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1
BY, INDU NATH S
M PHARM PART 1
PHARMACY PRACTICE
2
Ischaemic heart
disease
Angina pectoris
3
IHD
ANGINA
PECTORIS
DEFINITION
CLASSIFICATI
ON
EPIDEMIOL
OGY AND
PREVALENC
E
ETIOLOGY
AND RISK
FACTORS
PATHOPHYSIOL
OGY
CLINICAL
MANIFESTATI
ON
DIAGNOSIS
TREATMENT
CONCLUSI
ON
REFERENC
ES
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
DYSLIPED
AEMIA
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
13
III
Symptoms occurs
with usual
activities of daily
living.
Moderate
functional
impairment.
Patients can
perform to
completion any
activity involving
 or equal to 2
metabolic
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 2
metabolic
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
pulmonar
y HT.
Coronary
obstructiv
e lesion.
High intra
vascular
left
ventricula
r
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
Electroc
ardiogra
m
Cardiac
imaging
Cardiac
catheteri
zation
Echocar
diograph
y
Exercise
tolerance
testing
32
Electrocardiogra
m
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.
observa
tions
• 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.
Dyslipidaemia
For 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.
obesity
The treatment of obesity and accompanying risk factors is an
important component of management plan.
Modification of risk factors
49
Diabetes mellitus
It 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

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Angina pectoris

  • 1. 1
  • 2. BY, INDU NATH S M PHARM PART 1 PHARMACY PRACTICE 2 Ischaemic heart disease Angina pectoris
  • 4. 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. 5
  • 6. 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
  • 8. 8 Risk factor identification and modification are important for individualized patients with known or suspected IHD.
  • 9. 9
  • 10. 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. 11
  • 12. 12
  • 13. 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 13
  • 14. III Symptoms occurs with usual activities of daily living. Moderate functional impairment. Patients can perform to completion any activity involving  or equal to 2 metabolic 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 2 metabolic equivalents . 14
  • 15. 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. 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.
  • 18. 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. 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. 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. 21
  • 22. 22
  • 23. 23
  • 24. 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. 25
  • 26. 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. 27 Severe pulmonar y HT. Coronary obstructiv e lesion. High intra vascular left ventricula r pressure. Tachycardia.
  • 28. 28
  • 29. 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. 30
  • 33. 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. observa tions • 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. 34
  • 38. 38
  • 39. 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. 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. 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. 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. 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
  • 45. 45
  • 46. 46
  • 47. 47
  • 48. 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. Dyslipidaemia For 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. obesity The treatment of obesity and accompanying risk factors is an important component of management plan. Modification of risk factors
  • 49. 49 Diabetes mellitus It 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. 50
  • 52. 52
  • 53. 53
  • 54. 54
  • 55. 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. 56
  • 57. 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