presentation for drugs used to treat different types of angina pectoris : stable, unstable and vasospastic and the best for each type and side effects,

1. Antianginal drugs
Jomanah A. Hmood

3. What is angina pect oris?
"angina" means("strangling") , and the pectus means("chest")
thereforebecan translated as:
"astrangling feeling in thechest”
Anginapectoris:
isthechest discomfort that occurswhen
theheart isnot getting enough blood.

4. Angina is a symptom of myocardial
ischemia

5. This imbalance may result from:
Decrease supply
Spasm of vascular
smooth muscle
increase demand : exertion
Atherosclerosis in the coronary
artery

6. What the patient with angina
feels??
pain,
pressure,
fullness,
or squeezing
in the center of the chest

7. Somepatients(women, elderly, and diabetic) may have
different symptoms, such as:
 shortnessof breath
 A feeling of indigestion or heartburn
 nausea
 sweating
 dizziness
 fatigue
 Palpitations

8. which may be radiate to
neck
shoulder
jaw
arm

9. angina
stable unstable vasospastic

10. Stable angina
Called “ typical angina” ►►most common
Caused by
▼
The fixed obstruction of coronary artery
by atherosclerosis
▼
Blood supply ↕ when heart ↑ work

12. Stable angina
• Physical exertion
• Emotion
• Exposure to very cold temperatures
1. ↑work load
2. Coronary vasoconstriction
3. Sympatheticoadrenal hormones
• Heavy meals
• Smoking.

13. Stable angina
 Occurs when the heart must
work harder.
 Usually lasts a short time (5
minutes or less).
 Is relieved by rest or medicine.

14. Why is called “stable”angina?
1. Frequency of chest pain.
2. Amount of effort needed to trigger it .
↓↓
Don’t change from day to day or week to
week .

15. Unstable angina
Between stable | MI
Characterized by:
1. ↑ frequency, duration and intensity .
2. Often occurs at rest, while sleeping at
night, or with little physical exertion.
3. lasts more than 20(as long as 30
minutes).
4. Not relieved by rest .

17. atherosclerosis
Arterial wall thickening
Endothelium damage → cholesterol crosses
→ white blood cells stream in to digest
the LDL cholesterol → formation of plaque
• Which may be grow until block the artery
• Or rupture and allowing blood to clot
inside an artery.

19. Prinzmetal “ variant“
 It is coronary vasospasm
Uncommon “ 2% of cases of angina”
Occurs at rest “during the night or early morning
hours”
response to medication “coronary vasospasm”.

23. What diagnostic tests might pt has?
•Blood tests
•Electrocardiogram (EKG or ECG(
•Exercise stress test
•Cardiac catheterization
•Coronary angiogram

24. angina can be prevented:

25. Antianginal drugs action:

26. Variant angina

27. Organic nitrates

28. Organic nitrates
Are simple nitric and nitrous acid esters of
glycerol.
Used for all types of angina

29. Examples:
1. Isosorbide dinitrate →solid
2. Isosorbide mononitrates→solid
3. Nitroglycerin →volatile → therefore it
must be kept in tightly closed glass
containers

30. pharmacokinetics
• Nitroglycerin: rapidly disappears from the
blood
• half-life: only a few minutes
• Excretion: largely by extrahepatic
mechanisms.
• Isosorbide dinitrate, in contrast, must first be
converted in the liver to active mononitrates.
• half-life : 4 to 6 hours

32. Mechanism of action
•Nitrates work by dilating both arteries
and veins, both in the heart and
elsewhere.
1. Inhibit coronary spasm → variant angina
stable angina
1. Relax veins → ↓preload

36. adverse effects
1. Headache : 30-60% of patients.
2. Postural hypertension
3. Facial flushing high doses
4. Tachycardia

37. Tolerance
•"Decrease in the effect of a drug
•when administered in a long-acting form“
Is dose-dependent
•Disappears in 24 h. after stopping the drug
•The mechanisms of nitrate tolerance are therefore likely to be multifactorial,
involving vascular biochemical changes, physiologic compensation, and
possibly receptor regulation.
•result from vascular depletion of critical sulfhydryl groups, which are
necessary to bring about vasorelaxation from nitrates.
•While this mechanism of nitrate tolerance probably operates when isolated
blood vessels are exposed to high concentrations of nitrate in vitro
•Use of angiotensin converting enzyme inhibitors and diuretics in conjunction
with nitrates may alleviate the development of tolerance

38. B- blockers

39. B- blockers
• Lowering the rate and force of contractility
• Suppress the activation of heart by blocking B1
receptors
Heart work↓
Oxygen demand↓

40. B- blockers
They reduce oxygen demand both During
exertion and at rest
beta blockers are effective in improving the
amount of exercise that can be performed
without developing angina.
Vasospastic angina

42. B- blockers
• cardioselective
• Atenolol (Tenormin)
• Metoprolol (Lopressor, Toprol XL)
• Non selective :
• Propanolol
• Agents with intrinsic sympathomimetic
activity should be avoided.

43. side effects
 Bradycardia
 breathing difficulties in people who have
asthma or chronic lung disease.
 fatigue
 depression
 and erectile dysfunction.

44. side effects
• By Using cardioselective beta blockers ,
many of these side effects can be
avoided, because these have relatively
little effect on the blood vessels, lungs,
and central nervous system.
• But all B-blockers are non selective in high
doses.

45. ß-ADRENERGIC BLOCKERS
CONTRAINDICATIONS
•Hypotension: BP < 100 mmHg
•Bradycardia: HR < 50 bpm
•Chronic bronchitis, ASTHMA
•Severe chronic renal insufficiency

46. Calcium channel blockers

47. calcium channels
• Two voltage-dependent calcium channels:
• L-type calcium channel ('L' for Long-lasting)
• and T-type calcium channels ('T' for Transient)
• L-type channels are important in sustaining an
action potential
• while T-type channels are important
ininitiating them.
• L-type channels respond to higher membrane
potentials, open more slowly, and remain open
longer than T-type channels.

50. Calcium channel blockers
• Calcium is essential for muscular
contraction
• Ca influx ↑↑ in ischemia because :
Hypoxia →membrane depolarization ↑
→ ATP consuming enzymes →
↓energy

52. Calcium channel blockers
• Therefore, Calcium channel blockers
protect tissues by inhibiting the entrance
of Ca.
• It is used to treatment of variant angina.
• They are effective in treating hypertension
in patients with angina and diabetes.
• They don’t dilate the veins.

55. Calcium channel blockers
• High doses of short-acting calcium
channel blockers should be avoided
because of → increased risk of MI due to:
• excessive vasodilation
• and marked reflex cardiac stimulation.

57. Nifedipine
• is a dihydropyridine calcium channel
blocker.
• Has minimal effect on cardiac conduction
and heart rate.
• Administrated orally
• It undergoes hepatic metabolism .
• Eliminated in both urine and feces

58. Nifedipine
• Its main uses :
 antianginal (especially in Prinzmetal's
angina)
 antihypertensive
 Raynaud's phenomenon
 painful spasms of the esophagus such as
in cancer and tetanus patients

59. Side effects
headache
Flushing
hypotension
severe constipation and cramps.
Peripheral edema
Reflex tachycardia in sever peripheral
vasodilation →No sympathetic
antagonistic action

60. verapamil

61. Verapamil
 is an L-type calcium channel blocker of
the phenylalkylamine class.
 action:
 decrease impulse conduction through
the AV node
 dilate the blood vessel

62. Verapamil
It has been used in the treatment of :
hypertension
angina pectoris
cardiac arrhythmia
cluster headaches.
Verapamil is also used intra-arterially to
treat cerebral vasospasm.

63. Pharmacokinetic
Given orally
 absorption : 90–100% of Verapamil
 high first-pass metabolism , bioavailability(10–
35%)
 As its metabolites, 70% is excreted in the urine
and 16% in feces; 3–4% is excreted unchanged
in urine.
 Half-life : 5–12 hours
 not cleared by hemodialysis.
excreted in human milk

64. Side effects
• headaches,
• facial flushing,
• dizziness,
• swelling,
• increased urination,
• Fatigue
• and nausea

65. diltiazem
Diltiazem is a potent vasodilator → increasing
blood flow
strong depressor of A-V node conduction →
decreasing the heart rate
Its pharmacological activity is somewhat similar
to verapamil.
 reduces peripheral resistance and afterload.
Because of its negative inotropic effect,
diltiazem causes a modest decrease in heart
muscle contractility and reduces myocardium
oxygen consumption.

66. Indications
Stable angina (exercise-induced) – diltiazem
increases coronary blood flow and decreases
myocardial oxygen consumption, secondary to
decreased peripheral resistance, heart rate, and
contractility.
Variant angina coronary dilation.
supraventricular tachycardias
Atrial fibrillation
 hypertension

67. Contraindications
 In congestive heart failure, patients with reduced
ventricular function may not be able to counteract the
inotropic and chronotropic effects of diltiazem, the result
being an even higher compromise of function.
 With SA node or AV conduction disturbances : the use of
diltiazem should be avoided in patients with SA or AV
nodal abnormalities, because of its negative chronotropic
and dromotropic effects.
 Low blood pressure patients, with systolic blood
pressures below 90 mm Hg, should not be treated with
diltiazem.