Angina Pectoris Drugs Flashcards Preview

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Flashcards in Angina Pectoris Drugs Deck (12):

Amyl nitrite

- organic nitrite
- NO donor - generates nitric oxide
- inhaled
- fast onset, short (15 min) acting
- bad odor; limited use
- used by drug abusers for enhancement of sexual perception and pleasure as well as vasodilation of cerebral blood vessels along with warm sensations and facial flushing --> contribute to the users perception of a rush or high



- organic nitrate
- sublingual: fast onset, short (30 min) acting
- intravenous: immediate onset, transient short acting
- buccal (transmucosal): fast onset, long (6 hrs) acting
- oral: slow onset, long (8 hrs) acting
- transdermal: slow onset, long (24 hrs) acting
Nitroglycerin is adsorbed on lactose, colloidal silicone dioxide and silicone medical fluid
A layer of silicone adhesive ensures attachment to skin

Mechanism of action of nitrates:
Vasodilatory effect on different vessels: veins > larger arteries > arterioles. Nitroglycerin is denitrated in the tissues by mitochondrial aldehyde DH, and NO is liberated. Nitroglycerin is also denitrated in the liver by glutathione-S-transferase and nitrite ion is liberated, which is then reduced to NO by enzymes. Amount of nitric oxide (NO) liberated depends on different blood vessels. Venodilation causes pooling of blood in the large veins, less venous blood returns to the heart and there is decrease in the ventricular end‐diastolic volume and
Thus, pre‐load on the heart is decreased
NO stimulates soluble guanylate cyclase which increases intracellular cyclic guanosine monophosphate (cGMP) --> increase in cGMP results in relaxation of smooth muscle by dephosphorylation of phosphorylated myosin light chain.

Vasodilatory effect of nitrates on the arterioles decreases systemic blood pressure causing decrease in the after‐load on the heart
Decrease in pre‐load (due to venous pooling of blood) and after‐load (due to arteriolar
vasodilation and fall in BP) result in decrease in myocardial oxygen demand.
Decrease in myocardial oxygen demand is the most important mechanism by which nitrates relieve anginal pain

Nitroglycerin increases blood to cardiac ischemic areas whereas other vasodilator drugs like dipyridamole and hydrazine elicit the coronary steal phenomenon (both normal and ischemic vessels are dilated) and are not effective in relieving anginal pain

- cross run with Sildenafil (Viagra) - both cause increased cGMP so potentiation of cGMP induced hypotension may be dangerous in these patients

- side effects: because of venous pooling of blood postural hypotension associated with dizziness and weakness, dilation of meningeal blood vessels may cause headache, dilation of cutaneous vessels may cause flushing of the face


Isosorbide dinitrate

- organic nitrate
- sublingual: slow onset, long *2 hrs) acting
- oral: slow onset, long (10 hrs) acting
- NO donor - generates nitric oxide


Isosorbide mononitrate

- organic nitrate
- oral: slow onset, long (12 hrs) acting
- NO donor - generates nitric oxide


Erithrityl tetranitrate

- organic nitrate
- sublingual: slow onset, long (3 hrs) acting
- oral: slow onset, long (6 hrs) acting
- NO donor - generates nitric oxide


Pentaerythritol tetranitrate

- organic nitrate
- oral: slow onset, long (12 hrs) acting
- explosive
- NO donor - generates nitric oxide


Sodium nitroprusside

- inorganic nitroso compound
- NO donor - generates nitric oxide - unknown mech
- used for treatment of hypertensive emergencies and heart failure when short term reduction of cardiac pre-load and after-load is needed
- liberates CN ion (not good but should not be a problem in normal doses); mitochondrial enzyme rhodanase converts CN to less toxic thiocyanate in the presence of a sulfur donor
to prevent excessive CN formation, the drug must be prepared just before use and placed in an opaque container


Fatty acid oxidation inhibitors

mechanism of action
• Inhibitors of long‐chain 3‐ketoacylcoenzyme
A thiolase shift myocardial
metabolism toward greater use of
glucose as a substrate resulting in
reduced oxygen demand which is
helpful in patients with angina pectoris.
• Trimetazidine (a fatty acid oxidation
inhibitor) is not available in USA

Ranolazine: high concentrations of the drug are needed to serve as an inhibitor of fatty acid oxidation.



- at high concentrations serves as an inhibitor of FA oxidation
Ranolazine has been shown to inhibit late
sodium current (INa+) in the myocardial
ventricular muscle during ischemia.
• Increase in intracellular Na+ concentration, via
increase in INa+, in ischemic cardiac cells is
• Consequently, intracellular Ca++ concentration
is reduced in ischemic cardiac cells due to
lesser Na+/Ca++ exchange.
• Increase in diastolic ventricular muscle tension
during ischemia is reduced.
• Ventricular muscle MVO2 is reduced which is
useful in the treatment of angina pectoris.


Clopidogrel (Plavix)

- reduce platelet aggregation by blocking the adenosine diphosphate (ADP) receptor on platelets
- for unstable angina


Abciximab (ReoPro)
Tirofiban (Aggrastat)

- prevent platelet aggregation by inhibiting platelet glycoprotein IIb/IIIa receptor complex
- for unstable angina


beta blockers
calcium channel blockers

also anti-angina drugs