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Angina
- 1. ANGINA PECTORIS Presented by: Sk.samiya Y16MPH273 Deptof Pharmacology HINDU COLLEGE OF PHARMACY
- 2. • Definition • Classification •Signs and symptoms • Causes • Pathophysiology • Diagnosis • Treatment • Drug therapy Contents
- 3. A type ofchest pain caused by reduced blood flow to the heart.
- 4. • Angina pectorisis a clinical syndrome of IHD resulting from transient myocardial ischemia. • It is characterized by paroxysmal pain in the substernal or precordial region of the chest which is aggravated by an increase in the demand of the heart and relieved by a decrease in the work of the heart. • Often, the pain radiates to the left arm, neck, jaw or right arm. • It is more common in men past 5th decade of life. ANGINA
- 7. • Stable anginais the most common type of angina. • It occurs when the heart is working harder than usual. • Stable angina has a regular pattern. (“Pattern” refers to how often the angina occurs, how severe it is, and what factors trigger it.) • The pain usually goes away a few minutes after you rest or take your angina medicine. • Stable angina isn't a heart attack, but it suggests that a heart attack is more likely to happen in the future. Stable angina
- 8. • Unstable anginadoesn't follow a pattern. • It may occur more often and be more severe than stable angina. • Unstable angina also can occur with or without physical exertion, and rest or medicine may not relieve the pain. • Unstable angina is very dangerous and requires emergency treatment. • This type of angina is a sign that a heart attack may happen soon. Unstable Angina
- 9. • Variant anginais rare. • A spasm in a coronary artery causes this type of angina. • Variant angina usually occurs while you're at rest, and the pain can be severe. • It usually happens between midnight and early morning. • Medicine can relieve this type of angina. Variant (Prinzmetal's) Angina
- 10. • Chest discomfortrather than actual pain: • The discomfort is usually described as a – pressure, – heaviness, – tightness, – squeezing, – burning, – choking sensation. SIGNS AND SYMPTOMS
- 11. • Apart fromchest discomfort, anginal pains may also be experienced in the epigastrium (upper central abdomen), back, neck area, jaw, or shoulders. • It is exacerbated by having a full stomach and by cold temperatures. • Pain may be accompanied by breathlessness, sweating, and nausea in some cases.
- 12. 1) Major riskfactors CAUSES
- 13. 2) Other medicalproblems • Hyperthyroidism • Hypoxemia • Profound anemia • Uncontrolled hypertension 3) Other cardiac problems • Tachyarrhythmia • Bradyarrhythmia • Valvular heart disease • Hypertrophic cardiomyopathy
- 14. • Angina resultswhen there is an imbalance between the heart's oxygen demand and supply. • This imbalance can result from an increase in demand (e.g., during exercise) without a proportional increase in supply (e.g., due to obstruction or atherosclerosis of the coronary arteries). • However, the pathophysiology of angina in females varies significantly as compared to males Non-obstructive coronary disease is more common in females Pathophysiology
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- 20. • Organic nitratesare prodrugs and they release nitric oxide. • Nitrates are mainly venodilators also cause arteriolar dilation and as a result reduces both preload and afterload. • These compounds cause a rapid reduction in myocardial oxygen demand, followed by rapid relief of symptoms. Organic nitrates
- 21. Administered nitrates Increased nitratesin the blood Increased formation of nitric oxide Increased cGMP formation increased dephosphorylation of myosin Vascular smooth muscle relaxation • vasodilation
- 22. • The nitratesare inactivated in liver by glutathione or ganic nitrate reductase. • Therefore their oral bioavailability is considerably less due to their first-pass metabolism. • The sublingual route, which avoids first pass effect, is therefore preferred. • Duration of action lasts for about 25-30min pharmacokinetics
- 23. On other smoothmuscles: • Smooth muscles of bronchi, oesophagus, biliary tract, etc are relaxed by nitrates. Pharmacological actions of nitrates:
- 24. Venodilation arterial dilatation Peripheralpooling of blood PVR Venous return to the heart Afterload Preload Left and right end-diastolic volume and pressure Cardiac work O2 requirement of myocardium RELIEF OF PAIN Pharmacological action on vascular smooth muscles
- 25. • The mostcommon adverse effect of nitroglycerin, as well as of the other nitrates, is headache. • High doses of organic nitrates can also cause postural hypotension, facial flushing, and tachycardia. Sildenafil potentiates the action of the nitrates. • Over doses may cause methaemoglobinaemia. Adverse drug reactions
- 26. • Continuous exposureto nitrates in the chemical industry results in development of tolerance. • Workers may experience headache and dizziness on starting work during first few days. • As there is no exposure to chemicals over the weekend , tolerance disappears. • Symptoms disappear when they start work on Monday– “ Monday disease”. Tolerance
- 27. • Angina pectoris •Heart failure • Myocardial infarction • Cyanide poisoning • Oesophageal spasm • Biliary colic Therapeutic uses
- 28. • Sildenafil andother vasodilators potentiate the hypotensive action of nitrates • MI and sudden death have occurred. Drug interactions
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- 33. Nifedipine • Functions mainlyas an arteriolar vasodilator. • This drug has minimal effect on cardiac conduction or heart rate. • Nifedipine is administered orally, usually as extended-release tablets. It undergoes hepatic metabolism to products that are eliminated in both urine and the feces.
- 34. • The vasodilationeffect of nifedipine is useful in the treatment of variant angina caused by spontaneous coronary spasm. • Nifedipine can cause flushing, headache, hypotension, and peripheral edema
- 35. • The diphenylalkylamineverapamil slows cardiac atrioventricular (AV) conduction directly, and decreases heart rate, contractility, blood pressure, and oxygen demand. • Verapamil causes greater negative inotropic effects than nifedipine, but it is a weaker vasodilator. • The drug is extensively metabolized by the liver; therefore, care must be taken to adjust the dose in patients with liver dysfunction. Verapamil
- 36. • Verapamil iscontraindicated in patients with preexisting depressed cardiac function or AV conduction abnormalities. • It also causes constipation. • Verapamil should be used with caution in patients taking digoxin, because verapamil increases digoxin levels.
- 37. • It dilatesperipheral and coronary arteries but its dilating property is less marked than DHPs. • It also causes negative inotropic, chronotropic and dromotropic effects. • It is used in the treatment of angina, hypertension and supraventricular arrhythmias. Diltiazem
- 38. • Verapamil ordiltiazem should not be given with beta blockers as SA nodal depression, conduction defects or asystole may occur or be aggravated. • These should not be used with other cardiac depressants drugs like quinidine or disopyramide. • These drugs increase plasma digoxin levels by decreasing its excretion. DRUG INTERACTIONS
- 39. • All CCBsare well absorbed through GI tract but they undergo varying degree of first pass metabolism. • All are highly bound to plasma proteins, metabolized in the liver and excreted in urine. Pharmacokinetics
- 40. • Angina pectoris •Variant angina • Unstable angina • Supraventricular arrhythmias • Hypertension • Hypertropic cardiomyopathy • Migraine • Raynaud’s phenomenon Uses of CCBs
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- 43. • They are,however, contraindicated in patients with asthma, diabetes, severe bradycardia, peripheral vascular disease, or chronic obstructive pulmonary disease. Adverse effects: • Bradycardia • Heart block • Bronchospasm • hypoglycaemia
- 44. • Nitrates ×beta blockers • Nifedipine × β-blockers • Β-blockers × verapamil/diltiazem • Calcium channel blockers × nitrates • Nitrates + β-blockers + CCBs Combination therapy
- 46. • Voltage gatedK channels: These channels open when the cell is depolarized and therefore help in the process of repolarization. These are present mainly in vascular and other smooth muscles • Calcium activated K channels: An increase in intracellular ca+2 concentration causes opening of these channels, causes repolarization. • ATP sensitive K channels: These are present in cardiac muscle and beta cells of islets of Langerhans of pancreas Potassium channels
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- 54. 1. Lippincott's IllustratedReviews Pharmacology, 4th Edition 2. https://en.wikipedia.org/wiki/Angina_pe ctoris 3. Principles of Pharmacology SHARMA AND SHARMA 4. Pharmacology by Tara V Shanbhag. REFERENCES