By: dr. Yuri Savitri, M.Ked (Card), Sp.

JP, FIHA
 ANGINA
PECTORIS
A Chronic disease of CVS

Occurs with Interminent

chest pain spread along the
Chest, Shoulders and Arms.
• Angina pectoris: a heart condition marked by
paroxysms of chest pain due to reduced oxygen
to the heart

• Angina pectoris, or angina, as it is commonly

referred to, and coronary artery disease or
arteriosclerosis are closely related.

• Angina occurs in people who have some form

of blockage in the coronary arteries. In other
words, it occurs in people with coronary heart
disease.
•It occurs when the Oxygen Supply to
the Myocardium is insufficient for its
needs.
Factors affecting Oxygen Demand Supply Ratio
 Various Chemical Factors released from Ischeamic
Muscle like
1. K+
2. H+
3. Adenosine
are responsible to stimulate the Nociceptors i.e
Chest Pain when the muscles contract with
interrupted supply of blood.

 Also the same mediators that cause Coronary

Vasodilation are responsible for this Pain.
 Also may occur due to accumulation of the waste
products in the heart muscle and stimulate local nerve
endings.

 The usual discomfort is regarded as a

pressure, heaviness, tightness, squeezing, burning or
choking sensation.

 The angina – coronary occlusion occurs which leads to

the Anginal attack over a period of time.
ANGINA-CORONARY
OCCLUSION

CORONARY
OCCLUSION
CORONARY
CIRCULATION
 Most tissues can increase O2 extraction with demand.
 Heart extracts near maximal amount of O2 at rest.
 Therefore can increase O2 demand by increasing the
Coronary Blood Flow.

Various Coronary Arteries of

Heart
 Types Of Angina
1. Pectoris
Stable Angina

2. Unstable Angina

3. Variant Angina (Prinzmetal’s Angina)

4. Anginal Equivalent Syndrome

5. Syndrome- X

6. Silent Ischemia
STABLE
ANGINA
 Predictable
 Occurs on exercise, emotion or eating.
 Caused by increase demand of the heart and by a fixed
narrowing of coronary vessels, almost always by
atheroma.
 Coronary obstruction is ‘fixed’
 Blood flow fails to increase during increased demand
despite the local factors mediated ‘vasodilation’ and so
ischeamic pain is felt.
 So, the diastolic pressure increases and this causes a
endocrinal ‘crunch’ and thus causing Ischeamatic pain in
this region.
 Thus, a form of acutely developing and rapidly
reversible left ventricular failure results which is
relieved by taking rest and reducing the myocardial
workload.
UNSTABLE
ANGINA
 This is characterized by Pain that occurs with less
excertion , cumulating pain at rest.
 The pathology is similar to that involved in Myocardial
Infraction, namely platelet-fibrin thrombus associated
with a ruptured atheromatous
plaque, but without complete
occulation of the vessels.
 The risk of infraction is
subtanial, and the main aim
of therapy is to reduce this.
VARIANT ANGINA (PRINZMETAL’S
ANGINA)
 Uncommon
 Occurs at rest generally during sleep
 Caused by Large Coronary Artery Spasm
 Usually associated with atheromatous
disease
 Abnormally reactive and
hypertrophied segments
in the Coronary Artery
 Drugs aimed at preventing &
relieving Coronary Spasm.
ANGINAL EQUIVALENT
SYNDROME
 Patient’s with exertional dyspnea rather than
exertional chest pain

Caused by exercise induced left ventricular

dysfunction
ANGINA:
SYNDROME
 X
Typical , exertional angina
stress test
with positive exercise

Anatomically normal coronary arteries

Reduced capacity of vasodilation in
microvasculature
 Calcium channel blockers and Beta blockers are
effective.
ANGINA: SILENT
ISCHEMIA
 Very Common

 More episodes of Silent than Painful angina in the

same patient.
 Difficult to diagnose

 Gnerally Exercise testing.

DIAGNO
SIS
1. STRESS (EXERCISE) TEST.
2. ECG (ELECTROCARDIOGRAPHY)
3. CHEST X-RAY
4. CARDIAC ANGIOGRAPHY/
CARDIAC CATHETERIZATION
5. ERGONOVINE TEST
6. BLOOD TEST (BIO-MARKERS)
1. EXERCISE
TEST/STRESS TEST
 Used to measure heart’s response to exercise
 Patient asked to walk on a treadmill while the
physician takes the ECG
 So any changes in heart function can be determined
 Alternatively the patient recieves an injection of a
radioisotope (generally Thallium) which makes the
heart visible to a special-linked camera
 90% accurate
 But doesn’t identify the exactly where and how the
coronary arteries are blocked.
2. ELECTROCARDIOGRAM
(ECG)
 Measures electrical activity of the heart
 Provides info about the changes or damages to the
heart muscle
 Doesn’t detect the narrowing of the coronary arteries
 During an Anginal attack the ECG may show
1. S-T phase depression.
2. T- phase inversion and/or
3. Ventricular arrythmia
 ECG- more abnormal with Unstable Angina where
the elevation in S-T segment is found.
 STABLE ANGINA

At
Rest

After
Excercise
3. CHEST X-
RAY
 Performed to rule out any lung disease or heart
damage that may be causing the pain.
 Also may reveal enlargement of heart
4. CARDIAC
ANGIOGRAPHY/
CARDIAC
 Shows the precise size and location of blockages
within the Coronary arteries
CATHETERIZATION
 A cathereter is inserted through the blood vessels from
the forearm or groin
 It is snaked through arteries till it reaches the heart
 A fluid is pumped
 So the arteries and the heart are clearly visible
5. ERGONOVINE
TEST
 Generally done if the person is assumed to suffer from
Coronary Spasm
 Done along with angiography
 The artery-narrowing drug—Ergonovine or Ach is
given to cause Coronary Spasm
 The persons response to ergonovanine is measured
6. BLOOD
TEST/BIOMARKERS
 Blood test for amount of Lipids within the blood
 Because lipids major cause of anginal attack
 Lipid profile for :- 1. HDL 2. LDL 3. TRIGLYCERIDES
 Recently the newer biomarkers like the C-reactive
protein and B-type natriuretic protein have been
found out and the tests for each of them is done
 These tests are predictive of the moratality of heart
disease
TREATME
NT
 3 Classes of drugs used according their mode of action

1. NITRATES
2. - ADRENOCEPTOR ANTAGONISTS
3. CALCIUM CHANNEL ANTAGONISTS
4. ANTIPLATELET DRUGS
Improving Oxygen Demand:Supply
Ratio
a.Relaxation of resistance vessels (small arteries and
arterioles) ↓TPR → ↓BP → ↓Afterload
(Nitrates, calcium channel blockers and beta-
blockers)
b.Relaxation of capacitance vessels (veins and
venules) ↓Venous return, ↓heart size, ↓Preload
(Nitrates and calcium channel blockers)
c.Blockade or attenuation of sympathetic influence on
the heart ↓Contactility, ↓HR, ↓O2 demand (Beta-
blockers)
d.Coronary Dilation, Important mechanism for
NITRAT
ES
 Prodrugs
 Sources of Nitric Oxide
 Eg:- Nitroglycerin,
Isosorbide Dinitrate
Isosorbide-5-Mononitrate

 Mechanism Of Action
PHARMAC
O
-
LOGICAL
ACTIONS
OF
NITRATE
S
 Nitrates mainly give Vasoldilation effect
 The specificity of their action is in dilating the collaterals
 Unlike other vasodilators (dipyridamole) which dilate only
the arteries but not the collaterals
TOXICITY OF
NITRATES
 Headache
 Increased mortality
 Recurrence of Myocardial Infraction
 Dizziness
 Flushing
 Rapid heart beat
 Restlessness
 Dry mouth
 Skin rash
 Nausea
MARKETED
FORMULATIONS
 GTN Sorbitrate (PIRAMAL)

Nitroglyceride
Vasovin (TORRENT)

 ISMO retard (PIRAMAL) Isosorbide-5-

monophosphate
 Angicor (NOVARTIS)
CALCIUM CHANNEL
ANTAGONISTS
 Disrupt Ca++ through Ca++ channels
 -ve ionotrpic effect
 2 types:-
1. Dihydropyridine
(amlodipine, nifedipine, nicardipine)
2. Non-Dihydropyridine
1. Phenylalkylamine (verapamil, gallopamil)
2. Benzodiazapenes (diltiazem)
3. Non-selective (bepridil, mibefradil)
MECHANISM OF
ACTION
Pharmac
ological
Actions
TOXIC
EFFECTS
MARKETED
PREPARATIONS
 Calaptin (PIRAMAL)

Verapamil
Vasopten (TORRENT)
 Coriem XL Diltiazem
(RANBAXY)
 Dicard (INTAS)
Amplodipine
 Amtas (INTAS)
 Cadeut (PFIZER)
 -
ADRENOCEPT
 Important in prophylaxis of angina and treating
unstable angina
OR
 Decrease O2 consumption by the heart
 Effects on coronary vessels-not important
ANTAGONOSTS
 Avoided in variant angina
 As they increase the chances of spasm
 Eg:-
 Atenolol
 Propranolol
PHARMACOLOGICAL
ACTIONS
MECHANISM OF
ACTION
MARKETED
PREPARATIONS
 Betacard ( TORRENT)

 Aten (ZYDUS CADILA)

 Betacap (SUN PHARMA)

 Cardilax (INTAS)
ANTICOAGULA
NTS
 Anticoagulants are often called "blood thinners,"
although they don't really thin blood. They decrease
the blood's ability to clot.
 Eg Heparin, Dalteparin, Enoxaparin, Warfarin, Aspirin
COMPARITIVE TOXIC
EFFECTS
 COMBINATION
1. Nitrates + -blockers :- in stable angina
2. THERAPY
Ca++ channel blockers + -blockers :-in stable
angina when the treatment with nitrates and -
blockers has failed.
3. Ca++ channel blockers + Nitrates :- in unstable
angina
4. All 3 together:- when the combinations of 2 drugs
has failed, where:-
1. Nitrates:- decrease Preload
2. Ca++ channel Blockers:- decrease Afterload
3. -blockers:- decrease heart rate and myocardial
contractions
Recommended Drug therapy
for Angina with other
medications
NEWER DRUGS
 RANOLAZINE (Ranexa™; CV Therapeutics, Inc.), a
drug that has been in development for 20 years. It is a
Sodium Channel Blocker.

 NICORANDIL, a potassium channel activator, and also

has a Nitrogen Donating Moeity.

 IVABRADINE, inhibits the If channel in the sinus node

and thereby causes bradycardia without any negative
inotropic effects.
THANK
YOU!!!!