ANGINA PECTORIS

 Angina pectoris is the result of myocardial ischemia

caused by an imbalance between myocardial blood
supply and oxygen demand
occurs when the Oxygen Supply to the Myocardium is
insufficient for its needs.
ANGINA-CORONARY OCCLUSION

CORONARY OCCLUSION
Classification

Stable angina
 = effort angina, = angina related to myocardial ischemia.
 Typical presentations :
chest discomfort and associated symptoms precipitated by
some activity (running, walking, etc.) with minimal or non-
existent symptoms at rest.
STABLE ANGINA
 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
 a form of acutely developing and rapidly reversible left
ventricular failure results which is relieved by taking
rest and reducing the myocardial workload.
Classification
Unstable angina
 Unstable angina (UA) (also "crescendo angina;" this is a
form of acute coronary syndrome) is defined as angina
pectoris that changes or worsens.
 It has at least 1 of these 3 features:
 it occurs at rest (or with minimal exertion), usually lasting
>10 min;
 it is severe and of new onset (i.e., within the prior 4–6
weeks); and/or
 it occurs with a crescendo pattern (i.e., distinctly more
severe, prolonged, or frequent than before).
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.
Classification
Microvascular angina
 = Syndrome X
 characterized by angina-like chest pain
 The cause of Microvascular Angina is unknown, but it
appears to be the result of poor function in the tiny
blood vessels of the heart, arms and legs.
 prognosis is excellent.
ANGINA: SYNDROME X
 Typical , exertional angina with positive exercise
stress test
 Anatomically normal coronary arteries
 Reduced capacity of vasodilation in
microvasculature
 Calcium channel blockers and Beta blockers are
effective.
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: SILENT ISCHEMIA
 Very Common

 More episodes of Silent than Painful angina in the

same patient.

 Difficult to diagnose

 Generally Exercise testing.

DIAGNOSIS
1. STRESS (EXERCISE) TEST.
2. ECG
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
 Alternatively the patient recieves an injection of a
radioisotope (generally Thallium) which makes the
heart visible to a special-linked camera
 90% accurate
 doesn’t identify the exactly where and how the
coronary arteries are blocked.
2. ECG
 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 CATHETERIZATION
 Shows the precise size and location of blockages
within the Coronary arteries
 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
 Lipid profile
 C-reactive protein and B-type natriuretic protein
 These tests are predictive of the moratality of heart
disease
TREATMENT
 3 Classes of drugs used according their mode of action

1. NITRATES
2. - ADRENOCEPTOR ANTAGONISTS
3. CALCIUM CHANNEL ANTAGONISTS
4. ANTIPLATELET DRUGS
NITRATES
 Prodrugs
 Sources of Nitric Oxide
 Eg:- Nitroglycerin,
Isosorbide Dinitrate
Isosorbide-5-Mononitrate
TOXICITY OF NITRATES
 Headache
 Increased mortality
 Recurrence of Myocardial Infraction
 Dizziness
 Flushing
 Rapid heart beat
 Restlessness
 Dry mouth
 Skin rash
 Nausea
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
-ADRENOCEPTOR ANTAGONOSTS

 Important in prophylaxis of angina and treating

unstable angina
 Decrease O2 consumption by the heart
 Effects on coronary vessels-not important
 Avoided in variant angina as they increase the chances
of spasm
PHARMACOLOGICAL ACTIONS
MECHANISM OF ACTION
COMPARITIVE TOXIC EFFECTS
 COMBINATION THERAPY
1. Nitrates + -blockers :- in stable angina
2. 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