiac
markers.51 The availability of serum cardiac markers with
markedly enhanced

sensitivity for myocardial damage

enables clinicians to diagnose MI in about an additional

one-third of patients who would not have fulfilled criteria for
MI in the past.52 The increased use of more sensitive
biomarkers of MI combined with more precise imaging
techniques has necessitated establishment of new criteria
for MI.
The rate of appearance of these macromolecules in
the peripheral circulation depends on several factors,
including intracellular location, molecular weight, local blood

46

and lymphatic flow, and the rate of elimination from the

blood.53
Given the accelerated pace of decision-making in
patients with acute coronary syndromes and emphasis on
reduction of length of hospital stay, there is considerable
interest

in

evaluating

new

serum

cardiac

markers,

shortening assay time in the central chemistry laboratory,

and designing rapid whole blood bedside assays. 54 For ease
of clinical use, the marker should persist in blood for an
appropriate

length

of

time

to

provide

convenient

diagnostic time window.55

Creatine Kinease (CK)
Serum CK activity exceeds the normal range within 4 to 8
hours after the onset of STEMI and declines to normal
within 2 to 3 days. Although the peak CK occurs on average
at about 24 hours, peak levels occur earlier in patients who
have had reperfusion as a result of the administration of
fibrinolytic therapy or mechanical recanalization (as well as
in patients with early spontaneous fibrinolysis). Because the
time-activity

curve

of

serum

CK

is

influenced

by

47

reperfusion,

and

because

reperfusion

itself

influences

infarct size, reperfusion interferes with estimation of infarct

size by enzyme analysis.56
False-positive results can occur in patients with
muscle disease, alcohol intoxication, diabetes mellitus,
skeletal muscle trauma, vigorous exercise, convulsions,
intramuscular injections, thoracic outlet syndrome, and
pulmonary embolism.57
Creatinine Kinase Isoenzymes
Three isoenzymes of CK (MM, BB, and MB) have been
identified by electrophoresis. Extracts of brain and kidney
contain predominantly the BB isoenzyme; skeletal muscle
contains principally MM but does contain some MB (1 to 3
percent); and both MM and MB isoenzymes are present in
cardiac muscle. The MB isoenzymes of CK can also be
present in minor quantities in the small intestine, tongue,
diaphragm,

uterus,

and

prostate.

Strenuous

exercise,

particularly in trained long-distance runners or professional

atheletes, can cause elevation of both total CK and CKMB.58 Since CK-MB can be detected in the blood of healthy

48

subjects, the cutoff value for abnormal elevation of CK-MB

is usually set a few units above the upper reference limit for
a given laboratory.57 Creatine kinase MB is analyzed in most
laboratories

by

highly

sensitive

and

specific

enzyme

immunoassays that utilize monoclonal antibodies directed

against CK-MB.57 Mass assays report results in nanograms
per milliliter rather than units per milliliter and have been
confirmed to be more accurate than CK-MB activity assays,
especially in patients presenting within 4 hours of the onset
of STEMI. It has been proposed that a ratio (relative index)
of CK-MB mass to CK activity of about 2.5 is indicative of a
myocardial rather than a skeletal source of the CK-MB
elevation. Although this ratio may be satisfied by many
patients

with

STEMI,

it

is

inaccurate

in

several

circumstances: (1) when high levels of total CK are present

because of skeletal muscle injury (a large quantity of CKMB must be released from the myocardium to satisfy
criteria); (2) when chronic skeletal muscle injury releases
large

amounts

of

CK-MB;

and

(3)

when

total

CK

measurements are within the normal reference range for

the laboratory and CK-MB is elevated (possibly indicating

49

that

microinfarction

has

occurred).

Patients

with

minimally elevated CK-MB and normal CK have a prognosis

that is generally worse than that for patients with suspected
MI but no CK-MB elevation. Elevation of CK-MB following
PCI is associated with increased late (1-3 years) cardiac
mortality.59
In addition to STEMI secondary to coronary obstruction,
other forms of injury to cardiac muscle, such as those
resulting from myocarditis, trauma, cardiac catheterization,
shock, and cardiac surgery, may also produces elevated
serum CK-MB levels.57
Cardiac Specific Troponins
The troponin complex consists of three subunits that
regulate

the

calcium-mediated

contractile

process

of

striated muscle. These include troponin C, which binds Ca 2+,

troponin I (TnI), which binds to actin and inhibits actinmyosin interactions; and troponin T (TnT), which binds to
tropomyosin, thereby attaching the troponin complex to the
thin filament. Although the majority of TnT is incorporated
in the troponin complex, approximately 6 percent is

50

dissolved in the cytosol; about 2 to 3 percent of TnI is

found in a cytosolic pool.
Although both TnT and TnI are present in cardiac and
skeletal muscle, they are encoded by different genes and
the

amino

acid

sequences

differs.

This

permits

the

production of antibodies that are specific for the cardiac

form (cTnT and cTnI) and has led to the development of
quantitative assays for cTnT and cTnI that have been
approved by the Food and Drug Administration for clinical
use.75 Several studies have confirmed the reliability of these
new quantitative assays for detecting myocardial injury, and
measurement of cTnT or cTnI is now at the center of a new
diagnostic criteria for STEMI.60-61 Qualitative, rapid, bedside
assays for cTnT and cTnI have also been approved for
diagnosing MI.62

51

Fig. 4: Percutaneous coronary intervention

Source:http://www.nhlbi.nih.gov/health/dci/images/stent_l
owres.gif

52

Total occlusion.

Acute total Occlusion.

These patients frequently present with acute myocardial
infarction and absent or poorly developed collaterals. Unless
coronary flow is restored within 4-6 hours, myocardial
injury is permanent. Pathologically, the obstructed lumen
typically consists of ruptured plaque and fresh clot. These
types of acute occlusions are readily crossed with
conventional guidewires, accounting for procedural success
rates exceeding 90%. The likelihood of successful
recanalization decreases over the ensuing months as fresh
thrombus undergoes organization, fibrosis, and
calcification.63

53

Chronic Total Occlusion (CTO).

Defined as obstruction of a native coronary artery
with no luminal continuity and TIMI flow grade 0 or 1. The
duration of occlusion had to be more than 3 months,
estimated

from

clinical

events

such

as

myocardial

infarction, sudden onset or worsening of symptoms or

proven by previous angiography.

63

These patients frequently present with a change in anginal

status rather than acute MI. Well-developed collaterals may
provide flow equivalent to a 90-95% stenosis, which helps
maintain myocardial viability and prevents resting
myocardial ischemia. Overall contractile function may be
normal, or a regional wall-motion abnormality may be
present due to hibernating myocardium or non-Q-wave MI.
Pathologically, the major constituent of a chronic total
occlusion is fibrocalcific plaque. These obstructions are
often resistant to guidewire crossing, accounting for lower
success rates compared to nontotal occlusions.
PTCA of chronic total occlusions represents 10-20% of
all angioplasty procedures and poses a management

54

dilemma for the interventional cardiologist. Although

collaterals maintain myocardial viability under resting
conditions, they often fail to provide sufficient blood flow
during periods of increased oxygen demand, resulting in
lifestyle-limiting angina. Successful revascularization
improves anginal status, increases exercise capacity, and
reduces the need for late bypass surgery. However, PTCA of
a chronic total occlusion is associated with lower success
rates, higher equipment costs, increased radiation
exposure, and more restenosis compared to PTCA of
nontotal occlusions. Improved guidelines for case selection,
new interventional devices, and adjunctive
pharmacotherapy may favorably impact these patients.63

55

TABLE. 1. Total Coronary Occlusion: Clinical and

Pathological Features
Acute Occlusion

Chronic Occlusion

Presentation

Acute MI

Change in anginal
status; angina is
usually exertional
(collateral
insufficiency)

Histopathology

Ruptured fibrous
cap overlies soft
atheroma;

Complex fibrocalcific
atherosclerosis with

acute occlusive
thrombus is
common
Spontaneous

chronic organized
thrombus

Occasional

Rare

Intracoronary

Rare

Occasional (bridging
collaterals)

Intercoronary

Less common

Common

Myocardial

Uncommon unless
collaterals are
present

Collaterals sustain
viability; wall motion
may

recanalization
Collaterals

viability

be normal
PTCA success

High

Variable; depends on
duration and
morphology

56

CTO: Indications and Benefits of

Revascularization

63

Indications

Medically refractory angina

Large area of ischemia by noninvasive studies

Favorable angiographic appearance

Proven Benefits

Relief of exertional angina

Improvement in global and regional left ventricular

function and exercise capacity

Reduction in the need for late CABG by 50%

Possible Benefits

Potential source of collaterals to other vessels

Improvement in left ventricular remodeling following

MI.

Improvement in event-free survival

57

TABLE.2.CTO-Predictors of PTCA Outcome

Procedural Success
Functional occlusion
Occlusion age < 12 weeks

Procedural Failure
Total occlusion
Occlusion age > 12 weeks
Length > 15 mm

Length < 15 mm
Tapered stump
No sidebranch at point of
occlusion
No bridging collaterals

Abrupt cut-off
Sidebranch present
Extensive bridging collaterals
(Caput Medusa)

58

Fig.5. Chronic Total Occlusion: Lesion Morphology and

Procedural Success.

59

OBJECTIVE
To evaluate the technical success of percutaneous
coronary intervention of chronic total occlusion.

OPERATIONAL DEFINITIONS
Chronic total occlusion (CTO):
Defined as obstruction of a native coronary artery
with no luminal continuity and TIMI flow grade 0 or 1. The
duration of occlusion had to be more than 3 months,
estimated

from

clinical

events

such

as

myocardial

infarction, sudden onset or worsening of symptoms or

proven by previous angiography.

Technical success:

60

Defined as restoration of TIMI flow grade 3 with residual

stenosis <30% on coronary angiography.

MATERIALS AND METHODS

Setting.
Cardiology Department, Punjab Institute of Cardiology,
Lahore.
Duration of study.
The duration of study was six months after approval
of synopsis.
Study design
Observational study.
Sample size.
70 Patients fulfilling inclusion and exclusion criteria were
included after taking informed consent on a consent form
(Appendix I). A proforma (Appendix II) was used for data
Collection included parameters of study.

61

The study was conducted at Punjab Institute of Cardiology,

Lahore.
Duration of occlusion was defined as the elapsed time, in
months, from the onset of symptoms (acute myocardial
infarction or change of anginal pattern) or on coronary
angiography.
All patients received a loading dose of 300 mg of
clopidogrel and then 75 mg/d for 9 months in addition to
150 mg/d aspirin. All the PCIs of CTOs were performed by
experienced cardiologist. Local anesthesia was given at the
site of arterial puncture that was radial or femoral. A
fluoroscopy time of 30 minutes was

allocated to wire the

lesion. If the angioplasty guide wire failed to progress, or

complications

occurred

such

as

coronary

dissection,

perforation or hemodynamic instability the procedure was

abandoned

and

declared

unsuccessful.

Selection

of

angioplasty guide wires and supporting balloons was at the

discretion of PCI operators. Operators progressed from soft
to stiff wires. Balloon pre-dilatation was mandated before
stent placement. Stent assignment was blinded to both the

62

physician and the patient. Bare metal and drug eluting

stents were used of available lengths 8-18 mm lengths and
2.5, 3.0, and 3.5 mm diameters. They were identical in
appearance.
angiographic

Post

dilation

deployment.

was
During

done

to

the

optimize
procedure,

intravenous heparin boluses were administered.

The procedure was concluded on achievement of the
primary end point or any of the Secondary end points.
Primary end point
The primary end point of the study was procedural success.
Secondary clinical end point
Secondary end point included failure of guide wire to cross
the lesion, perforation, dissection, peri-procedural instability
or death.

Sample technique.
Non probability, purposive sampling.

63

SAMPLE SELECTION
Inclusion criteria:
1. All patients with chronic total occlusion having TMI flow 01 degree undergoing percutaneous coronary interventions
were included.
Exclusion criteria:
1. Renal dysfunction, raised S Creatinine>1.4.
2. History of prior PCI.
3. History of prior CABG.

DATA COLLECTION
After fulfilling inclusion criteria patients admitted for
study were included after taking informed consent. They
were explained about procedure of study.

64

STATISTICAL ANALYSIS
Data was analyzed on SPSS version 14.0. Nominal variables
were presented as the frequencies and percentages and
continuous variables were expressed as the mean
standard deviation. Since it was an observational study so
no test of significance were applied.

ETHICAL ISSUES
All

patients

or

their

legally

authorized

representatives were explained about the study and written

informed consent was obtained.

65

RESULTS
Results were compiled after studying the specific variables.
70 patients were included in this study that fulfilled
inclusion criteria.
Mean age of patients was 52.79.9, mean height was
167.22 6.4 cm and mean weight was 76.39 kg.

Out of 70 patients 57 (81.4%) were male 13 (18.6) were

female. Regarding coronary artery risk factors 22 (31.4%)
were

Diabetic,

39

(55.7%)

hypertensive,

34(48.6%)

smokers, 17(24.3%) with family history of ischemic heart

disease and 13(13%) had previous history of ischemic
heart disease.
Diseased artery was LAD in 32 (45.7%), LCX in 9(12.9%)
and RCA in 29 (41.4%).
Regarding lesion characteristics of CTO Distal vessels
visualized in 56 (80%), Antegrade Flow was found in
45(64.3%) ,Retrograde Flow

25(35.7%), and

Calcification found in 9(12.9%).

66

Regarding Procedural characteristics JR Guider was used in

42(41.4%)
and XB-3 Guider was used 41(58.6%). Wire crossed with
balloon support 54(77%). TIMI III flow achieved
54(77%) and Technical success was 54(77%),
Residual stenosis was fonund >30%

16(22.9%)

Predictors of successful PCI Stump shape was Tapering in

46(65.7%) and Flat in 24(34.3%).
Collaterals were found in 36(51.4%), Bridging collaterals
were in 13(18.6%), Side branch collatrals were in
42(60%)
Length of leison was <10mm in 4(5.7%), 10-20mm in
30(42.9%), >20mm in 36 (51.4%).

67

TABLE 1. Baseline characteristics

Numbers
(n=70)

(%)

Characteristics
Age mean years
Gender

Men

52.79.9
57

81.4

13

18.6

Smoking

34

48.6

Diabetes mellitus

22

31.4

Hypertension

39

55.7

Previous MI

13

13

Family history of IHD

17

24.3

Women
Hypercholesterolemia

Table 2 Angiographic variables

68

Varaiables

Numbers (percentage)

Height mean (cm)

167.226.4

Weight mean (kg)

76.39

Diseased vessel
LAD

32 (45.7%)

LCx

9 (12.9%)

RCA

29(41.4%)

Table 3 Angiographic lesion chraterstics of CTO

69

Varaiables

Numbers (percentage)

Distal vessels visualized

56 (80%)

Antegrade Flow

45(64.3%)

Retrograde Flow

25(35.7%)

Calcification

9(12.9%)

Table 4 : Procedural characteristics

Characteristics
Guider used

Numbers (%)

70

JR-4

29(41.4%)

XB-3

41(58.6%)

Wire crossed with balloon

54(77%)

support

TIMI III flow achieved

54(77%)

Technical success

54(77%)

Residual stenosis >30%

16(22.9%)

Table 5: Predictors of successful PCI

Variables

Numbers (%)

Stump shape
Tapering

46(65.7%)

Flat

24(34.3%)

71

36(51.4%)

Collaterals

Bridging collaterals

13(18.6%)

Side branch

42(60%)

Length of Leison
<10mm

4(5.7%)

10-20mm

30(42.9%)

>20mm

36(51.4%)

DISCUSSION
In the current study the procedural success rate was 77%
The success rate of PCI was higher than the success rates
reported in the meta-analyses (53-68%)64 but similar to the
70-75% reported by a few authors,65-68 probably because
the proportion of late chronic lesions was high in the
present study. Puma et al

69

in their meta-analysis, reported

that chronicity is the most important factor in successful

72

intervention and that the success rate in late chronic

occlusion was significantly lower than that in early chronic
occlusion.
In our study, the factors affecting the success of transradial
PCI for CTO were also similar to these previous reports.
Although

the

success

of

CTO

intervention

might

dependent on experience, the lesion type, and indications

for intervention, the devices used for the procedure are
critically important to the outcome, particularly in the case
of transradial intervention. When the radial approach for
CTO intervention is attempted, availability of sufficient
guiding support becomes a major concern since it is
generally not feasible to use a guiding catheter larger than
7

Fr. Accordingly, transfemoral coronary intervention is

often preferred over transradial PCI for CTO because 7 or 8

Fr guiding catheters may be used to obtain greater back-up
support, as compared to the 6 Fr guiding catheters
frequently used in the transradial approach. However,
because catheter materials have improved a great deal, and
because special curvature is available to increase support,

73

we were able to achieve sufficient guiding support with a 6

Fr guiding catheter in most cases.
In this study, the selection of guiding catheters was based
on the lesion characteristics and the radial artery size. A 6
Fr guiding catheter was most frequently used. The type of
guiding catheters used for CTO was similar to those needed
for transradial PCI for other coronary lesions. In our study,
transradial PCI for a CTO lesion was possible using XB 3.0
guiding catheters in 58.6% when the lesion was in the left
coronary artery and in 41.4% Judkins right guiding catheter
was used for lesions in the right coronary artery. The
Judkins

right

guiding

catheter

was

used

less

often,

compared with the results reported by Lotan et al70 who

reported that Judkins (JL) guiding catheters were used in
49% of cases for the left coronary artery, while Judkins (JR)
guiding catheters were used in 57% of cases for the right
coronary artery in transradial PCI.
Kim et al80 evaluated the feasibility of the transradial
coronary intervention (TRCI) in 85 consecutive patients
with chronic total occlusion (CTO). Clinical, angiographic

74

and procedural factors were compared between the success

and failure groups. An overall success rate of 65.5% (57 of
87 lesions) was achieved with TRCI, and the most common
cause of failure was an inability to pass the lesion with a
guidewire. A multivariate analysis demonstrated that the
most significant predictor of failure was the duration of
occlusion. The procedural success rate improved with use of
new-generation hydrophilic guidewires. The 6 Fr guiding
catheters were used in the majority of the 70 cases (81%).
Five cases were crossed over to a femoral artery approach
due to engagement failure of the guiding catheter into the
coronary ostium because of severe subclavian tortuosity
and stenosis in two cases, radial artery looping in one case,
and poor guiding support in two cases. There were no
major entry site complications.8
Park et al71 reported a total of 195 patients had total
occlusion

lesions

(7.4%).

Percutaneous

coronary

interventions were attempted in 136 total occlusion lesions

(66.0%) in 134 patients. Successful recanalization with
stent implantation was accomplished in 89 lesions, with a
procedural success rate of 66.4%. One procedure-related

75

death occurred because of no-reflow phenomenon. After

excluding 8 patients with bundle branch block, Q and T
wave inversions were observed in 60 (32.1%) and 78
patients (41.7%), respectively. The presence of Q waves
was

associated

ventricular

with

ejection

severe
fraction,

angina,
regional

decreased
wall

left

motion

abnormality, and T wave inversion, but was not related to

procedural success. Percutaneous coronary intervention is a
safe and useful procedure for the revascularization of
coronary chronic total occlusion lesions. The procedural
success rate was not related to the presence of pathologic
Q waves, which were associated with severe angina and
decreased left ventricular function.71
Hoye et el72 reported a total of 874 consecutive patients
were treated for 885 CTO lesions. Mean follow-up time was
4.47+2.69

years.

occurrence

of

Patients

major

were

adverse

evaluated

cardiac

events

for

the

(MACE)

comprising death, acute myocardial infarction, and need for

repeat revascularization with either coronary artery bypass
surgery or PCI. Successful revascularization was achieved in
576 lesions (65.1%), in which stent implantation was used

76

in 81.0%.

At 30

days,

the

overall

MACE rate

was

significantly lower in those patients with a successful

recanalization. At 5 years, survival was significantly higher
in those patients with a successful revascularization. In
addition, there was a significantly higher survival free of
MACE, with the majority of events reflecting the need for
repeat intervention. Independent predictors for survival
were successful revascularization, lower age, and the
absence of diabetes mellitus and multivessel disease. Hoye
et

al73

concluded

that

successful

percutaneous

revascularization of a CTO leads to a significantly improved

survival rate and a reduction in major adverse events at 5
years.

Most

events

relate

to

the

need

for

repeat

reintervention, and the introduction of drug-eluting stents,

with low-restenosis rates, encourages the development of
technologies

to

improve

recanalization

success

rates.

However, failed recanalization may be associated acutely

with an adverse event, and new technologies must focus on
a safe approach to successful recanalization.

77

CONCLUSION

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Clinical Outcomes of Percutaneous Coronary,

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Eu Heart J 2006;

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PROFORMA
TITLE:
TECHNICAL SUCCESS OF PERCUTANEOUS CORONARY
INTERVENTION OF CHRONIC TOTAL OCCLUSION
S.NO:

Registration NO:

Name:

Age:

Height:

Weight:

Sex: M / F

Address:

94

CONVENTIONAL CORONARY ANGIOGRAPHIC LESION

DESCRIPTION:
LAD: Prox: Y / N

Mid: Y / N

Distal: Y / N Vessel diameter:

Mid: Y / N

Distal: Y / N Vessel diameter:

Lesion length
LCx: Prox: Y / N
Lesion length
Intermediate:Prox: Y / N

Mid: Y / N Distal: Y / N Vessel diameter:

Lesion length
RCA: Prox: Y / N

Mid: Y / N

Distal: Y / N Vessel diameter:

Lesion length
Side branch location within 2 mm of lesion: Y / N
Stump shape: Tapering:

Y / N Flat: Y / N

Duration of CTO:

Calcification: Y / N

Collaterals: Y / N

Bridging collaterals: Y / N

CTO vessel: LAD / RCA / LCX / Intermediate

Distal vessel visualized: Y / N
LESION LENGTH:
<10 mm: Y / N

10-20 mm: Y / N

>20 mm: Y / N

95

FLOW DYNAMICS ACROSS LESION:

Antegrade flow: Y / N

Retrograde flow: Y / N

Guider used:
PROCEDURE VARIABLES:
Guide wire used to cross the lesion:

with or without balloon

support:
Balloon used:

Inflations given:
Single: Y / N

Multiple: Y / N

Stent brand:

Deployment pressure:

Flouro time:

Procedure time:

TIMI flow grade 3:

Y/N

Stenosis <30%:

Y/N

Technical success:

Y/N

Procedure successful:

Y/N

Failure of guide wire to cross the lesion:

Y/N

Dissection:

Y/N

Perforation:

Y/N

96

CK-MB Level Raised:

Y/N

Cardiac Tamponade:

Y/N

Peri-procedural death:

Y/N