Antianginals Flashcards
Angina
Transient episodes of pressure like discomfort resulting from myocardial ischemia that do not cause cell death (MI) and last for fifteen seconds to fifteen minutes
Class 0 Angina
Asymptomatic
Class 4 Angina
Occurs at any level of exertion
Treatment rationale
Increasing oxygen delivery through coronary vasodilators or antithrombotic agents, or decreasing oxygen demand via vasodilators and cardiac depressants; decreasing the oxygen demand is the only therapy that can be used in Prinzmetal angina
Isosorbide mononitrate class
Organic Nitrates
Isosorbide dinitrate class
Organic nitrates
Nitroglyceran class
Organic nitrate
Sodium Nitroprusside class
Organic nitrate
Organic nitrate description
Indicated for ALL anginas
Mimic the action of endogenous NO
Rapid reduction in myocardial oxygen demand via systemic vasodilation and relief of symptoms
Functions of NO:
Vasodilation
Anti-thrombotic
Antiinflammatory
Functions of NO
Vasodilation
Anti-thrombotic
Anti inflammatory
Organic nitrate mechanism
Nitrates activate guanylyl cyclase which converts GTP into cGMP; elevated cGMP aids in the de phosphorylation of myosin light chains -> smooth muscle relaxation
Decreased coronary vasoconstriciton -> increased myocardial perfusion
Large venous dilation -> decreased preload and work of the heart
Isosorbide mononitrate indication
Oral prophylaxis
Longer onset and duration than nitroglyceran
Isosorbide mononitrate PK
Metabolites are active
Onset > 1 hr
Isosorbide mononitrate adverse effect
Headache -> cerebral vasodilation
Postural hypotension
Flushing
Reflex tachycardia
Desensitization-> nitrate free interval of 10-12 hours needed
Organic nitrates contraindications
Sildenafil inhibits PDE5 which breaks down cGMP leading to an even greater increase in cGMP
Isosorbide dinitrate indication
ongoing attack
Isosorbide dinitrate PK
similar to nitroglyceran but longer action
Isosorbide dinitrate adverse
Headache -> cerebral vasodilation
Postural hypotension
Flushing
Reflex tachycardia
Desensitization-> nitrate free interval of 10-12 hours needed
Nitroglycerin adverse
Headache -> cerebral vasodilation
Postural hypotension
Flushing
Reflex tachycardia
Desensitization-> nitrate free interval of 10-12 hours needed
Nitroglyceran indication
IV -> unstable angina and acute HF
Sublingual -> 1st line treatment of acute symptoms
Nitroglyceran PK
High 1st pass metabolism ->parental admin
Onset in 2-5 mins
Lasts 30 mins
Sodium nitroprusside indication
Direct NO donor -> immediate vasodilation used in EMERGENCY settings
Sodium nitroprusside PK
Continuous IV infusion
Protect from light due to conversion to cyanide
Sodium nitroprusside adverse
Headache -> cerebral vasodilation
Postural hypotension
Flushing
Reflex tachycardia
Desensitization-> nitrate free interval of 10-12 hours needed
**Cyanide poisoning*
Anti-anginal beta blockers
Acebutolol
Atenolol -cardio selective
Metoprolol - cardio selective
Propranolol - not cardioselective
Beta blcokers mechanism
Decrease heart rate and contractility
**Decrease oxygen demand **
Decrease frequency and severity of stable/unstable angina attacks
Beta blockers indication
Recommended in all patients with stable angina who have LV dysfunction
Beta blockers adverse
Rebound HTN or angina if drug is discontinued abruptly (upregulate receptors)
Beta blocker contraindications
Asthma, COPD
Diabetes, PVD
Severe bradycardia
Prinzmetal angina
Calcium channel blocker drugs for angina
Amlodipine, Felodipine
Verapamil
Diltiazem
Calcium channel blockers for angina description
Calcium is increased in ischemia due to hypoxia induced membrane depolarization
Angina is improved by coronary and peripheral vasodilation and reducing contractility
DOC for variant angina
Use with beta blockers when they aren’t successful or replace them when contraindicated
Amlodipine and Felodipine mechanism
Minimal effect on conduction or heart rate
Entry of calcium blocked -> decrease smooth muscle tone and PVR -> arteriolar vasodilation -> decrease BP
Calcium channel blockers adverse
Flushing Headache Hypotension Peripheral edema **Constipation for verapamil**
Verapamil mechanism for angina
Slows AV conduction directly -> decreases HR, contractility, BP, O2 demand
Diltiazem mechanism for angina
slows AV conduction similar to Verapamil, but decreases HR to a lesser extent
Verapamil and Diltiazem contraindications
Pre-existing depressed cardiac function or AV conduction abnormalities
Use with caution in patients on digoxin
Sodium channel blocker for angina
Ranolazine
Ranolazine description
Sodium/calcium exchanger reverses direction in sichemia
Indirectly decreases calcium levels by blocking this exchanger
May also produce myocardial relaxation
Ranolazine mechanism
decreases contractility
decreases O2 demand
May modify fatty acid oxidation
Ranolazine PK
metabolized by CYP3A4
Ranolazine Adverse
QT prolongation***
Nausea, constipation, Dizziness
Treatment strategy for Stable/unstable angina
Acute attacks are promptly relieved by rest or nitroglycerin; maintenance therapy is best with long acting nitrates and beta blockers; Calcium channel blockers are used when beta blockers are not successful or contraindicated; Ranolazine is a last ditch effort when all else fails. Patients should also take aspirin and modify their lifestyle.
Treatment strategy for Prinzmetal (variant) angina
Symptoms respond to nitroglycerin and calcium channel blockers (all types)
