CHD drugs
Wonder Me!
CHD: Acute MI, Acute Coronary Syndrome, Angina
All drugs work to reduce myocardial Oxygen demand

Drug Class
Drug Group
Specific MOA
Special notes
Drugs
Vasodilators
 
Nitrates
(DOC)
Stimulate nitric oxide => Increase cGMP => Vasodilation throughout body1
SL: acute angina
Oral: prevent angina
Intermittent dosing 2 avoid tolerance
Acute, unstable & chronic angina
Isosorbide dinitrate,
Isosorbide mononitrate 30mg PO daily
SL NTG 0.4mg q5min prn CPx3
Calcium chanel blockers
Blocks Ca2+ entry into cells => vasodilation2,4
Stable angina: may be used as monotherapy when unale to tolerate betablockers
Amlodipine 5mg PO daily
Felodipine 2.5mg PO daily
Antiarrythmias
Calcium chanel blockers
Blocks Ca2+ entry into nodes => Decrease impulse 3,5
Stable angina: may be used as monotherapy when unale to tolerate betablockers
Verapamil, diltiazem
Adrenergic antagonists
Beta-blockers
Decreases cardiac contractility (negative inotropy)6
DOC to prevent angina symptoms
Do NOT discontinue abruptly
Metoprolol 25mg PO BID
Atenolol 25 mg PO daily
Unknown
Ranolazine
Unknown
Adjunct
For chronic stable angina
Ranolazine 500mg PO BID
 (max 1000mg PO BID)
Arterio & Veno dilators
ACE-I
Prevents Angiotensin I to Angiotensin II => dilation7
Adjunct
Lisinopril, captopril
Blood thinners
Anti-platelet
prevent blood cells called platelets from clumping together to form a clot8
Adjunct
Aspirin, Clopidogrel
Anti-Coagulant
work on chemical reactions in your body to lengthen the time it takes to form a blood clot.9
Adjunct
For acute coronary syndromes (ACS)10
Heparin, LMWH
~Wonder me! 

 1Nitrovasodilators are prodrugs that donate NO by various mechanisms. Nitrates undergo chemical reduction, likely mediated by enzymes. Molsidomine and nitroprusside already contain nitrogen in the right oxidation state (+2) and liberate NO without the aid of enzymes.
NO stimulates the soluble form of the enzyme guanylate cyclase in the smooth muscle cells of blood vessels. Guanylate cyclase produces cyclic guanosine monophosphate (cGMP) from guanosine triphosphate (GTP). cGMP in turn activates cyclic nucleotide-dependent protein kinase G, which phosphorylates various proteins that play a role in decreasing intracellular calcium levels, leading to relaxation of the muscle cells and thus to dilation of blood vessels.
The most important effect in angina is the widening of veins, which increases their capacity to hold blood ("venous pooling") and reduces the pressure of the blood returning to the heart (the preload). Widening of the large arteries also reduces the pressure against which the heart has to pump, the afterload. Lower preload and afterload result in the heart needing less energy and thus less oxygen. Besides, NO donated by nitrovasodilators can reduce coronary spasms, increasing the heart's oxygen supply. Source: https://en.wikipedia.org/wiki/Nitrovasodilator#Mechanism_of_action  
2 Calcium channels are also present in the smooth muscle lining blood vessels. By relaxing the tone of this smooth muscle, calcium channel blockers dilate the blood vessels.
3Verapamil's mechanism in all cases is to block voltage-dependent calcium channels. In cardiac pharmacology, calcium channel blockers are considered class-IV antiarrhythmic agents. Since calcium channels are especially concentrated in the sinoatrial and atrioventricular nodes, these agents can be used to decrease impulse conduction through the AV node, thus protecting the ventricles from atrial tachyarrhythmias.
4 The pain of angina is caused by a deficit in oxygen supply to the heart. Calcium channel blockers like verapamil dilate blood vessels, which increases the supply of blood and oxygen to the heart.[ This controls chest pain, but only when used regularly. It does not stop chest pain once it starts. A more powerful vasodilator such as nitroglycerin may be needed to control pain once it starts.
5verapamil and diltiazem slow AV conduction and decrease SA node automaticity, they also decrease heart rate. Diltiazem is used in the treatment of variant angina because of its coronary antispasmodic properties. (Source: http://pharmacologycorner.com/calcium-channel-blockers-classification-mechanism-of-action-indications/)
6Chronotropy:  decreasing heart rate (chronotropy) and myocardial contractility (inotropy) (source: http://cvpharmacology.com/cardioinhibitory/Cardioinhibitory)
7ACE inhibitors block the conversion of angiotensin I (AI) to angiotensin II (AII).[4] They thereby lower arteriolar resistance and increase venous capacity; decrease cardiac output, cardiac index, stroke work, and volume
8 An antiplatelet drug (antiaggregant) is a member of a class of pharmaceuticals that decrease platelet aggregation [1] and inhibit thrombus formation. They are effective in the arterial circulation, where anticoagulants have little effect.
9 https://www.nlm.nih.gov/medlineplus/bloodthinners.html
10 Though ACS is usually associated with coronary thrombosis, it can also be associated with cocaine use.

Acute coronary syndrome (ACS) refers to a group of conditions due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies.[1] The most common symptom is chest pain, often radiating to the left arm or angle of the jaw, pressure-like in character, and associated with nausea and sweating. Acute coronary syndrome usually occurs as a result of one of three problems: ST elevation myocardial infarction (STEMI, 30%), non ST elevation myocardial infarction (NSTEMI, 25%), or unstable angina (38%).[2] These types are named according to the appearance of the electrocardiogram (ECG/EKG) as non-ST segment elevation myocardial infarction and ST segment elevation myocardial infarction.[3] There can be some variation as to which forms of myocardial infarction (MI) are classified under acute coronary syndrome.[4] ACS should be distinguished from stable angina, which develops during exertion and resolves at rest. In contrast with stable angina, unstable angina occurs suddenly, often at rest or with minimal exertion, or at lesser degrees of exertion than the individual's previous angina ("crescendo angina"). New onset angina is also considered unstable angina, since it suggests a new problem in a coronary artery.
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