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ASSIGNMENT REPORT
ON
ANGINA PECTORIS
Guided by
Prof Mrs Anjali M. Wankhade
Submitted by
Miss Shruti R.Gautam
VIDYABHARTI COLLEGE OF PHARMACY
CAMP ROAD AMRAVATI 444602
Defination
 Angina, also known as angina pectoris, is chest pain
or pressure, usually due to not enough blood flow to
the heart muscle.
 Angina is usually due to obstruction or spasm of the
coronary arteries. Other causes include anemia,
abnormal heart rhythms and heart failure.
Classification
 Classical angina
 Variant angina
 Unstable angina
Stable Angina
 Stable angina is chest pain or discomfort that most
often occurs with activity or emotional stress. Angina
is due to poor blood flow through the blood vessels in
the heart.
 Stable angina is less serious than unstable angina, but
it can be very painful or uncomfortable
Variant Angina
 Attack occur at rest or during sleep and are
unpredictable
 They are due to recurrent location coronary
vasospasm which may be superimposed on
arteriosclerotic coronary artery disease
Unstable Angina
 Unstable angina is a condition in which your heart
doesn’t get enough blood flow and oxygen. It may
lead to a heart attack.
 Angina is a type of chest discomfort caused by poor
blood flow through the blood vessels (coronary
vessels) of the heart muscle (myocardium)
Pathogenesis
• Oxygen is delivered to the heart by larger surface vessels (epicardial
vessels) and intramyocardial arteries and arterioles, which branch
out into capillaries. In a healthy heart, there is little resistance to
blood flow in the epicardial vessels. When atherosclerotic plaques
are present, blood flow is impeded, but the process of autoregulation
can compensate to a degree. Autoregulation is the dilation of the
myocardial vessels in response to decreased oxygen delivery.
Through autoregulation, blood flow to the heart changes rapidly as a
result of higher demand. The most important mediators involved in
myocardial perfusion are adenosine (a potent vasodilator), other
nucleotides, nitric oxide, prostaglandins, carbon dioxide, and
hydrogen ions. Obstructions to the coronary blood flow can be fixed,
as with atherosclerosis, or dynamic, as with coronary spasm. Some
patients may have both characteristics, and this is termed mixed
angina
Cause
• Major risk factor
• Age (≥ 45 years for men, ≥ 55 for women)
• Smoking
• Diabetes mellitus
• Dyslipidemia
• Family history of premature cardiovascular disease (men <55 years, female <65
years old)
• Hypertension
• Kidney disease (microalbuminuria or GFR<60 mL/min)
• Obesity (BMI ≥ 30 kg/m2)
• Physical inactivity
• Prolonged psychosocial stress
• Routine counselling of adults to advise them to improve their diet and increase their
physical activity has not been found to significantly alter behaviour, and thus is not
recommended. Conditions that exacerbate or provoke angina
Symptoms
• Angina symptoms include:
• Chest pain or discomfort, possibly described as
pressure, squeezing, burning or fullness
• Pain in your arms, neck, jaw, shoulder or back
accompanying chest pain
• Nausea
• Fatigue
• Shortness of breath
• Sweating
• Dizziness
DIAGNOSIS
• Angina should be suspected in people presenting
tight, dull, or heavy chest discomfort that is
• Retrosternal or left-sided, radiating to the left
arm, neck, jaw, or back.
• Associated with exertion or emotional stress and
relieved within several minutes by rest.
• Precipitated by cold weather or a meal.
Drugs used in Angina
I. Nitrates and Nitrites
a) Relief of anginal pain
 Nitroglycerin
 Amyl nitrite
b) Prevention of anginal attack
 Pentaerythrityl Tetranitrate
 Erythrityl Tetranitrate
 Mannitol Hexanitrate
 Isosorbide Dinitrate
 Isosorbide Mononitrate
c) Treatment of Cynaide Poisoning
 Sodium Nitrate
2) Beta blocker
 Propanolol
 Nedolol
 Atenlol
 Metoprolol
3) Calcium channel blocker
 Verapamil
 Nifedipin
 Diltiazem
4) Potassium channel opener
 Nicorandil
5) Other
 Dipyridamole
 Trimetazidine
 Ranolazine
 Ivabradine
 Oxyphedrine
Nitrates and Nitrites
Nitrate dilate vein more than arteries
peripheral pooling of blood
decrease venous return ie preload on heart reduced
end-diastolic size and pressure are reduced
decreased cardiac work.
 MECHANISM OF ACTION
Nitrates are rapidly denitrated enzymatically in the smooth
muscle cell to release the active free radical nitric oxide
 ADVERSE EFFECT :
Fullness in the head, throbbing headache, some
degree of tolerance develop,
flushing, weakness, sweating, palpitation, dizziness,
fainting
 INTERACTION
sildenafil causes dangerous potentiation nitrate action, MI
and death are on record
Beta blocker
 These drugs do not dilate coronaries or another blood
vessel, total coronary flow rather reduced due to
blockade of dilator β2 receptor .
 β blocker limit increase in cardiac work that occurs
during exercise or anxiety by antiadrenergic action on
the heart.
 β blocker are nearly equally effective in decrease
frequency and severity of the attack
Calcium channel blocker
• Calcium channel blocker are a heterogeneous group of drugs
that reduce intracellular calcium transfer thereby limiting
calcium-triggered ATP release and thus reducing contractility
of the muscle cell
 Mechanism of action
• When cardiac cell potential reaches its threshold the membrane
permeability for sodium increase rapidly and markedly .this is
called fast channel is responsible for the influx of sodium and
is blocked by the tetrodotoxin. The time required for the
second inward the current to reach its maximum is longer .this
current is caused mainly by the movement of calcium ions into
the cell through a membrane pore, This second channel is
known as the slow channel. the movement of calcium through
this slow channel is inhibited by manganese
Adverse effect
• Constipation is the most common side effect
• Headache, vertigo, weakness, nervousness, flushing
• Perceptual disorder, hyperprolactinaemia, and
galactorrhoea
Drug interaction
• Calcium antagonists and beta blocker is risky as the
cardiac function can be adversely affected
• A potential interaction between nifedipine and quinidine
leads to a decline in quinidine concentration
• Verapamil administered with an antihypertensive
agent may have an additive effect in lowering blood
pressure
Potassium channel opener
• This dual mechanism antianginal drug activities ATP
sensitive K channel thereby hyperpolarizing vascular
muscle the vasodilator action is partly antagonised
by K channel blocker glibenclamide. like nitrate, it
acts as NO donor relaxed blood vessel by increasing
cGMP
RECENT DRUG
• The FDA has approved Ranexa, a new drug for the
treatment of chronic angina (chest pain).
• Ranexa is the first drug approved to treat chronic
angina in more than 10 years. The precise way
Ranexa works isn't fully understood, though several
of its pharmacological activities have been described,
states an FDA news release. Because Ranexa affects
electrical conduction in the heart, the drug should
only be used by patients who haven't responded to
other angina drugs, states the FDA.
PREVENTION
• Adopting a heart-healthy lifestyle can help you keep
your cholesterol and blood pressure down, keep your
arteries clear, and prevent angina.
• Eat lots of fruits, vegetables, whole grains, and low-
fat sources of protein such as nuts and fish.
• Exercise regularly.
• Maintain a healthy weight and keep diabetes under
control.
• Quit smoking
The goal of antianginal therapy
• Relieve ischemia
• Reducing the frequency and severity of anginal
attacks
• To prevent a heart attack.
REFERENCE
• Essential Of Medical Pharmacology by K.D. Tripathi
seventh edition page no 539
• Essential of pharmacotherapeutics by F.S.K Barar
page no 268
• www.webmd.com
THANK YOU

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Angina

  • 1. ASSIGNMENT REPORT ON ANGINA PECTORIS Guided by Prof Mrs Anjali M. Wankhade Submitted by Miss Shruti R.Gautam VIDYABHARTI COLLEGE OF PHARMACY CAMP ROAD AMRAVATI 444602
  • 2. Defination  Angina, also known as angina pectoris, is chest pain or pressure, usually due to not enough blood flow to the heart muscle.  Angina is usually due to obstruction or spasm of the coronary arteries. Other causes include anemia, abnormal heart rhythms and heart failure.
  • 3. Classification  Classical angina  Variant angina  Unstable angina
  • 4. Stable Angina  Stable angina is chest pain or discomfort that most often occurs with activity or emotional stress. Angina is due to poor blood flow through the blood vessels in the heart.  Stable angina is less serious than unstable angina, but it can be very painful or uncomfortable
  • 5. Variant Angina  Attack occur at rest or during sleep and are unpredictable  They are due to recurrent location coronary vasospasm which may be superimposed on arteriosclerotic coronary artery disease
  • 6. Unstable Angina  Unstable angina is a condition in which your heart doesn’t get enough blood flow and oxygen. It may lead to a heart attack.  Angina is a type of chest discomfort caused by poor blood flow through the blood vessels (coronary vessels) of the heart muscle (myocardium)
  • 7. Pathogenesis • Oxygen is delivered to the heart by larger surface vessels (epicardial vessels) and intramyocardial arteries and arterioles, which branch out into capillaries. In a healthy heart, there is little resistance to blood flow in the epicardial vessels. When atherosclerotic plaques are present, blood flow is impeded, but the process of autoregulation can compensate to a degree. Autoregulation is the dilation of the myocardial vessels in response to decreased oxygen delivery. Through autoregulation, blood flow to the heart changes rapidly as a result of higher demand. The most important mediators involved in myocardial perfusion are adenosine (a potent vasodilator), other nucleotides, nitric oxide, prostaglandins, carbon dioxide, and hydrogen ions. Obstructions to the coronary blood flow can be fixed, as with atherosclerosis, or dynamic, as with coronary spasm. Some patients may have both characteristics, and this is termed mixed angina
  • 8. Cause • Major risk factor • Age (≥ 45 years for men, ≥ 55 for women) • Smoking • Diabetes mellitus • Dyslipidemia • Family history of premature cardiovascular disease (men <55 years, female <65 years old) • Hypertension • Kidney disease (microalbuminuria or GFR<60 mL/min) • Obesity (BMI ≥ 30 kg/m2) • Physical inactivity • Prolonged psychosocial stress • Routine counselling of adults to advise them to improve their diet and increase their physical activity has not been found to significantly alter behaviour, and thus is not recommended. Conditions that exacerbate or provoke angina
  • 9. Symptoms • Angina symptoms include: • Chest pain or discomfort, possibly described as pressure, squeezing, burning or fullness • Pain in your arms, neck, jaw, shoulder or back accompanying chest pain • Nausea • Fatigue • Shortness of breath • Sweating • Dizziness
  • 10. DIAGNOSIS • Angina should be suspected in people presenting tight, dull, or heavy chest discomfort that is • Retrosternal or left-sided, radiating to the left arm, neck, jaw, or back. • Associated with exertion or emotional stress and relieved within several minutes by rest. • Precipitated by cold weather or a meal.
  • 11. Drugs used in Angina I. Nitrates and Nitrites a) Relief of anginal pain  Nitroglycerin  Amyl nitrite b) Prevention of anginal attack  Pentaerythrityl Tetranitrate  Erythrityl Tetranitrate  Mannitol Hexanitrate  Isosorbide Dinitrate  Isosorbide Mononitrate c) Treatment of Cynaide Poisoning  Sodium Nitrate
  • 12. 2) Beta blocker  Propanolol  Nedolol  Atenlol  Metoprolol 3) Calcium channel blocker  Verapamil  Nifedipin  Diltiazem
  • 13. 4) Potassium channel opener  Nicorandil 5) Other  Dipyridamole  Trimetazidine  Ranolazine  Ivabradine  Oxyphedrine
  • 14. Nitrates and Nitrites Nitrate dilate vein more than arteries peripheral pooling of blood decrease venous return ie preload on heart reduced end-diastolic size and pressure are reduced decreased cardiac work.
  • 15.  MECHANISM OF ACTION Nitrates are rapidly denitrated enzymatically in the smooth muscle cell to release the active free radical nitric oxide  ADVERSE EFFECT : Fullness in the head, throbbing headache, some degree of tolerance develop, flushing, weakness, sweating, palpitation, dizziness, fainting  INTERACTION sildenafil causes dangerous potentiation nitrate action, MI and death are on record
  • 16. Beta blocker  These drugs do not dilate coronaries or another blood vessel, total coronary flow rather reduced due to blockade of dilator β2 receptor .  β blocker limit increase in cardiac work that occurs during exercise or anxiety by antiadrenergic action on the heart.  β blocker are nearly equally effective in decrease frequency and severity of the attack
  • 17. Calcium channel blocker • Calcium channel blocker are a heterogeneous group of drugs that reduce intracellular calcium transfer thereby limiting calcium-triggered ATP release and thus reducing contractility of the muscle cell  Mechanism of action • When cardiac cell potential reaches its threshold the membrane permeability for sodium increase rapidly and markedly .this is called fast channel is responsible for the influx of sodium and is blocked by the tetrodotoxin. The time required for the second inward the current to reach its maximum is longer .this current is caused mainly by the movement of calcium ions into the cell through a membrane pore, This second channel is known as the slow channel. the movement of calcium through this slow channel is inhibited by manganese
  • 18. Adverse effect • Constipation is the most common side effect • Headache, vertigo, weakness, nervousness, flushing • Perceptual disorder, hyperprolactinaemia, and galactorrhoea Drug interaction • Calcium antagonists and beta blocker is risky as the cardiac function can be adversely affected • A potential interaction between nifedipine and quinidine leads to a decline in quinidine concentration
  • 19. • Verapamil administered with an antihypertensive agent may have an additive effect in lowering blood pressure
  • 20. Potassium channel opener • This dual mechanism antianginal drug activities ATP sensitive K channel thereby hyperpolarizing vascular muscle the vasodilator action is partly antagonised by K channel blocker glibenclamide. like nitrate, it acts as NO donor relaxed blood vessel by increasing cGMP
  • 21. RECENT DRUG • The FDA has approved Ranexa, a new drug for the treatment of chronic angina (chest pain). • Ranexa is the first drug approved to treat chronic angina in more than 10 years. The precise way Ranexa works isn't fully understood, though several of its pharmacological activities have been described, states an FDA news release. Because Ranexa affects electrical conduction in the heart, the drug should only be used by patients who haven't responded to other angina drugs, states the FDA.
  • 22. PREVENTION • Adopting a heart-healthy lifestyle can help you keep your cholesterol and blood pressure down, keep your arteries clear, and prevent angina. • Eat lots of fruits, vegetables, whole grains, and low- fat sources of protein such as nuts and fish. • Exercise regularly. • Maintain a healthy weight and keep diabetes under control. • Quit smoking
  • 23. The goal of antianginal therapy • Relieve ischemia • Reducing the frequency and severity of anginal attacks • To prevent a heart attack.
  • 24. REFERENCE • Essential Of Medical Pharmacology by K.D. Tripathi seventh edition page no 539 • Essential of pharmacotherapeutics by F.S.K Barar page no 268 • www.webmd.com