ANGINA PECTORIS

1. MAIN EXIT NEXT
Definition
Types of Angina
Management of Angina
Antianginal drugs

2. Transient MyocardialTransient Myocardial
ischemiaischemia
Severe Chest painSevere Chest pain
Myocardial Blood Flow
Myocardial O2 Demands
Angina Pectoris
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3. Chest pain caused by transient
myocardial ischemia due to an
imbalance between myocardial
oxygen supply and demand.
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4. Types of AnginaTypes of Angina
1. Stable Angina.
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2. Unstable Angina.
3. Variant Angina.

5. HOME
1.1. Stable Angina .
Retrosternal painRetrosternal pain
Radiating to left arm &Radiating to left arm &
shouldershoulder
The commonest cause isThe commonest cause is ADVANCEDADVANCED
ATHEROSCELEROSISATHEROSCELEROSIS
Lasting less than 15 min.Lasting less than 15 min.
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6. ExertionExertion
EmotionEmotion
Heavy mealsHeavy meals
Exposure to coldExposure to cold
weatherweather
Predisposing factors Relieving
factors
RestRest
sublingual
nitroglycerin
Stable Angina
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7. Exercise ECG showing typical severe down slopingExercise ECG showing typical severe down sloping STST
segmentsegment ::
Anginal pain is often associated with DepressionAnginal pain is often associated with Depression
ofof STST segmentsegment
Standing 1 min. 3 min. 7 min. 9 min.
Stable Angina
In between attacksIn between attacks :: ECG is entirelyECG is entirely NORMALNORMAL
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8. 2.2. Unstable Angina .
Increased frequencyIncreased frequency,, severity or durationseverity or duration
of pain in a patient of Stable Anginaof pain in a patient of Stable Angina
Myocardial infarction may occur in 10-20% of patients.Myocardial infarction may occur in 10-20% of patients.
N.B.N.B.
Pain occurs with less exertionPain occurs with less exertion
or at restor at rest
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9. The underlying cause isThe underlying cause is
•Atheroscelerotic changesAtheroscelerotic changes
Fissuring of atheroscelerotic plaquesFissuring of atheroscelerotic plaques
Platelet aggregationPlatelet aggregation
ThrombosisThrombosis
Coronary artery spasmCoronary artery spasm
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10. 3.3. Variant Angina .
(Prinzmetal)
Chest pain at rest due toChest pain at rest due to
coronary artery spasmcoronary artery spasm
ECGECG
changeschanges::
Acute elevation ofAcute elevation of STST
segmentsegment
The baseline ECG
With chest pain ,
marked ST segment
elevation
Return of the ST segment to
the baseline after
nitroglycerin administration
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11. Management of Angina
Management of Stable Angina
Management of UnstableManagement of Unstable AnginaAngina
Management of Variant Angina
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12. Management of Stable
Angina
1-1- General measures.General measures.
2-2- Drug Treatment.Drug Treatment.
3-3- Coronary arteryCoronary artery
revascularization.revascularization.
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13. Stop smokingStop smoking Reduce weightReduce weight
Treat Hypertension ,Treat Hypertension ,
HypercholestrolimiaHypercholestrolimia
and Diabetesand Diabetes
AVOIDAVOID
SevereSevere
exertionexertion
Heavy mealHeavy meal EmotionsEmotions Cold WeatherCold Weather
General measures
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•Graduated exercise may open new
collaterals

14. a.a. For an acute attackFor an acute attack
b.b. For immediate pre-exertionalFor immediate pre-exertional
prophylaxisprophylaxis
c.c. For long-term prophylaxisFor long-term prophylaxis
d.d. Antiplatelet therapy.Antiplatelet therapy.
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15. Treatment of an acute attack of angina
SublingualSublingual nitroglycerinnitroglycerin (0.5 mg ) or isosorbide(0.5 mg ) or isosorbide
dinitrate (5 mg )dinitrate (5 mg ) or
Oral sprayOral spray nitroglycerinnitroglycerin (0.4 mg/metered(0.4 mg/metered
dose),dose), isosorbide dinitrateisosorbide dinitrate(1.25 mg/metered(1.25 mg/metered
dose)dose)
Relief within 1-3 min. Persistence of pain
Repeat nitroglycerin at 5 min.Repeat nitroglycerin at 5 min.
interval (3 tab. max.)interval (3 tab. max.)
Relief not relieved
InfarctionHOSPITALIZATION
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16. Immediate pre-exertional prophylaxis of AnginaImmediate pre-exertional prophylaxis of Angina
Sublingual nitroglycerin (0.5 mg) or isorbide
dinitrate (5 mg) should be taken 5 min.
before effort.
For Long term prophylaxis:For Long term prophylaxis:
Long acting nitrates, Ca++
channel blockers,
β-blockers or combinations of these drugs.
Antiplatelet therapy:Antiplatelet therapy:
Aspirin in small dose (75-150 mg daily orally)Aspirin in small dose (75-150 mg daily orally)
or Dipyridamole (75 mg t.d.s orally)or Dipyridamole (75 mg t.d.s orally)
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17. Coronary artery bypass graftingCoronary artery bypass grafting
(CABG)(CABG)
Percutaneous TransluminalPercutaneous Transluminal
coronary Angioplasty (PTCA)coronary Angioplasty (PTCA)
For patients not responding toFor patients not responding to
adequate medical therapyadequate medical therapy
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18. Management of Unstable
Angina
NitrateNitrate
++
ββ-blocker-blocker
++
Aspirin (low dose) and/orAspirin (low dose) and/or
Heparin orHeparin or
Thrombolytic (stryptokinase)Thrombolytic (stryptokinase)
to minimize risk of infarctionto minimize risk of infarction
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19. Management of Variant
Angina
Nitrates andNitrates and/or/or Ca++Ca++
Channel blockersChannel blockers
For the acute attack &For the acute attack &
prophylaxisprophylaxis
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20. What are the antianginal drugs?
Organic nitrates.
Calcium channel blockers.
β- adrenoceptor blockers.
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21. NITRATESNITRATES
VeinsVeins
ArteriesArteries
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Relaxation of smoothRelaxation of smooth
muscles Dilatationmuscles Dilatation

22. Cellular Mechanism of Vasodilatation
NitratesNitrates Formation ofFormation of
Nitric oxide (NO)Nitric oxide (NO)
Activation ofActivation of
Guanylate cyclaseGuanylate cyclase
Synthesis ofSynthesis of
cyclic GMPcyclic GMP
Relaxation of VascularRelaxation of Vascular
smooth musclessmooth muscles
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N.B. (-SH) groups are required
for formation of NO.

23. Effect of Nitrates :Effect of Nitrates :
On Stable Angina :On Stable Angina :
Venodilatation
Arteriolar
dilatation
PreloadPreload AfterloadAfterload
MyocardialMyocardial
Oxygen demandOxygen demand
2- Redistribution of coronary flow towards
subendocardium
3- Dilatation of coronary collateral vessels.
1-1-

24. On Variant Angina :On Variant Angina :
Relax smooth muscles of the
epicardial coronaries → relieve
coronary artery spasm
On Unstable Angina :On Unstable Angina :
Dilatation of epicardial coronary
arteries + reducing O2 demands
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26. Preparations :
Short actingShort acting
For acute attacksFor acute attacks
Long actingLong acting
For antianginal prophylaxisFor antianginal prophylaxis
NitroglycerinNitroglycerin
(sublingual, buccal(sublingual, buccal
spray)spray)
IsosorbideIsosorbide
dinitrate(sublingual,dinitrate(sublingual,
buccal spray)buccal spray)
NitroglycerinNitroglycerin
oral SR (6.25-12mg) 2-4oral SR (6.25-12mg) 2-4
times/daytimes/day
- 2% ointment (1-1.5- 2% ointment (1-1.5
inch/4hrs)inch/4hrs)
- patches (1 patch=25mg)/day- patches (1 patch=25mg)/day
Isosorbide dinitrate (oral) 10-Isosorbide dinitrate (oral) 10-
40mg t.d.s.40mg t.d.s.
Isosorbide mononitrate (oral)Isosorbide mononitrate (oral)
20mg/12 hrs.20mg/12 hrs.
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27. Duration of Action of Various Preparations of
Organic Nitrates
Preparation
Duration of
action
" Short-acting"
1-Nitroglycerin
2- Isosorbide dinitrate
a) Sublingual
b) Spray
a) Sublingual
b) Spray
10-30 min
10-30 min
Up to 60 min.
1.5 hours
" Long-acting"
1-Nitroglycerin
2- Isosorbide dinitrate
3-Isosorbide mononitrate
a) Oral; sustained release
b) Ointment
c) Transdermal patches
Oral
Oral
4-8 hours
3-6 hours
8-12 hours
4-6 hours
6-10 hours

28. Adverse Reactions :Adverse Reactions :
1- Postural Hypotension &1- Postural Hypotension &
SyncopeSyncope
2- Tachycardia2- Tachycardia
5- Throbbing Headache5- Throbbing Headache
4- Facial Flushing4- Facial Flushing
3- Drug Rash3- Drug Rash
6- Prolonged high dose6- Prolonged high dose
MethaemoglobinaemiaMethaemoglobinaemia
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29. How does it occur?
The main limitation of chronic nitrate therapy is
TOLERANCE
It develops as SH groups in vessel wall become oxidized by
constant exposure to nitrates, this prevents the production of
NO & hence stimulation of Guanylate cyclase which is
believed to be fundamental to smooth muscle relaxation
produced by the drugs.
Tolerance to the antianginal effect occurs as a result
of chronic administration
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“NITRATE FREE INTERVAL” of 8-10 hrs reduces or prevents
development of nitrate tolerance.e.g. isosorbide dinitrate is given
at 7am, noon and 5pm; trnsdermal patches should be used for
about 12 hrs daily

30. What are nitrosamines & what is their medical
importance ?
What is the effect of nitroglycerin on platelet
aggregation ?
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These are small molecules formed from the combination of
nitrates and nitrites with amines.
They are also found in tobacco and cigarette smoke. Some of
them may cause cancer in humans, but there is no evidence
that the small doses of nitrates used in treatment of angina
result in significant body levels of nitrosamines.
It decreases platelet aggregation.

31. β-blockers are effective in STABLE & UNSTABLE
angina
In contrast they are not useful for
vasospastic angina (Variant) {Prinzmetal}&
may worsen the condition. This deleterious
effect is likely due to an increase in coronary
resistance caused by the unopposed effects of
catecholamines acting at α-adrenoceptors.

32. The effectiveness ofThe effectiveness of ββ-adrenoceptor blockers in the-adrenoceptor blockers in the
treatment of exertional angina is attributable to a falltreatment of exertional angina is attributable to a fall
in myocardial Oin myocardial O22 requirement at rest & duringrequirement at rest & during
exertion due to :exertion due to :
1- A -ve chronotropic effect (particularly during1- A -ve chronotropic effect (particularly during
exercise).exercise).
2- A -ve inotropic effect.2- A -ve inotropic effect.
3- A reduction in arterial blood pressure (particularly3- A reduction in arterial blood pressure (particularly
systolic pressure) during exercise.systolic pressure) during exercise.
Mechanism of antianginal action:Mechanism of antianginal action:
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33. 33
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However the net effect of β-blockers is to ↓
myocardial O2 requirement particularly during
exercise; their potentially deleterious effects
can be balanced by concomitant use of nitrates
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Rate & contractility
Undesirable effects of β-blockers in treatment of angina:
Systolic ejection period & left
ventricular end diastolic vol.
Myocardial O2 requirements

34. Dosage and Route of Administration
Drug Route Dosage
Propranolol Oral 30-360 mg/day in 2-4 divided
doses
Nadolol Oral 40-80 mg ONCE daily
Atenolol Oral 50-100 mg ONCE daily
Metoprolol Oral 50-100 mg TWICE daily

35. Adverse ReactionsAdverse Reactions ::
CHFCHF A-V blockA-V block BronchospasmBronchospasm
ColdCold
extremitiesextremities WorseningWorsening
symptoms of PVDsymptoms of PVD
HypotensionHypotension
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36. Fatigue &Fatigue &
weaknessweakness
Mask signs ofMask signs of
HypoglycemiaHypoglycemia
Nightmares , Hallucinations ,Nightmares , Hallucinations ,
Depression.Depression.
Plasma Triglycerides & HDLPlasma Triglycerides & HDL
CholesterolCholesterol Discontinuation afterDiscontinuation after
long ttt exacerbateslong ttt exacerbates
AnginaAngina
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Adverse ReactionsAdverse Reactions ::

37. CHFCHF A-V blockA-V block
PeripheralPeripheral
VascularVascular
diseasedisease
HypotensionHypotension
Contraindications :Contraindications :
BronchialBronchial
asthmaasthma
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38. Verapamil (80-160 mg) /8 hr(80-160 mg) /8 hr
Diltiazem (60-120 mg) /8 hr(60-120 mg) /8 hr
Dihydropyridine group
Nifedipine (10-40mg) /8 hr
Amlodipine 5mg/day
Used in treatment of all types of angina.
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39. BlockBlock
Voltage -dependent calciumVoltage -dependent calcium
channels (L-type) in cardiac andchannels (L-type) in cardiac and
smooth muscles.smooth muscles.
CC
AA
LL
CC
II
UU
MM

40. Mechanism of anti-anginal action :Mechanism of anti-anginal action :
1 - Coronary artery dilatation and relief
of coronary spasm (variant angina)
•(Verapamil & Diltiazem)
•Decrease HR.
•Decrease contractility
•Decrease AV conductivity
•Arteriolar
dilatation
Vascular
resistance
Afterload
2 -Decrease myocardial O2 demand due to:

41. Dosage and Route of Administration
Drug Route Dosage
Verapamil Oral 80-160 mg every 8 hours
Nifedipine Oral 10-40 mg every 8 hours
Diltiazem Oral 60-120 mg every 8 hours

42. Adverse reactions :Adverse reactions :
DizzinessDizziness
AnkleAnkle
edemaedema
HypotensionHypotensionHeadacheHeadache
FlushingFlushing
ConstipationConstipation
A-V block & HFA-V block & HF onlyonly
with Verapamil &with Verapamil &
DiltiazemDiltiazem
ReflexReflex
TachycardiaTachycardia
with Nifedipinewith Nifedipine

43. 3 - Bradycardia.
Contraindications ofContraindications of
Verapamil & Diltiazem:Verapamil & Diltiazem:
1 - HF
2 - Sinus or A-V node
disease.

44. β-blocker + Long
acting Nitrate
β-blocker +
Nifedipine
Verapamil or
Diltiazem +
Nitrate
β-blocker +
Nitrate +
Nifedipine
??
??
??
??

45. β-blockers block reflex tachycardia
produced by nitrates
•Nitrates attenuate the increased left
ventricular end-diastolic volume associated
with β-blockers

46. β-blockers decrease reflex
tachycardia produced by nifedepine.

47. •Verapamil or Diltiazem decrease
tachycardia produced by nitrates.

48. •In patients with stable angina not
controlled by two types of
antianginal drugs the use of three
agents may provide improvement.