By: group c

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.

 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 Pectoris

1. Stable Angina 2. Unstable Angina 3. Variant Angina (Prinzmetals 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 (PRINZMETALS 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

Patients with exertional dyspnea rather than

exertional chest pain

Caused by exercise induced left ventricular dysfunction

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.

ANGINA: SILENT ISCHEMIA

Very Common
More episodes of Silent than Painful angina in the

same patient.
Difficult to diagnose Gnerally Exercise testing.

DIAGNOSIS
1.
2. 3. 4. 5. 6.

STRESS (EXERCISE) TEST. ECG (ELECTROCARDIOGRAPHY) CHEST X-RAY CARDIAC ANGIOGRAPHY/ CARDIAC CATHETERIZATION ERGONOVINE TEST BLOOD TEST (BIO-MARKERS)

1. EXERCISE TEST/STRESS TEST

Used to measure hearts 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 doesnt 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 Doesnt 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 drugErgonovine 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

TREATMENT
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 relieving vasospastic angina, O2 supply (Nitrates)

NITRATES
Prodrugs Sources of Nitric Oxide Eg:- Nitroglycerin,

Isosorbide Dinitrate Isosorbide-5-Mononitrate

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

CALCIUM CHANNEL ANTAGONISTS

Disrupt Ca++ through Ca++ channels
-ve ionotrpic effect 2 types:-

Dihydropyridine (amlodipine, nifedipine, nicardipine) 2. Non-Dihydropyridine

1.
1. 2. 3.

Phenylalkylamine (verapamil, gallopamil) Benzodiazapenes (diltiazem) Non-selective (bepridil, mibefradil)

-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 Eg:

Atenolol Propranolol

ANTICOAGULANTS
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

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.
1. 2. 3.

COMBINATION THERAPY

Nitrates:- decrease Preload Ca++ channel Blockers:- decrease Afterload -blockers:- decrease heart rate and myocardial contractions

THANK YOU!!!!