Pharmacology of Angina + MI

• - MOA: releases NO into smooth muscle; activates guanylyl cylase; increases cGMP; increased Ca sequestration into SR; smooth muscle relaxation & vasodilation
• - Effect: vasodilation of arteries & veins reduce afterload & preload (decrease O2 demand, decrease wall stress)

• - AE: hypotension, reflex tachycardia, tachyphylaxis (tolerance)
• - Interactions: lethal hypotension + Sildenafil (erectile dysfxn)

- Nitrovasodilator

- Nitrovasodilator

• - MOA: bind to α1 subunit of L-type calcium channel in smooth muscle; inhibit calcium influx; decrease intracellular calcium levels; decrease contractile force of myocardium
• - Effect: decrease myocardial contractility

• - AE: hypotension, constipation, gingival hyperplasia, AV node depression 
• - Contraindication: CHF (exc. Amlodipine)
• - Interactions: CYP3A4 drugs

• - CCB
• - Dihydropyridine

• - CCB
• - Dihydropyridine
• - Only CCB not contraindicated in CHF

• - CCB
• - Non-dihydropyridine
• - Extensive CYP3A4 interactions

• - CCB
• - Non-dihydropyridine
• - Extensive CYP3A4 interactions
• - Higher incidence of constipation

• - MOA: competitive antagonist of beta-adrenergic receptors
• - Effect: block sympothetic increases of HR, BP, & contractility; decrease O2 demand

• - Contraindications: asthma, uncompensated heart failure, cardiogenic shock
• - Do not stop abruptly
• - Indicated in pt's post-MI with angina

- BB, Nonselective

- BB, Selective for B1

• - MOA: inhibits late sodium current; decreases intracellular calcium levels, decreases contract contractility
• - Effect: decrease myocardial contractility

• - Interactions: CYP3A4
• - Warning: prolongs QT interval (worry about arrhythmias)
• - Indication: rx chronic angina

- Late sodium current inhibitor (only one)

M - Morphine: blocks pain -/-> anxiety -/-> sympathetic ns -/->  elevated HR, BP, contractility -/-> worsened ischemia -/-> more pain -/-> etc.

O - Oxygen (nasal): support blood oxygen levels

N - Nitroglycerin: vasodilation of arterial --> reduced afterload --> reduced wall stress; AND vasodilation of veins --> reduced preload

A - Aspirin: anti-platelet therapy

- Statins are the only drug class known to have atheroprotective properties

• - ACE Inhibitors also have been shown to reduce mortality to MI (also lower BP, thus decrease risk factor for atherogenesis)
• - Amlodipine (CCB) has been shown to reduce mortality in pt's with CAD & in HF pt's

• - All atheroprotective drugs are shown to increase NO
• - Exercise also increases NO