PH1.28 Describe the mechanisms of action, types, doses, side effects, indications and contraindications of the drugs used in ischemic heart disease (stable, unstable angina and myocardial infarction), peripheral vascular disease
PH1.28 Describe the mechanisms of action, types, doses, side effects, indications and contraindications of the drugs used in ischemic heart disease (stable, unstable angina and myocardial infarction), peripheral vascular disease
This document discusses anti-platelet drugs used to treat arterial thrombi, specifically newer P2Y12 receptor antagonists. It provides details on Clopidogrel, Prasugrel, and Ticagrelor which are widely used due to being more potent than Aspirin. Clinical trials including TRITON-TIMI 38, TRILOGY-ACS and PLATO compared the drugs and found Ticagrelor and Prasugrel superior to Clopidogrel in reducing ischemic events without increasing major bleeding risk. The document concludes the drugs have differences in efficacy against stent thrombosis and risk of bleeding.
Myocardial Infarction Treatment
Classes of drugs used in the treatment of myocardial infarction
Vasodilators
General Pharmacology
Cardiac depressant drugs
Antiarrhythmics
Anti-thrombotics
Thrombolytics
Analgesics
General Mechanisms of Action
Pharmacological Use of drugs in heart failure Ebtisam ~
This document discusses pharmacological treatment options for heart failure. It lists common medications used including ACE inhibitors, ARBs, beta-blockers, digoxin, diuretics, blood vessel dilators, aldosterone inhibitors, calcium channel blockers, and aspirin. These drugs work to block chemicals that affect the heart and blood vessels, increase heart contraction strength, relieve heart failure symptoms, and reduce inflammation and blood clots. Lifestyle changes and monitoring are also part of first-line treatment, while advanced options like surgery may be used for worsening conditions.
This document summarizes fibrinolytics and antiplatelet drugs. It describes the fibrinolytic system and how fibrinolytics like streptokinase, urokinase, alteplase work to activate plasminogen and lyse clots. Newer fibrinolytics like reteplase and tenecteplase are discussed. Antiplatelet drugs discussed include aspirin, dipyridamole, clopidogrel, abciximab and how they inhibit platelet aggregation by blocking TXA2 synthesis, increasing cAMP, or blocking ADP/GP-IIb-IIIa receptors. Their uses for coronary artery disease and procedures are highlighted.
This document provides an overview of hemostasis and antithrombotic drugs. It discusses the four phases of hemostasis - vascular, platelet, coagulation, and fibrinolytic. Antithrombotic drugs include antiplatelet drugs that inhibit platelet activation and aggregation, anticoagulants that inhibit fibrin formation, and fibrinolytic agents that degrade fibrin. The document focuses on antiplatelet drugs, describing their mechanisms of action, types including aspirin, clopidogrel, prasugrel, ticagrelor, and glycoprotein IIb/IIIa antagonists. Their uses, pharmacokinetics, adverse effects, and interactions are summarized.
This document discusses cardiac glycosides, which are drugs that increase the force of contraction of the heart without increasing oxygen consumption. It specifically focuses on digitalis, which is derived from foxglove. Digitalis increases myocardial contractility in a failing heart, improving cardiac output. It acts by increasing the intracellular calcium levels in cardiac muscle cells. The document covers the chemistry, pharmacology, mechanisms of action, effects on cardiac electrophysiology, pharmacokinetics, uses, and adverse effects of digitalis and other cardiac glycosides in detail over several pages.
some reports that procainamide follows nonlinear pharmacokinetics, for the purposes of clinical drug dosing in patients, linear pharmacokinetic concepts and equations can be effectively used to compute doses and estimate serum concentrations.
Cardiac electrophysiology is the study of the electrical activities of the heart. It is used to assess and treat arrhythmias by evaluating electrocardiograms and assessing the risk of future arrhythmias. The normal electrical conduction in the heart begins with an impulse from the sino-atrial node through the atria and atrioventricular node to the ventricles. The cardiac action potential produces contractions through five phases: rapid sodium influx in Phase 0; potassium channel activation and repolarization in Phase 1; calcium influx and balance of potassium efflux in Phase 2; calcium channel closure and potassium efflux in Phase 3; and resting potential in Phase 4.
Drugs used for the treatment of myocardial ischemiask-yasmeen
This document provides information on drugs used for the treatment of myocardial ischemia. It discusses the types of myocardial ischemia including stable, unstable, and variant angina. It then describes the heart and coronary arteries and risk factors for myocardial ischemia. The main drug classes used for treatment are discussed in detail, including nitrates, calcium channel blockers, beta blockers, potassium channel activators, antiplatelet drugs, ACE inhibitors, and cholesterol lowering medications. Adverse effects, pharmacokinetics and contraindications are summarized for each drug class. Additional treatments beyond medications are also mentioned.
This document summarizes thrombolytic drugs, which are used to treat life-threatening blood clots. It discusses how thrombolytic drugs work by activating plasminogen to form plasmin, which breaks down fibrin and dissolves blood clots. The main thrombolytic drugs discussed are tissue plasminogen activator (tPA), streptokinase, urokinase, and their uses, mechanisms of action, advantages, and disadvantages in treating conditions like myocardial infarction and pulmonary embolism. The document also mentions antifibrinolytic drugs that inhibit fibrinolysis.
Beta receptor blockers are a class of drugs that are commonly used to treat cardiovascular conditions by blocking beta-1 and beta-2 receptors. They have several therapeutic uses including hypertension, congestive heart failure, angina, myocardial infarction, and cardiac arrhythmias. They work by decreasing heart rate, contractility, and blood pressure. Common side effects include fatigue, bronchospasm, and metabolic abnormalities. First generation blockers are non-selective while later generations are more cardioselective. Carvedilol is used for heart failure, atenolol for hypertension, and esmolol for emergencies. Propranolol is effective for migraine prevention. Timolol eye drops are used for glaucoma treatment by decreasing
This document discusses the physiology of cardiac rhythm, classification of arrhythmias, and anti-arrhythmic drugs used to treat arrhythmias. It covers the phases of the cardiac action potential, mechanisms of arrhythmia production, Vaughan Williams classification of anti-arrhythmic drugs based on their effects on the action potential, and details several important anti-arrhythmic drugs including their mechanisms, uses, and potential adverse effects. The document concludes that treatment of arrhythmias depends on the type of arrhythmia and patient's condition, as anti-arrhythmic drugs are efficacious but can have serious side effects, and non-pharmacological therapies are also used.
This document discusses different types of angina and drugs used to treat them. It describes stable angina, which is predictable and relieved by rest. Unstable angina occurs with less exertion and may happen at rest. Prinzmetal angina typically happens at rest and is caused by coronary artery spasms. Common drugs to treat angina include nitrates like nitroglycerin, beta blockers, calcium channel blockers, and aspirin. Nitroglycerin works by dilating blood vessels to increase blood flow and reduce oxygen demands on the heart. Beta blockers prevent reflex heart rate increases from nitrates and both drug classes reduce oxygen needs.
1. Arrhythmias occur when the heart beats too fast, too slow, or with an irregular rhythm due to problems with the heart's electrical conduction system.
2. Several classes of antiarrhythmic drugs are used to treat arrhythmias by blocking sodium, calcium, or potassium channels to suppress abnormal automaticity or conduction in the heart.
3. Common antiarrhythmic drugs include quinidine, mexiletine, flecainide, propranolol, amiodarone, dofetilide, verapamil and diltiazem. These drugs have different mechanisms of action and potential side effects like cardiac toxicity that require careful monitoring.
Angina pectoris is chest pain due to an imbalance between the heart's oxygen demand and supply. There are three types: stable angina occurs during exercise and is relieved by rest; variant angina occurs at rest due to coronary artery spasm; unstable angina is unpredictable and may lead to heart attack. Risk factors include age, sex, smoking, diabetes, and hypertension. Treatment includes nitrates, beta blockers, and calcium channel blockers to reduce symptoms and mortality from coronary artery disease progression.
Nitrates work by relaxing smooth muscle in blood vessels via the production of nitric oxide. This leads to vasodilation and reduced preload and afterload, lowering oxygen demand on the heart. Common side effects include headaches and hypotension. Tolerance develops with chronic use and can be prevented through intermittent dosing schedules and adjunctive treatments that replenish nitric oxide stores. Nitrates are available in various oral, topical, and intravenous formulations for use in angina and heart failure.
The document discusses various thrombolytic drugs (fibrinolytics), which are used to lyse blood clots and recanalize occluded blood vessels. It describes the mechanism of action of thrombolytic drugs like streptokinase, urokinase, alteplase, reteplase and tenecteplase. It provides details on the therapeutic uses, indications, contraindications and adverse effects of thrombolytic drugs in treating conditions like acute myocardial infarction, pulmonary embolism, deep vein thrombosis and more. The document is authored by Dr. Lokendra Sharma, Professor of Pharmacology at SMS Medical College in Jaipur.
1. Diuretics are drugs that cause increased excretion of water and sodium in urine. They are classified based on their mechanism and efficacy as high ceiling loop diuretics, medium efficacy thiazides, weak carbonic anhydrase inhibitors, and potassium-sparing diuretics.
2. Loop diuretics like furosemide inhibit sodium reabsorption in the ascending loop of Henle. Thiazides like hydrochlorothiazide act in the distal convoluted tubule. Carbonic anhydrase inhibitors inhibit the enzyme carbonic anhydrase.
3. Diuretics are used to treat heart failure, liver cir
This document provides an overview of nitrates in the management of angina pectoris. It defines angina pectoris and its types, and describes the pathophysiology and rationale for using nitrates. It discusses the class and examples of nitrates, their mechanisms of action, effects, dosages, and interactions. It describes nitrate tolerance and the benefits of nitrate combinations with beta-blockers or calcium channel blockers. In conclusion, the document states that nitrates decrease preload while calcium channel blockers decrease afterload, and beta-blockers decrease heart rate and contractions, making all three drugs beneficial when used together for treating angina.
Similar to PH1.28 Describe the mechanisms of action, types, doses, side effects, indications and contraindications of the drugs used in ischemic heart disease (stable, unstable angina and myocardial infarction), peripheral vascular disease
Angina pectoris is chest pain due to ischemia of the heart muscle. It is usually felt as a tightness or pressure in the middle of the chest that may spread to the neck, jaw, or arm. There are three main types - stable angina brought on by exertion, unstable angina that occurs at rest, and Prinzmetal or variant angina caused by coronary artery spasm. Treatment involves medications to relieve symptoms like nitrates, beta blockers, calcium channel blockers, and newer drugs that open potassium channels or have a cytoprotective effect. Combination therapy with two or more classes is often used for better management of angina.
This document provides learning objectives and content on the management of ischemic heart disease. It defines stable and unstable angina, describing their underlying pathologies. It classifies drugs used to treat angina, describing the mechanisms of action, uses, and side effects of nitrates, calcium channel blockers, beta blockers, nicorandil, and ivabradine. The management of myocardial infarction is also covered, outlining treatment strategies for pain, oxygenation, hemodynamics, arrhythmias, and use of antiplatelet/anticoagulant drugs and thrombolysis.
The document discusses various drugs used to treat angina pectoris and myocardial infarction. It describes the classes of drugs which include nitrates, beta blockers, calcium channel blockers, nicorandil, aspirin, ACE inhibitors, and captopril. It explains the mechanisms of action, pharmacokinetics, indications, contraindications and side effects of these drug classes and examples like nitroglycerin, atenolol, nifedipine, verapamil, aspirin, and captopril.
This document discusses antianginal drugs used to treat angina pectoris and coronary artery disease. It describes the types and causes of angina, the classes of antianginal drugs including their mechanisms of action, effects, examples, and uses. The main classes discussed are nitrates, beta blockers, calcium channel blockers, and potassium channel openers. Adverse effects and pharmacokinetics are also summarized for several drug classes and examples.
This document discusses antianginal drugs used to treat angina pectoris, or chest pain caused by reduced blood flow to the heart. There are three main classes of drugs used: organic nitrates, beta-blockers, and calcium channel blockers. Organic nitrates like nitroglycerin work by dilating blood vessels to increase blood flow to the heart and reduce its workload. Beta-blockers lower the heart rate and force of contraction to decrease oxygen demand. Calcium channel blockers inhibit calcium entry into heart and blood vessel cells to relax vessels and reduce workload. Each drug class is described in more detail regarding mechanisms, effects, pharmacokinetics, uses, and side effects.
Anti anginal drugs ppt by anjali kotwalanjali kotwal
This document discusses various anti-anginal drugs used to treat angina pectoris. It describes three main classes of drugs: nitrates, beta-blockers, and calcium channel blockers. Nitrates work by dilating blood vessels to increase oxygen supply and decrease oxygen demand. Beta-blockers lower heart rate and contractility to reduce myocardial oxygen consumption. Calcium channel blockers inhibit calcium entry into cardiac and vascular muscle to produce vasodilation and reduce myocardial work. Combination therapy using drugs from different classes is often most effective for treating angina due to their additive effects on myocardial oxygen balance.
This document discusses various drugs used to treat angina pectoris. It begins by defining angina and describing its causes as inadequate blood flow through the coronary arteries. It then discusses the different types of angina - stable, unstable, and Prinzmetal's variant angina. The main drugs used to treat angina are described - nitrates, beta-blockers, calcium channel blockers, and newer drugs like ranolazine. Nitrates work by dilating blood vessels to reduce preload and afterload. Beta-blockers reduce heart rate and contractility. Calcium channel blockers inhibit calcium entry to arteries and heart muscle. Ranolazine inhibits sodium channels to reduce oxygen demand. Combinations of these drugs
Anti-Angina & Anti arryhthias Drugs .pptssuser504dda
This document discusses drugs used to manage angina and arrhythmias, and current guidelines for managing acute coronary syndrome (ACS). It describes the classification and pathophysiology of angina, then focuses on pharmacological management including nitrates like nitroglycerin, calcium channel blockers like nifedipine, beta blockers like atenolol, and alpha/beta blockers like carvedilol. It provides details on their mechanisms of action, indications, interactions, and side effects in treating conditions like angina, heart failure and ACS.
The document discusses different types of angina pectoris and treatments for angina. It defines typical angina, variant angina, and unstable angina. It then explains drugs that can be used to treat angina by decreasing oxygen demand and/or increasing oxygen supply, including nitrates, calcium channel blockers, and beta blockers. Nitrates are described as being effective for treating acute angina by dilating blood vessels and reducing workload. Calcium channel blockers and beta blockers are also outlined as treatments that reduce oxygen demand. Combination therapies are noted to provide additive effects.
The document discusses different types of angina pectoris and treatments for angina. It defines typical angina, variant angina, and unstable angina. It then explains drugs that can be used to treat angina by decreasing oxygen demand and/or increasing oxygen supply, including nitrates, calcium channel blockers, and beta blockers. Nitrates are described as being effective for treating acute angina by dilating blood vessels and reducing workload on the heart. Calcium channel blockers and beta blockers are also outlined as treatments that decrease oxygen demand. Combination therapies are noted to provide additive effects in managing angina.
The document discusses different types of angina pectoris and treatments for angina. It defines typical angina, variant angina, and unstable angina. It then explains drugs that can be used to treat angina by decreasing oxygen demand and/or increasing oxygen supply, including nitrates, calcium channel blockers, and beta blockers. Nitrates are described as being effective for treating acute angina by dilating blood vessels and reducing workload on the heart. Calcium channel blockers and beta blockers are also outlined as treatments that decrease oxygen demand. Combination therapies are noted to provide additive effects in managing angina.
The document discusses different types of angina pectoris and treatments for angina. It defines typical angina, variant angina, and unstable angina. It then explains drugs that can be used to treat angina by decreasing oxygen demand and/or increasing oxygen supply, including nitrates, calcium channel blockers, and beta blockers. Nitrates are described as being effective for treating acute angina by dilating blood vessels and reducing workload. Calcium channel blockers and beta blockers are also outlined as treatments that reduce oxygen demand. Combination therapies are noted to provide additive effects.
Recent advances in ischemic heart diseasessaachslides15
This document provides an overview of ischemic heart diseases and recent advances in treatment. It discusses the types of angina pectoris and myocardial infarction. Current treatment strategies include nitrates, beta blockers, calcium channel blockers, and potassium channel openers. Newer agents that are discussed include trimetazidine, ranolazine, and ivabradine which lower cardiac oxygen demand and improve symptoms of angina. Combination therapies are also used to maximize antianginal effects while minimizing side effects.
Ischemic heart disease occurs when coronary arteries become narrowed by atherosclerosis, reducing blood flow to the heart muscle. Angina, myocardial ischemia, and myocardial infarction can result. Myocardial infarction is caused by sudden blockage of a coronary artery and leads to cell death in the affected region. Treatment focuses on pain relief, oxygenation, volume maintenance, acidosis correction, and preventing/treating arrhythmias. Drugs like nitrates, beta blockers, and calcium channel blockers aim to reduce oxygen demand and increase supply.
Stable angina occurs when myocardial ischemia is caused by fixed atherosclerotic narrowing of one or more coronary arteries. Vasospastic angina occurs when ischemia is caused by coronary artery spasm, with or without endothelial dysfunction. Microvascular angina refers to ischemia without an obstructed epicardial artery, potentially caused by microvascular or endothelial dysfunction. The main classes of antianginal drugs are organic nitrates, calcium channel blockers, and beta blockers. They work by decreasing myocardial oxygen demand, increasing supply, and inhibiting platelet aggregation. Organic nitrates like nitroglycerin are enzymatically converted to nitric oxide, causing smooth muscle relaxation and vasodilation to treat all types of angina.
principle action of drugs,types of angina classification of drugs ,nitrates,calcium channel blockers pharmacological actions ,combination therapy and its sid effects
Anti Anginal Drugs and its side affect and useswajidullah9551
This document discusses anti-anginal drugs used to treat angina pectoris. There are three main classes of drugs: nitrates, beta blockers, and calcium channel blockers. Nitrates work by reducing preload and afterload, increasing coronary blood flow and oxygen supply. Beta blockers decrease oxygen demand by lowering heart rate and contractility. Calcium channel blockers increase oxygen supply by dilating coronary arteries and reduce afterload by decreasing peripheral resistance. The document provides details on the mechanisms, effects, and examples of drugs in each class.
This document discusses different types of angina and drugs used to treat them. It defines angina as chest pain caused by inadequate blood flow to the heart. The main types of angina discussed are stable angina, unstable angina, and Prinzmetal's variant angina. The document outlines several classes of drugs used to treat angina, including nitrates, beta-blockers, calcium channel blockers, and some newer drugs. It provides details on the mechanisms and effects of these drug classes and recommendations for treating different angina types.
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PH1.37 Describe the mechanism of action, types, doses, side effects, indications and contraindications of the drugs used as sex hormones, their analogues
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PH1.28 Describe the mechanisms of action, types, doses, side effects, indications and contraindications of the drugs used in ischemic heart disease (stable, unstable angina and myocardial infarction), peripheral vascular disease
1. PH1.28 Describe the mechanisms of action, types,
doses, side effects, indications and
contraindications of the drugs used in ischemic
heart disease (stable, unstable angina and
myocardial infarction), peripheral vascular disease
Dr Pankaj Kumar Gupta, MD
Assistant Professor,
Department of Pharmacology,
ESIC Medical College & Hospital,
Faridabad (HARYANA) INDIA
3. Objectives
• Definition of Myocardial Ischemia
• Definition, Pathophysiology & types of Angina
• Anti-anginal drugs Pharmacology
Nitrates
B-blockers
Calcium Channel blockers
• Newer drugs for Angina
• Drug therapy in myocardial infarction
• Drug therapy in Peripheral Vascular Disease (PVD)
4. Myocardial ischemia
• Myocardial ischemia is a condition
when blood flow to heart is
reduced, preventing the heart
muscle from receiving enough
oxygen.
• The reduced blood flow is usually
the result of a partial or complete
blockage of coronary arteries.
• A sudden, severe blockage of
coronary artery can convert
myocardial ischemia to myocardial
infarction.
7. Angina
• Angina (an-JIE-nuh or AN-juh-
nuh) is a type of chest pain
caused by reduced blood flow
to the heart.
• Angina is a symptom of
coronary artery disease.
• Angina is also called angina
pectoris.
• Angina pain is often described
as squeezing, pressure,
heaviness, tightness or pain in
the chest. It may feel like a
heavy weight lying on the
chest.
https://www.mayoclinic.org/diseases-conditions/angina/symptoms-causes/syc-20369373
8. Pathophysiology of Angina/IHD
• Chest pain/discomfort related to a decrease
in oxygen-rich blood flow
• Usually due to coronary artery disease (CAD)
• Atherosclerosis
– Build up of plaque over time that narrows the
internal diameter of the vessel
• Arteriosclerosis
– Stiffening of vessels over a period of time which
makes them less pliable
8
11. Stable Angina
• Most common form
• Pain occurs when oxygen
demand is greater than
the supply during
periods of increased
workload of the heart
• Usually treated with rest
and medication (i.e.
nitroglycerin)
11
12. Unstable Angina
• Pain that is unpredictable
and can occur at rest
• May not stop with rest
and/or medication
• Event to be taken
seriously
– May be predicting an
imminent acute MI in
the near future
12
13. Variant Angina
• Occurs when vessel is in spasm
• Very painful
• Often occurs at night
• Controlled with medication
13
15. NITRATES
MODE OF ACTION
• Acts directly on vascular smooth muscle to
produce arterial and venous dilatation
EFFECT DURING ANGINA
• Reduces myocardial oxygen demand (lowers pre-
load and after load)
• Increases myocardial oxygen supply (coronary
vasodilatation)
17. BETA BLOCKERS
MODE OF ACTION
• Lowers myocardial oxygen demand by
A. Reducing heart rate
B. Reducing blood pressure
C. Reducing myocardial contractility
18. • All β- blockers except those with intrinsic
sympathomimetic activity are equally effective in
decreasing frequency & severity of attacks & in
increasing exercise tolerance in classical angina but
the cardio-selective are preferred over non-selective
blockers.
• Commonly used β- blockers:
• Atenolol 50-200 mg daily
• Metoprolol SR 50-200 mg daily
• Bisoprolol 5-10 mg daily
20. Limitations of β blockers
• Can exacerbate symptoms of peripheral vascular disease.
• May provoke bronchospasm in patients with obstructive
airway disease e.g asthma.
• Non-selective beta blockers may aggravate coronary
vasospasm (variant angina) by blocking the coronary artery β-
2 receptors & due to unopposed α receptor mediated
vasoconstriction.
• β-blockers should not be withdrawn abruptly because of the
possibility of a rebound effect and the risk of precipitating
arrhythmias, worsening angina or causing myocardial
infarction (the ‘beta-blocker withdrawal syndrome).
21. Calcium Channel Blockers
MODE OF ACTION
• Decreases myocardial oxygen demand by reducing blood
pressure and myocardial contractility
TYPES
A. Dihydropyridine CCBs:
• Often cause reflex tachycardia
• best used in combination with beta blocker
• Eg. Nifedipine, Nicardipine
B. Phenylalkylamine-Verapamil
C. Benzothiazepine- Dilitiazem
• Both suitable for patients who are not receiving beta blockers as
they decrease the heart rate (dangerous additive effect)
• May reduce myocardial Contractility to a degree that can aggravate
or precipitate Heart failure
22. Status of CCBs in Angina
• All the CCBs have been used for treating angina. However, the most
commonly used for this purpose are the longer-acting forms of
Diltiazem and Verapamil, Amlodipine, or Felodipine.
• Nifedipine, especially its short-acting forms, should be avoided in
people with angina since the pronounced blood vessel dilation
produced by this drug can increase in adrenaline, leading to a more
rapid HR, and consequently an increase in cardiac oxygen
requirements which led to worsen cardiac ischemia.
• CCBs should be tried in patients who cannot tolerate beta-blockers.
• CCBs should be added to beta-blockers in patients who have
insufficient relief of symptoms with beta-blockers.
https://www.verywellhealth.com/calcium-channel-blockers-for-treating-angina-1745910
23. POTASSIUM CHANNEL ACTIVATORS: NICORANDIL
Mode of action 1. Dilates arteries and veins
2. Does not exhibit tolerance seen with nitrates
Mechanism of
action
1. This a novel anti-anginal drug activates ATP sensitive K+
channels leading to hyperpolerization of vascular smooth
muscle.
2. It also acts as a NO donor and relaxes blood vessels by
increasing cGMP.
2. Coronary blood flow is increased, dilatation of both
epicardial conducting vessels and deeper resistance vessel.
3. Mitochondrial K+ ATP channel opening exert myocardial
protection by preconditioning which appears to reduce
myocardial stunning, arrhythmias and infarct size.
Side effect 1. Flushing, palpitation, weakness, headache, dizziness
2. Large painful aphthous ulcers of mouth.
Dose 1. Nicorandil Dose- 5-20 mg BD (NIKORAN)
24. RANOLAZINE
Mode of action 1. ↓ myocardial contractility
2. Cardioprotective effect
Mechanism of
action
1. Act mainly by reducing a late, prolonged sodium current in
myocardial cells. (Late INa)
2. The decrease in intracellular sodium causes an increase in
calcium expulsion via the Na/Ca transporter and a reduction in
cardiac force and work.
3. By inhibiting LC3KAT Spare fatty acid oxidation during
ischemia & ↑ O2 efficient carbohydrate oxidation.
4. Ranolazine is moderately effective in angina prophylaxis.
Pharmacokinetics 1. Oral absorption- slow (4-6 hrs), BA-30-50%
2. Metabolism CYP3A4, t1/2- 7 hrs
3. Excretion-urine
Side effect 1. Dizziness, weakness, constipation, postural hypotension,
headache, dyspepsia
Dose 1. 0.5- 1 g BD (RANOZEX)
25. DIPYRIDAMOLE
Mode of action 1. Coronary dilator
2. Adjuvant anti-platelet drug
Mechanism of action 1. It is a powerful coronary dilator
2. ↑ total coronary flow by preventing uptake and
degradation of adenosine. (local mediator involved in auto-
regulation)
3. It dilates resistance vessels (both in ischemic & non-
ischemic zone vessels) and abolishes auto-regulation. So, fails
to relieve anginal symptoms & avert ECG changes. (Coronary
steal phenomena- pharmacological success but therapeutic
failure)
4. Not useful as an anti-anginal drug but used for prophylaxis
of Coronary and cerebral thrombosis in post-MI and post stoke
patients.
5. Inhibit platelet aggregation. (PGI2 potentiation)
26. Diagrammatic representation of coronary haemodynamics.
A—in classical angina,
B — Selective nitrate action on conducting vessels,
C—Dipyridamole action on all resistance vessels increases blood flow to non-ischaemic zone
27. TRIMETAZIDINE
Mode of action 1. pFOX inhibitor (fatty acid oxidation pathway)
2. Anginal frequency is reduced and exercise capacity is increased.
Mechanism of action 1. Improve cellular tolerance to ischemia by
• Inhibiting mitochondrial long chain 3-ketoacyl-CoA- thiolase
(LC3-KAT) a key enzyme in fatty acid oxidation
• Increasing glucose metabolism in myocardium. (oxidation of fatty
acid requires more more O2 to glucose for same amount of ATP
generation)
• Limiting intracellular acidosis and Na+ and Ca++ accumulation
during ischemia.
• Protecting against O. free radical induced membrane damage
Pharmacokinetics 1. Oral absorption
2. Partial metabolism
3. Excretion in urine-unchanged, t1/2- 6 hrs
Side effect 1. Well tolerated
2. Gastric burning, dizziness, fatigue, muscle cramps
3. Reversible parkinsonism
Dose & use 1. 20 mg TDS (FLAVEDON)
2. Used as an add-on medication to conventional therapy in angina,
post-MI patients.
28. IVABRADINE
Mode of action 1. This is a‘pure’ heart rate lowering antianginal drug.
Mechanism of action 1. It blocks the cardiac pacemaker (sino-atrial) cell ‘f’ channels,
which are ‘funny’ cation channels that open during early part of
slow diastolic (phase 4) depolarization.
2. The resulting inward current (If) determines the slope of phase 4
depolarization, thus decreasing heart rate.
3. Heart rate reduction decreases cardiac O2 demand and
prolongation of diastole tends to improve myocardial perfusion
(O2 supply).
Pharmacokinetics 1. Well absorbed orally, BA-40%
2. Metabolism by CYP3A4
3. Excretion in urine, t1/2-2 hrs
Side effect 1. Excess bradycardia, visual disturbance, extrasystoles, prolongation
of P-R interval, headache, dizziness and nausea.
Dose & use 1. Initially 5 mg BD, increase to 7.5 mg BD (IVABRAD)
29. DRUG COMBINATIONS
I. β blocker + long-acting nitrate combination
II. slow acting DHP (in place of nitrate) with β blocker.
III. Nitrates and CCBs
IV. All 3 classes
31. Acute Coronary Syndromes (ACS)
•According to severity, the acute coronary syndrome (ACS)
may be graded into:
•Unstable Angina (UA)
•Non-ST segment Elevation Myocardial Infarction (NSTEMI)
•ST segment Elevation Myocardial Infarction (STEMI)
•Myocardial Infarction (MI) is ischaemic necrosis of a
portion of the myocardium due to sudden occlusion of a
branch of coronary artery.
•Ischemia means the absence of blood flow to the organ or
body tissues, while Infarction implies the death of tissues
due to reduced blood supply.
32. Acute Coronary Syndromes (ACS)
Unstable Angina (UA)
NSTEMI
(Non-ST segment
Elevation Myocardial
Infarction)
STEMI
(ST segment Elevation
Myocardial Infarction)
1 Vascular obstruction is
incomplete
Vascular obstruction is
incomplete, but occlusion &
micro-embolization has
started
Vascular obstruction is
complete (complete
occlusion)
2 Myocardial necrosis is
absent
Smaller area of myocardial
necrosis
Full thickness of ventricular
wall & larger area of
myocardium is necrosed
3 Biochemical biomarkers
of ischemia (myoglobin,
CK-MB, Troponin-I) do not
appear in blood
Biochemical biomarkers of
ischemia appear in blood
Biochemical biomarkers of
ischemia appear in blood
prominently
4 ST segment not elevated
in ECG
ST segment not elevated in
ECG
ST segment is elevated in
ECG
34. DRUG THERAPY IN MYOCARDIAL
INFARCTION
1 Pain, anxiety and
apprehension
•GTN, Morphine, Diazepam
2 Oxygenation
3 Maintenance of blood
volume
•Slow IV infusion of saline/dextrose
4 Correction of acidosis •Due to lactic acid production
•IV Sodium bicarbonate infusion
5 Prevention and
treatment of
arrhythmias
Beta blockers, Lidocaine
•Arrythmias- Prophylactic Metoprolol (IV/Oral) &
continued for few days ↓ incidence of arrhythmias,
mortality & infarct size
•Tachyarrhythmias- IV
Lidocaine/Procainamide/Amiodarone
•Bradycardia/Heart block- Atropine/Electrical Pacing
35. DRUG THERAPY IN MYOCARDIAL
INFARCTION
6 Pump failure •The objective is to increase c.o. and/or decrease
filling pressure without unduly increasing cardiac work
or lowering BP.
•Vasodilators (GTN slow IV)
•Inotropic agents (Dopamine/dobutamine IV infusion)
•Diuretics (Furosemide if pulmonary wedge pressure
>20 mm Hg)
7 Prevention of thrombus
extension, embolism,
venous thrombosis
•Aspirin (162–325 mg), then continued at 80–160
mg/day
8 Thrombolysis and
reperfusion
•Fibrinolytic agents: Plasminogen activators—
streptokinase/ urokinase/alteplase/ PCI
9 Prevention of remodeling
and subsequent CHF
•ACE inhibitors/ARBs
36. DRUG THERAPY IN MYOCARDIAL
INFARCTION
10 Prevention of future
attacks
• Platelet inhibitors: aspirin/clopidogrel on long
term basis
• β blockers: ↓ risk of re-infarction, CHF and
mortality, all pts should be on suitable β blocker
for at least 2 years
• Statins: for control of hyperlipidaemia
• ACE-I/ARBs: ↓vascular remodeling & BP
37. Approach to a patient with Acute Corornary Syndromes
38. Peripheral Vascular Disease (PVD)
• A slow and progressive circulation disorder.
• Narrowing, blockage, or spasms in a blood vessel can
cause PVD.
• Primarily due to atherosclerosis.
• The atherosclerotic process may gradually progress to
complete occlusion of medium-sized and large
arteries.
• The legs and feet are most commonly affected. It has
the potential to cause loss of limb or even loss of life.
https://emedicine.medscape.com/article/761556-overview
https://www.hopkinsmedicine.org/health/conditions-and-diseases/peripheral-vascular-disease
40. Drugs Properties
Cyclandelate •Papaverine like general smooth muscle relaxant
•MOA: ↑ cutaneous, skeletal & cranial blood flow
•Uses: In PVD- minor role, restricted to vasospastic PVD
•ADR: flushing, palpitation, headache
•Dose: 200-400 mg TDS (CYCLOSPASMOL)
Xanthinol
Nicotinate
•A compound of xanthine & nicotinic acid (both are vasodilators)
•Uses: Promoted for cerebrovascular disorders & PVDs
•Therapeutic benefits are insignificant
•Dose: 300-600 mg TDS Oral, 300 mg IM/slow IV (COMPLAMINA)
Pentoxiphylline •An analogue of theophylline
•Weak phosphodiesterase inhibitor
•Rheological action (property of flow- ↓blood viscosity & ↑flexibility
of RBCs) is responsible for therapeutic benefit
•ADRs: Well tolerated, in some- nausea, vomiting, dyspepsia, bloating
•Uses: intermittent claudication due to occlusion, trophic leg ulcers,
TIAs, chronic cerebrovascular insufficiency
•Overall benefits are minimal
•Dose: 400 mg BD/TDS, 300 mg/15 ml for slow IV (TRENTAL,
FLEXITAL)
41. Drug Properties
Cilostazol •MOA: PDE-3 inhibitor- ↑ intracellular cAMP in platelets &
vascular smooth muscle cells- antiplatelet & vasodilator effect
•↑walking distance in intermittent claudication pts
•More effective than Pentoxyphylline
•PK: metabolized by CYP3A4/CYP2C19
•ADRs: headache, palpitation, dizziness, nausea, vomiting,
weakness, ↑ventricular ectopic
•Use: Intermittent claudication in patient with no rest pain or
heart failure
•Dose: 100 mg BD 30 min before/2 hr after food
42. References
• Tripathi, K. D. (2018). Essentials of medical pharmacology (8th ed.). Jaypee
Brothers Medical.
• https://www.mayoclinic.org/diseases-conditions/angina/symptoms-causes/syc-
20369373
• https://www.verywellhealth.com/calcium-channel-blockers-for-treating-angina-
1745910
• https://emedicine.medscape.com/article/761556-overview
• https://www.hopkinsmedicine.org/health/conditions-and-diseases/peripheral-
vascular-disease