1

BY, I NDU NAT H S

M PHARM PART 1

PHARM AC Y PRACT I CE

2

Ischaemic heart disease

Angina pectoris

3

IHD

ANGINA PECTORIS

DEFINITION

CLASSIFICATION

EPIDEMIOLOGY AND

PREVALENCE

ETIOLOGY AND RISK FACTORS

PATHOPHYSIOLOGY

CLINICAL MANIFESTATI

ON

DIAGNOSIS

TREATMENT

CONCLUSION

REFERENCES

CONTENTS

ISCHAEMIC HEART

DISEASE4

Ischaemic heart disease is a condition in which, there is an inadequate

supply of blood and oxygen to a portion of the

myocardium.

5

Common cause of myocardial ischaemia is atherosclerotic

disease of epicardial coronary artery.

That cause a regional reduction in myocardial blood

flow and inadequate perfusion of myocardium supplied by involved

coronary artery.Also known as coronary artery

disease.Chest pain is the cardinal

symptom of IHD due to CAD.

6

MAJOR RISK FACTORS

DYSLIPEDAEMIA

SMOKING

Sedentary life style

Hyper tension

Glycemic control in

DM

7

8

Risk factor identification and modification are

important for individualized

patients with known or suspected IHD.

9

Definition

A clinical syndrome due to

myocardial ischaemia characterized

by precordial discomfort or

pressure, typically precipitated by

exertion and relieved by rest or

sub-lingual nitroglycerine.

Tightness or squeezing sensation. The pain radiate to

the neck, chin, or down the left arm to the elbow. Lasts 2-3

min .Crescendo -decrescendo nature.

Literally means “strangled chest “, a severe pain that

usually accompanies with

MI.

10

11

12

classification

class

New York heart association functional

classification

Specific activity scale

I Symptoms occurs with unusual activity.Minimal or no functional impairment.

Patients can perform to completion any activity involving or equal to 7 metabolic equivalents

II

Symptoms occurs with prolonged or slightly more than usual activity.Mild functional impairment.

Patients can perform to completion any activity involving or equal to 5 metabolic equivalents but cannot perform to completion any activity involving or equal to 7 metabolic

13

III

Symptoms occurs with usual activities of daily living.Moderate functional impairment.

Patients can perform to completion any activity involving or equal to 2metabolic equivalents but cannot perform to completion any activity involving or equal to 5 metabolic equivalents.

IV

Symptoms occurs at rest.Severe functional impairment.

Patients can perform to completion any activity involving or equal to 2metabolic equivalents .

14

Some other forms of angina…15

Unstable angina

Characterized by a progressive increase in anginal symptoms, new onset of rest (angina decubitus) or nocturnal angina, or onset of prolonged angina.

It is precipitated by an acute increase in coronary obstruction due to rupture of the fibrous plaque covering an atheroma with consequent platelet adhesion.

Pain is more when compared to stable angina.

16

Variant angina

• Angina pectoris i.e. usually secondary to large vessel spasm.

• Characterized by discomfort at rest and by ST segment elevation during the attack.

• Have significant obstruction of at least one major coronary artery.

Also known as prinzmetal’s

angina.

17

Epidemiology

18

Epidemiology and prevalence

Leading cause of death , disability and incurs world wide.

Major cause of death in both developed and developing countries.

Greater economic costs than any other illness in the developed countries. Most common in us 13 million.

6 million angina and 7 million MI.

In USA and Europe more among low income groups than high income group.

Prevalence is more in low and middle income countries.

Predominant in male and increase with age.

Annual incidence rate of angina is 1.5% depending on the age, gender and risk factor profile.

Angina is more in women than in men.

Female to male ratio is 1.7:1.

Prevalence of 4.6 million in women and 3.3 million in men.

19

High rate of STEMI (61%) than high income countries (15-25%).

Highest burden of acute coronary syndrome in the world.

Common risk factors include smoking (40%), high BP (38%), and diabetes (30%) .

The mean age the patient is 58 yrs.

53 % of lower middle class and 20% were from poor middle class.

In India 98 % receiving anti platelet drugs.

51-61% receiving ACE inhibitors or ARB.

57-54 % receiving lipid lowering therapy .

20

Mortality rate per 100,000, 382 for men and 128 for women.

60 % death in men and 40 % death in women . It occur before the age of

68 yrs.

CAD results in high economic burden.

Prevalence of heart disease in rural Kerala is 7%.

21

22

23

24

Etiology and risk factors

When cardiac workload and MVO2 demand exceed, the ability of coronary arteries

to supply an adequate amount of oxygenated blood

decrease.

Atherosclerosis ,

Coronary artery spasm, rarely coronary artery

embolism.

Increased age, male sex, family history of CAD,

smoking, diabetes mellitus, HT.

Soft factors include stress, anxious personality, obesity,

alcohol consumption.

causes

25

26

Prime determinants of myocardial

oxygen demand.

Heart rate, Contractility, and Wall

stress .

Increase in HR contractility,

ventricular vol or pressure will increase

MVO2.upset the demand results in

angina .

Coronary blood flow.

Depends on a pressure gradient b/w aorta and

intra myocardial coronary arteriole.

Reduction of the coronary gradient will reduce coronary flow

and result angina.

pathophysiology

27

Severe pulmonary HT.

Coronary obstructive lesion.

High intra vascular left ventricular pressure.

Tachycardia.

28

29

Clinical manifestation

Angina presents as substernal, retrosternal, or transsternal discomfort.

Pain radiates to the left jaw, shoulder, and arm.

Discomfort is a dull pain, strangling or constricting

sensation.

Patient describes the discomfort as pressure,

heaviness, fullness, squeezing, burning,

aching, gas or anxiety.

Severity of discomfort ranges from slight to

disabling pain. It have a gradual onset and lasts

from0.5 to 30 mins.

Provocation of anginal episodes include physical

exertion, emotion, exposure to cold, heat and

humidity, meals.

30

31

Diagnosis

Diagnosis

Electrocardiogra

m

Cardiac imaging

Cardiac catheteri

zation

Echocardiograph

y

Exercise tolerance

testing

32

Electrocardiogram

33

Exercise tolerance testing

ETT

• Test of choice for evaluating most patients of intermediate risk for CAD.

BRUCE PROTOC

OL

• Consist of 3-min stages of increasing treadmill speed and incline. BP, HR, and ECG are monitored throughout the study and the recovery period.

observations

• study is considered positive if,

• New ST segment depression of 1 mm in multiple leads

• Hypotensive response to exercise

• Sustained ventricular arrhythmias are precipitated by exercise.

34

35

Cardiac imaging

36

Echo cardiograph

37

Coronary angiography

38

39

MOA : Indirectly via reduction in the MVO2 secondary to venodilation and arterial- arteriolar dilation, leading to a reduction in wall stress from reduced ventricular vol and pressure.

• Dosage SL : 0.4 mg every 5 min, Topical: 0.5-2 iv : 10-200 mcg/min .

NTG is contraindicated in sildenafil due to severe risk of hypotension .

• Nitrates are contraindicated in patients with severe aortic stenosis and hypertrophic obstructive cardiomyopathy.

Nitrates

Pharmacological TREATMENT

40

Dose

2-4 mg

IV.

Patient whose symptoms are not relieved after three serial

sublingual nitroglycerine tablets or whose symptoms recur with adequate anti-

ischemic therapy.

Contraindicated in hypotension, respiratory depression, confusion, obtundation .

Morphine

41

MOA of beta blocker is it decrease HR, contractility, and BP reduce MVO2 and oxygen demand in patients with effort induced angina.

Dose :

Metoprolol : 5 mg IV or 25 mg PO qid.

Atenolol : 50-200 mg PO daily.

Propranolol : 20-80 mg PO bid.

Beta blockers reduce s the risk of recurrent ischemia, myocardial infarction and mortality in patients with UA/NSTEMI.

BETA BLOCKERS

42

MOA : Direct actions include vasodilation of systemic arterioles and coronary arteries, leading to a reduction of arterial pressure and coronary vascular resistance and myocardial contractility.

Dose : amlodipine 5-10 mg daily.

Verampamil 80-160 mg tid.

Nifidipine 30 -180 mg daily.

Short acting nifidipine should use along with beta blocker otherwise risk of myocardial infarction and death.

Verampamil should be avoided in patients with severe LV dysfunction, pulmonary congestion, or AV block.

Calcium channel blockers

43

It reduces the risk for formations of

a clot in the narrowed artery by interrupting

the clotting process

Once daily therapy treatment

with low dose aspirin,75-325mg is recommended.

Aspirin

44

Non pharmacological therapy

MODIFICATI

ON of risk

factors

CABG

pci

45

46

47

48

Diet A diet low in saturated and trans unsaturated fatty acids and a

caloric intake to achieve optimal body weight is essential in the management of chronic IHD.

DyslipidaemiaFor long term relief from angina treatment of dyslipidaemia is essential. Control of lipids can be achieved by the combination

of low fatty diet, exercise and weight loss.

obesityThe treatment of obesity and accompanying risk factors is an

important component of management plan.

Modification of risk factors

49

Diabetes mellitusIt accelerates coronary and peripheral atherosclerosis, it frequently

associated with dyslipidemia and increase in the risk of angina. Control of dyslipidemia and HT is essential for diabetic patient.

Smoking Cigarette smoking accelerates coronary atherosclerosis in both sexes

and at all ages. So patient must be strongly advised to give up smoking completely.

Hypertension

Long term, effective treatment of HT can decrease the occurrence of adverse coronary events.

50

51

Newer Therapies

52

53

54

55

CAD can be managed by

pharmacological and non

pharmacological treatment.

Risk factor identification

and modification.

Chest pain is cardinal

symptom.

IHD is caused due to coronary atherosclerosis.

Conclusion

56

57

Davidson’s Principle and Practice of Medicine by Nicholas.N.Boon, Niki. R.colledge, Brain. R. Walker Page No: 424 – 434,20 th edition.

Text book of therapeutics- Drug and Disease Management, by Eric. T. Herfintal, Dick .R.Gourley; page no : 917 – 934,7th edition.

Pharmacotherapy- A pathophysiological approach, by Joseph. T. Dipiro, Robert. L. Talbert, Gary. C. Yee, Gary. R. Matzke , Barbara. G. Wells, L. Michael Posey; Page No: 261 – 287,6 th edition.

Harrison’s Principle of Internal Medicine ,Vol 1 by Longo, Fauci Kasper, Hasper, Jamesoli Page No: 1514 – 1531,18 th edition.

Oxford text book of medicine , vol 3 , David . A . Warrell , Timothy . M . Cox , John . Difirth. Page no : 2318 -2331,4th

editon.

References