ISCHEMIC HEART DISEASE

Presenter: Dr. Mounika

Moderator: Dr. Jayapal Rao
MD,HOD,Dept of Pathology

ISCHEMIC
HEART DISEASE

PLAN OF STUDY
1.
2.
3.
4.
5.
6.
7.

Need for study

Definition
Risk factors
Pathogenesis
Effects of Ischemia
Angina
MI

8.Investigations
9. Complications
10.DD
11.Management
12. Conclusion
13. Homoeopathic
approach
14. Bibliography

Need for study

EPIDEMOLOGY:
IHD causes more deaths and disability
and incurs greater economic costs than
any other illness in the developed world.
IHD is the single most important cause of
premature death in developed world. It is
serious, chronic, life-threatening illness.

 With urbanization in the developing world,

the prevalence of risk factors for IHD is
increasing rapidly in these regions such
that a majority of the global burden of IHD
is now occurring in low-income and
middle-income countries. Population
subgroups that appear to be particularly
affected are men in South Asian countries,
especially India.

Speciality of cardiac muscle?

No fatigue?
No tetanus?

Blood supply
The two coronary arteries, left and right,
arise from the left and right sinus of
Valsalva, respectively. In 10% of
individuals the circulation is considered as
"left dominant" as the circumflex artery
gives off the posterior descending artery.
In 90%, the circulation is right dominant as
the posterior interventricular artery is given
off from the right coronary artery

Supply to heart occurs during

Systole or Diastole?

Factors that maintain circulation

Pumping action of heart

Elastic recoil of the arteries\
Pressure gradient
Respiration
Muscular exercise
Effect of gravity

Factors regulating nutrition &

action of heart

O2 supply
Blood pressure
Temperature
Inorganic ions
Neuroharmones

Factors influencing coronary

circulation

Mean aortic pressure

Cardiac output
Metabolic factors
O2 supply

Conduction & nerve supply

Autorhythmic
Sympathetic & parasympathetic

DEFINITION OF IHD
The World Health Organisation has
defined ischaemic heart disease (IHD) as
myocardial impairment due to imbalance
between coronary blood flow and
myocardial requirements.
The most common cause of IHD is
atherosclerotic coronary artery
disease[CAD]

Aetiology
MAJOR RISK FACTORS
CONSTITUTIONAL
Age
Sex
Genetic
Familial

Acquired
Hyperlipidaemia
Hypertension
DM
Smoking

Minor risk factors

Environmental influences
Obesity
Infections
Harmones
Physical inactivity
Stressful life
Role of alcohol
Homocystinuria

PATHOPHYSIOLOGY OF
MYOCARDIAL ISCHAEMIA
Myocardial ischaemia occurs as a result of
imbalance between O2 supply and
demand.

Etiopathogenesis
1.Coronary atherosclerosis:
Distribution:[ SVD, TVD]
Location.

 2. Superadded changes in coronary

atherosclerosis:
Acute changes
coronary artery thrombosis
platelet aggregation

3.Non atherosclerotic causes:

Vasospasm,
Arteritis
Embolism
Trauma
Aneurysm
Compression.

Effects of Myocardial Ischemia: Depending

on suddenness of onset , Duration,
Degree, Location, Extent of area affected
by ischemia.

Asymptomatic state
Angina pectoris
Acute myocardial infarction
Chronic ischemic heart disease
Sudden cardiac death

ANGINA
It is derived from the greek word
STRANGULATION.
It is a syndrome SENSE OF BAND
AROUND CHEST. Patient presses his
sternum with clenched fist to locate the
pain.
Progressive constriction of coronary
arteries cardiac pain called angina.

The types of angina include

1. Stable angina,
2. Unstable angina,
3. Prinzmetals angina
4. Post infarction angina

Stable angina or effort angina

Also called Heberdeens angina, it occurs
on known physical effort, and is relieved
with rest, standing or sublingual
nitroglycerine.
Modalities
Temperature,
Emotions,

 Diurnal
Even sometimes smoking, sexual act,
shaving, straining at stool

Some cases pain is absent , Anginaequivalent symptoms breathlessness,

fatigue, symptoms of decreased cardiac
output.

Variants:
Start-up or Walk- through angina,
Nocturnal angina,
Decubitius angina,
Post Prandal angina,
Ammunition factories.

Class

New York Heart Association Functional

Classification

Canadian Cardiovascular Society

Functional Classification

Patientshavecardiacdiseasebutwithout
theresultinglimitationsofphysicalactivity.
Ordinaryphysicalactivitydoesnotcause
unduefatigue,palpitation,dyspnea,or
anginalpain.

Ordinaryphysicalactivity,such
aswalkingandclimbingstairs,
does not cause angina.Angina
presentwithstrenuousorrapid
orprolongedexertionatworkor
recreation.

II

Patientshavecardiacdiseaseresultingin Slight limitationofordinary

slight limitationofphysicalactivity.Theyare activity.Walkingorclimbing
comfortableatrest.Ordinaryphysical
stairsrapidly,walkinguphill,
activityresultsinfatigue,palpitation,
walkingorstairclimbingafter
dyspnea,oranginalpain.
meals,incold,orwhenunder
emotionalstressoronlyduring
thefewhoursafterawakening.

III

Patientshavecardiacdiseaseresulting Marked limitationof

inmarked limitationofphysicalactivity. ordinaryphysicalactivity.
Theyarecomfortableatrest.Lessthan Walkingonetotwoblocks
ordinaryphysicalactivitycauses
onthelevelandclimbing
fatigue,palpitation,dyspnea,oranginal morethanoneflightof
pain.
stairsinnormal
conditions.

IV

Patientshavecardiacdiseaseresulting Inabilitytocarryonany
ininabilitytocarryonanyphysical
physicalactivitywithout
activitywithoutdiscomfort.Symptoms discomfortanginal
ofcardiacinsufficiencyoroftheanginal syndromemaybepresent
syndromemaybepresentevenatrest. atrest.
Ifanyphysicalactivityisundertaken,
discomfortisincreased.

 Physical examination in patients with

angina pectoris is often normal. However,
there may be indication of coronary risk
factors like xanthelasma or xanthomas.
Palpation may reveal thickened arteries
and reduced or absent pulses as signs of
generalised atherosclerosis. LV
enlargement, S3 or S4 gallop.

INVESTIGATIONS
1. X-ray chest for cardiomegaly or
pulmonary congestion. 2. Lipid profile 3.
Blood sugar, serum uric acid and urine
examination
Electrocardiogram : In 50% of patients
with angina, the resting ECG is normal
between anginal episodes. During an
anginal episode transient ST-T depression
may be noted which disappears with rest
or with sublingual nitroglycerine

Prinzmetal angina
Also called variant angina, it was
described by Prinzmetal in 1959. The pain
usually occurs at rest at night or in the
early morning hours. It is associated with
ST elevation on the ECG, responds to
sublingual nitroglycerine, and is caused by
spasm of the coronary artery.

 Exercise stress testing may fail to induce

ischaemic changes. The spasm can be
induced by smoking, hyperventilation .
The cause of spasm may be increased
alpha-adrenergic activity during the early
morning hours or platelet aggregation.
Coronary angiography may reveal normal
coronary arteries.

Unstable angina
Also called intermediate coronary
syndrome and Preinfarction angina, it is a
serious form of angina and needs special
attention since 20% of these patients are
likely to develop fatal or nonfatal
myocardial infarction within 4 months.
There is a higher incidence of left main
coronary artery disease in these patients.

 Unstable angina includes (i) angina of

recent onset (less than 60 days); (ii) stable
angina with symptoms more severe in
intensity, frequency or duration and more
easily provoked; (iii) angina at rest; (iv)
angina following myocardial infarction
(within days or weeks).

 ST-T depression in the ECG is common...

About 25% of these patients have
coronary artery thrombosis. In the others,
spasm plays an important role. Patients
have associated severe coronary artery
obstructive disease.

Management
Thrombolytic agents
PTCA
CABG

Post infarction angina

Some patients with myocardial infarction
develop angina 2 days to 8 weeks
following the acute infarction. Most
patients have multivessel disease or
partially recanalised coronary arteries with
residual myocardial ischaemia.

MYOCARDIAL INFARCTION
The area of muscle that has either zero
flow or so little flow that it cannot sustain
cardiac muscle function process called
Infacrtion.

 Myocardial infarction is a serious

complication of atherosclerotic coronary
heart disease. In most patients (80-95%) it
results from thrombotic occlusion of the
infarct-related vessel. Myocardial
ischaemia and necrosis set in within about
20-40 minutes

 This occurs as a wave-front starting from

the subendocardial region and
progressing to the subepicardial region.
The entire process usually takes 6 hours
to complete. Therefore any intervention for
limiting infarct size should be initiated in
this "time window" of 6 hours.

Etiopathogenesis:
Mechanism of Myocardial ischemia:
Diminished coronary blood flow, Increased
myocardial demand, Hypertrophy of heart
without increase in coronary blood flow.

 Infarcts may be transmural versus

subendocardial infarcts: Transmural
most common type 95%. Subendocardial
infarct genesis is due to reduced coronary
perfusion without critical stenosis

Transmural
Full thickness
Superimposed thrombus in
atherosclerosis
Focal damage

Sub-endocardial
Inner 1/3 to half of ventricular
wall
Decreased circulating blood
volume( shock, Hypotension,
Lysed thrombus)
Circumferential

Types of infarcts:
1. Acc to anatomical region of left
ventricle: Anterior, lateral, septal,
circumferential or combinations.
2. Acc to degree of thickness : Transmural,
Subendocardial.
3. Acc to age old, new [ healed & fresh].

Location of infarcts:
Infarcts are most frequently located in left
ventricle . Right ventricle is less
susceptible to infarction due to its thin wall
less metabolic requirement.

3 common regions of MI:

1. Stenosis of left anterior descending coronary
artery is most common[40% to 50%]
2. Stenosis of right coronary artery[30% to 40%]
3. Stenosis of left circumflex coronary
artery[ 15% to 20%]

Morphology[ Pathological changes]

light microscopy
First 0-6hrs- Streching of fibres.
6-12hrs after MI Coagulative
necrosis & neutrophils begins
Up to 3 days = Coagulative necrosis,
neutrophils
1-2 weeks = Granulation tissue
3 weeks = fine scar
2 months = dense scar

CLINICAL FEATURES
The presenting symptoms vary from
severe pain in the chest to minimal
symptoms with the disease being
unrecognised. In most patients, there is
substernal pain of varying intensity,
radiating to the arms, jaws or back or the
epigastric region, with sweating. The pain
lasts for 20 minutes or more and is
unrelieved or partially relieved by
sublingual nitroglycerine

 The discomfort may be felt as

compression of chest or a burning
sensation, associated with anxiety and
feeling of impending death. Continuing
discomfort is a symptom of ongoing
ischaemia and evolving infarction. As the
infarction is completed, the pain may
subside completely..

 In 15-30% of patients the infarction may go un

recognised because of absence of typical
symptoms. About 5% of such patients have
silent infarction. This is common in diabetics
and elderly patients. In others, breathlessness
as in acute left ventricular failure, syncope,
giddiness, fatigue, abdominal pain, nausea
and vomiting and unexplained hypotension
may be the presenting manifestation

C/F

Pain
Indigestion
Apprehension
Shock
Oliguria
Low grade fever
Acute pulmonary oedema

 Physical examination reveals a pale

patient who is sweating, restless, in agony
due to pain, and tossing in the bed in an
attempt to get relief. The pulse may be
rapid or slow, and regular or irregular.
Bradycardia may be a prominent feature
in the early hours especially in those with
inferior wall infarction

Blood pressure may be normal, low or high.

Auscultation may reveal S3 or S4 gallop.
Paradoxical splitting of the second heart sound
may be made out. Right ventricular infarction
may result in increased jugular venous
pressure and signs of right heart failure.

Cardiac reserve
Maximum amount of cardiac output that
can increase above normal. It is 400%
blood per min more than body requires.

Coronary steal syndrome

The degree of cellular death = degree of
ischemia x degree of metabolism of heart .
[ Increase exertion
Increase metabolism- decrease blood
supply to ischemic areas leaving the blood
through coronary vessels.]

INVESTIGATIONS
Leucocytosis with polymorphonuclear
reaction and high ESR due to tissue
necrosis are present during the first week.

 Electrocardiographic changes : The earliest

changes are ST elevation occurring with the
onset of chest pain. Q waves appear when
transmural infarction occurs. ST segment
changes start reversing early (within 24
hours or so) and T waves begin to get
inverted.).

 Anterior wall infarction is diagnosed by

changes in leads V1 to V4,
Lateral by changes in L1, aVL, V5 and V6,
and
Inferior wall infarction by changes in L2, L3
and aVF
Posterior wall LV infarction is diagnosed by
ST depression, upright T wave and tall R
wave in V1 and V2.

 The initial ECG changes may be present

in only about 50-75% of patients. In
others, a typical history and serial serum
enzyme changes provide diagnostic help.
Serial ECGs improve the diagnostic yield
to 85%.

 Serum enzymes: Necrosis of myocardial

cells releases enzymes in the blood.
SGOT (AST) starts to rise within a few
hours, reaching a peak at 24 hours and
declining over the next 48-72 hours; it is
not specific for cardiac muscle injury since
it is present in red blood cells, liver and
skeletal muscle.

 Serum creatinine phosphokinase (CPK) rises

immediately 4 to 6hrs ; it falls to normal values
within 48 hours. This enzyme is also not
specific for cardiac cells and is present in
skeletal muscle and brain tissue. The CPK
isoenzyme, CPK-MB, is more specific for
cardiac tissue; its levels have been related to
the extent of myocardial infarction.

 Serum LDH levels increase late after

myocardial infarction. The increase starts
during the first day, peak levels are
achieved during the 3rd or 4th day, and
they may remain high for 14-15 days. LDH
cardiac isoenzyme (LDH1) is more
specific.
Troponin level is increased in AMI 4 to
6hrs and is a more sensitive indicator of
myocardial neurosis high for 7 to 10 days.

MANAGEMENT
Almost 30-35% of patients with AMI die
due to arrhythmias, LV failure and
cardiogenic shock. Half of these deaths
occur in the first 1-2 hours after onset of
symptoms and 70-80% in the first 24
hours. Further, the Time window for
salvaging the ischaemic myocardium at
risk of necrosis is about 6 hours

Reperfusion
An occluding thrombus is responsible for
myocardial infarction in almost 85% of
patients. It is known that the infarction is
completed after several hours. An attempt
should therefore be made to remove the
obstruction and achieve reperfusion to reestablish blood flow to the jeopardised
myocardium and so limit the size of the
infarct.

Cell injury induced by free radicals, particularly

reactive oxygen species, is an important
mechanism of cell damage in many pathologic
condition ischemia-reperfusion injury (induced
by restoration of blood flow in ischemic tissue) .
On perfusion excess of sodium and calcium
ions due to cell membrane damage.

 For approximately 30 minutes after the

onset of even the most severe ischemia,
myocardial injury is potentially reversible.
Thereafter, progressive loss of viability
occurs that is complete by 6 to 12 hours.
The benefits of reperfusion are greatest
when it is achieved early, and are
progressively lost when reperfusion is
delayed

Ischemic Heart Disease

 Thrombolytic agents, viz. streptokinase,

urokinase, acetylated streptokinase, and
tPA. It achieves recanalisation in about
50% of patients, recanalisation rates are
reportedly higher (75%). A major factor is
the high cost of the drug.

 All thrombolytic agents should be given within

4-6 hours after the onset of chest pain. Some
of the complications that can occur include
reperfusion arrhythmias and bleeding.
Thrombolysis is generally avoided in patients
following recent operations, those with recent
cerebrovascular accidents, those who have
bleeding diathesis or following
cardiopulmonary resuscitation.

 Thrombolytic agents help in reducing

short-term mortality and improving LV
function. Following thrombolytic therapy,
intravenous Herapin is given for the next
24-48 hours to prevent reocclusion..

 PTCA has been used as a method of

reperfusion with a success rate of 9095%.. It is a procedure of immense value
in patients with cardiogenic shock, severe
LV failure and large anterior myocardial
infarction.

 INDICATIONS OF PTCA:
Coronary arteriography is indicated in (1)
patients with chronic stable angina
pectoris who are severely symptomatic
despite medical therapy and who are
being considered for revascularization,
i.e., a percutaneous coronary intervention
(PCI) or coronary artery bypass grafting
(CABG)

 patients with troublesome symptoms that

present diagnostic difficulties in whom
there is a need to confirm or rule out the
diagnosis of IHD.

 Coronary bypass surgery as a method of

reperfusion is limited to patients who do
not respond to thrombolytic therapy and
continue to get angina and are not
suitable candidates for PTCA.
Complications and mortality are higher.

 Anastomosis of one or both of the internal

mammary arteries or a radial artery to the
coronary artery distal to the obstructive
lesion is carried out. For additional
obstructions that cannot be bypassed by
an artery, a section of a vein (usually the
saphenous) is used to form a connection
between the aorta and the coronary artery
distal to the obstructive lesion.

 Occlusion of venous grafts is observed in

1020% of patients during the first
postoperative year, in approximately 2%
per year during 5- to 7-year . Long-term
patency rates are considerably higher for
internal mammary and radial artery
implantations than saphenous vein grafts

 The survival benefit is greater in patients

with abnormal LV function (ejection
fraction <50%) the fraction of end diastolic
volume.

Complications of Acute Myocardial

Infarction
Arrhythmias
Heart failure
Cardiogenic shock
Sudden death. Rupture of interventricular
septum
Thrombosis in LV causing cerebral
embolism

 Rupture of ventricle into pericardial sac causing

cardiac tamponade
Deep vein thrombosis in legs causing
pulmonary embolism
Pericarditis during massive infarction
Aneurysm of ventricle with thrombosis and
thrombo-embolic phenomenon
Dresslers syndrome (post myocardial infarction
syndrome)

Dresslers syndrome occurs a few days to

6 weeks following myocardial infarction
and is characterised by fever,
Pleuropericarditis, joint pains and raised
ESR. It results from an autoimmune
reaction to the necrosed myocardial tissue

ASYMPTOMATIC [SILENT] CORONARY

ARTERY DISEASE
Several autopsy studies in accident victims
or in military personnel dying in the
battlefield, stress testing in asymptomatic
individuals subjected to executive health
check-ups, and coronary angiographic
studies in individuals may have coronary
artery disease without any symptoms. In
many of them the first event may be sudden
cardiac death or myocardial infarction.

 Some of these patients exhibit higher

thresholds to electrically induced pain,
others show higher endorphin levels, and
still others may be diabetics with
autonomic dysfunction.[ Endorphins are
derived from a substance found in Pitutary
gland , naturally and have pain relieving
properties.]

 In addition, patients with asymptomatic

ischemia after suffering a myocardial
infarction are at greater risk for a second
coronary event. The widespread use of
exercise ECG during routine examinations
has also identified some of these
heretofore unrecognized patients with
asymptomatic CAD

CHRONIC IHD
Ischemic Cardiomyopathy or Diffuse
fibrosis in the myocardium
characterstically found in elderly age
group.CHF is gradually developed
decompensation over a period of years
[Chronic anaemia]

SUDDEN CARDIAC DEATH AND

CARDIAC ARREST
It is estimated that in 20% or more of
patients with coronary artery disease, the
first presenting feature may be sudden
cardiac death, defined as death within few
minutes to 2 hours after onset of
symptoms. The usual cause is ventricular
fibrillation or cardiac asystole and
occasionally electromechanical
dissociation.

Differential Diagnosis
1. Pericarditis Hours to days; may be
episodic Sharp Retrosternal or toward
cardiac apex; may radiate to left shoulder
May be relieved by sitting up and leaning
forward <cough, swallowing, lying in
leftsided supine.
Pericardial friction rub

 Aortic dissection : Abrupt onset of

unrelenting pain Tearing or ripping
sensation; knifelike Anterior chest, often
radiating to back, between shoulder
blades.

 Pulmonary embolism: Abrupt onset;

several minutes to a few hours Pleuritic
Often lateral, on the side of the embolism
Dyspnea, tachypnea, tachycardia, and
hypotension, haemoptysis.

 Esophageal reflux -1060 min, Burning

Substernal, epigastric, Worsened by
postprandial recumbency.
Relieved by antacids.
Esophageal spasm- 230 min ,Pressure,
tightness, burning retrosternal, Can
closely mimic angina,

 Peptic ulcer- Prolonged Burning

Epigastric, substernal relieved with food or
antacids.
Acid peptic disease: < Early mrng
[ acid secretions are not neutralised by
food.]

 Musculoskeletal disease- Variable, Aching

< movement
May be reproduced by localized pressure
on examination[ chondrosternal,
costochondral .]

 Emotional and psychiatric conditions

tightness & aching; may be fleeting
Variable; may be retrosternal, Situational
factors may precipitate symptoms
Anxiety or depression often detectable
with careful history

Prognosis
Depends on:
1.Number of diseased vessels
2. Degree of LV dysfunction

MANAGEMENT [ADAPTATION]
Myocardial ischemia is caused by a
discrepancy between the demand of the
heart muscle for oxygen and the ability of
the coronary circulation to meet this
demand. Most patients can be helped to
understand this concept and utilize it in
the rational programming of activity.

 Many tasks that ordinarily evoke angina

may be accomplished without symptoms
simply by reducing the speed at which
they are performed. Patients must
appreciate the diurnal variation in their
tolerance of certain activities and should
reduce their energy requirements in the
morning, immediately after meals, and in
cold or inclement weather.

On occasion, it may be necessary to

recommend a change in employment or
residence to avoid physical stress.
However, with the exception of manual
laborers, most patients with IHD can
continue to function merely by allowing
more time to complete each task. In
some patients, anger and frustration may
be the most important factors
precipitating myocardial ischemia. If
these cannot be avoided, training in
stress management may be useful.

 A treadmill exercise test to determine the

approximate heart rate at which ischemic
ECG changes or symptoms develop may
be helpful in the development of a specific
exercise program.

EXERCISES
A regular program of isotonic exercise
[muscles contract & there is movement]
that is within the limits of each patient's
threshold for the development of angina
pectoris and does not exceed 80% of the
heart rate associated with ischemia on
exercise testing should be strongly
encouraged.
Avoid Isometric exercises[muscle
contract increase in tension but does not
move]

CONCLUSION
Chest discomfort is one of the most
common challenges for clinicians in the
office or emergency department. The
differential diagnosis includes conditions
affecting organs throughout the thorax and
abdomen, with prognostic implications that
vary from benign to life-threatening.

 Failure to recognize potentially serious

conditions such as acute ischemic heart
disease, aortic dissection, tension
pneumothorax, or pulmonary embolism
can lead to serious complications,
including death. Conversely, overly
conservative management of low-risk
patients leads to unnecessary hospital
admissions, tests, procedures, and
anxiety.

Homoeopathic approach
Physiological action basis said by
Dr.Richard Hughes:
Aconite: In all diseases of heart
characterised by increased action when
leftside is chiefly
involved.[ Physiologically cardiac
depressent][ Fear, anxiety, mental
restlessness]
Dr. Clark: Rapidity of action relieved
sometimes so painful & distressing spasm

Arsenic: For incidence of cardiac cachexy.

Nights are troubled by oppression and
anguish.
Dr. Clark: Ars.Iod: Act on heart muscle
arresting degeneration & restoring vitality.

Dr. Boerick- Same character of

pain as in Angina
Cactus: Pain as if constricted by Iron
band[ It is a stimulant on ganglionic
centres in the cardiac walls.]
Haemotoxylon: Sense of constriction is
characteristic. Sensation as if bar lay
across chest
Lactrodectus. Mactans: Picture of Angina,
constriction of chest muscles.

Hydrocyanic acid: Spasmodic

constriction& tightness in chest, torturing
pain in chest.
Anacardium: Also has band like
sensation.

 Glonine : Nitroglycerine[ palliative non

homoeopathic]
Amy.Nitrosum:For palliation in Coronary
spasm.

 Tabacum: Prove the most homoeopathic

drug for Angina pectoris, Constriction of
heart.[ Nausea, vomiting ,death like pallor]
Camphor: As a heart stimulant for
emergency use is most satisfactory
remedy.[ collapse]
Veratrum: Best heart stimulant.

 Iberis:Posess efficacy in cardiac

diseases.Wakes at 2 am with palpitation.
Ophidia [Naja, Bothrops][ Symptoms of
thrombotic phenomena]
Craetagus: Solvent power upon
crustaceous and calcareous deposits in
arteries.

 Type A Personality: Aggressiveness,

Competitive drive, Ambitiousness, Sense
of urgency [ risk factors & modalities].
Environmental influences. Helpful in
selection of remedy.

BIBLIOGRAPHY

Textbook of pathology by Dr. Harshmohan

API textbook of medicine
Harrisons Internal medicine.
Textbook of medical physiology by Guyton

THANKYU
THANKYU