Chapter 18: Antianginal Drugs Flashcards
What are the types of angina? (5)
- Effort induced angina, classic or stable: reductiong of coronary perfusion due to fixed obstruction of a coronary artery by atherosclerosis; relieved with nitroglycerin which decreases myocardial O2 demand
- Unstable angina: between stable angina and MI; not relieved with nitroglycerin; requires hospital admission and more aggressive therapy
- Prinzmetal, variant, vasospastic, or rest angina: occurs at rest due to coronary artery spasm; symptoms caused by decreased blood flow to the heart; symptoms unrelated to physical activity, HR, or BP
prinzmetal angina responds promptly to vasodilators such as nitroglycerin or Ca2+-channel blockers - Mixed forms of angina: angina during excertion and at rest suggesting fixed obstruction
- Acute coronary syndrome: rupture of atherosclerotic plaque that causes thombosis of a coronary artery; may present as STEMI or NSTEMI; MI presents with an elevation of biomarkers
What are the types of angina? (5)
- Effort induced angina, classic or stable: reductiong of coronary perfusion due to fixed obstruction of a coronary artery by atherosclerosis; relieved with nitroglycerin which decreases myocardial O2 demand
- Unstable angina: between stable angina and MI; not relieved with nitroglycerin; requires hospital admission and more aggressive therapy
- Prinzmetal, variant, vasospastic, or rest angina: occurs at rest due to coronary artery spasm; symptoms caused by decreased blood flow to the heart; symptoms unrelated to physical activity, HR, or BP
- Mixed forms of angina:
- Acute coronary syndrome:
What are the types of antianginal drugs? (4 categories)
Organic Nitrates: isosorbide dinitrate, isosorbide mononitrate, nitroglycerin
B-blockers: acebutolol, atenolol, metoprolol, propranolol
Ca2+ channel blockers: amlodipine, diltiazem, felodipine, nicardipine, nifedipine, verapamil
Na+ channel blockers: ranolazine
What is the MOA, effects on the cariovascular system, pharmokinetics and adverse effects of organic nitrates?
Ex: nitroglycerin,
MOA: inhibit coronary vasoconstriction, venodilation, decrease preload and decrease O2 demand; effective in treating effort induced angina (classic angina); basically these just convert over to nitric oxide which results in smooth muscle relaxation
Effect: sublingual nitroglycerin causes dilation of large veins, resulting in blood pooling which diminishes preload and reduces work of the heart
sublingual nitroglycerin also dilates the coronary vasculature which provides an increased blood supply to the heart
basically: nitroglycerin decreases myocardial O2 consumption
Pharmokinetics: nitroglycerin action: 1minute
isosorbide mononitrate: 1hr
-take sublingually or transdermal patch to prevent first pass metabolism
Adverse Effects: headache, postural hypotension,
Tolerance: develops rapidly; nitate free interval after 12 hours then remove for 12 hours (usually at night)
What is the MOA, effects on the cardiovascular system, pharmokinetics and adverse effects of organic nitrates?
Ex: nitroglycerin,
MOA: inhibit coronary vasoconstriction, venodilation, decrease preload and decrease O2 demand; effective in treating effort induced angina (classic angina); basically these just convert over to nitric oxide which results in smooth muscle relaxation
Effect: sublingual nitroglycerin causes dilation of large veins, resulting in blood pooling which diminishes preload and reduces work of the heart
sublingual nitroglycerin also dilates the coronary vasculature which provides an increased blood supply to the heart
basically: nitroglycerin decreases myocardial O2 consumption
Pharmokinetics: nitroglycerin action: 1minute
isosorbide mononitrate: 1hr
-take sublingually or transdermal patch to prevent first pass metabolism
Adverse Effects: headache, postural hypotension,
Tolerance: develops rapidly; nitate free interval after 12 hours then remove for 12 hours (usually at night)
What is the MOA, effects on the cardiovascular system, pharmokinetics and adverse effects of B-adrenergic blockers?
Ex: propanolol, metoprolol, atenolol
MOA: block B1 receptors which results in lowering HR, contractility, CO, and BP; O2 demand reduced both at exertion and at rest; should not be used in vasospastic angina
indications: drug of choice to treat effort induced angina
- no intrinsic sympathomimetic activity metoprolol is useful in treatment of patients with MI
- patients with classic angina: B-blockers used with nitrates to increase excersise tolerance
pharmokinetics: all B blockers are non selective at high doses (propanolol is generally non selective)
adverse effects: contraindicated in patients with asthma, diabetes, severe bradycardia, peripheral vascular disease, and COPD
What is the MOA, effects on the cardiovascular system, pharmokinetics and adverse effects of B-adrenergic blockers?
Ex: propanolol, metoprolol, atenolol
MOA: block B1 receptors which results in lowering HR, contractility, CO, and BP; O2 demand reduced both at exertion and at rest; should not be used in vasospastic angina
indications: drug of choice to treat effort induced angina
- no intrinsic sympathomimetic activity metoprolol is useful in treatment of patients with MI
- patients with classic angina: B-blockers used with nitrates to increase excersise tolerance
pharmokinetics: all B blockers are non selective at high doses (propanolol is generally non selective)
adverse effects: contraindicated in patients with asthma, diabetes, severe bradycardia, peripheral vascular disease, and COPD
What is the MOA, indications, pharmokinetics and adverse effects of Ca2+- channel blockers?
-Ca2+ increases in ischemia because of membrane depolarization that hypoxia produces; all Ca2+ blockers decrease BP and may worsen heart failure due to negative inotropic effect
MOA: inhibit entrance of Ca2+ into cardiac and smooth muscle system of the heart; all are vasodilators of the coronary arteries
indications: used in the treatment of effort induced angina to reduce oxygen consumption by decreasing afterload
What is the MOA, indications, pharmokinetics and adverse effects of Nifedipine?
MOA: arteriolar vasodilator with minimal effect on cardiac conduction of HR
indications: variant angina caused by spontaneous coronary spasm
pharmokinetics: orally as extended release tablets undergoing hepatic metabolism and being eliminated in urine and feces
adverse effects: flushing, headache, hypotension, and peripheral edema, constipation (with all Ca2+ blockers), no sympathetic activity so it may cause reflex tachycardia if peripheral vasodilation occurs
What is the MOA, indications, pharmokinetics and adverse effects of Verapamil?
MOA: slows cardiac AV conduction directly and decreases HR, contractility, BP and O2 demand
-greater negative inotropic effect with weak vasodilator action
indications: mainly affects myocardium
pharmokinetics: metabolized by liver
adverse effects: contraindicated in patients with preexisting depressed cardiac function or AV conduction abnormalities, constipation
What is the MOA, indications, pharmokinetics and adverse effects of Diltiazem?
MOA: similar to verapamil
-slow AV conduction and decreases firing rate of the sinus node pacemaker, reduces HR and decreases BP
indications: relieve coronary artery spasms in patients with variant angina
pharmokinetics: extensively metabolized by the liver
adverse effects: same as other Ca2+ blockers
What is the MOA, indications, pharmokinetics and adverse effects of Diltiazem?
MOA: similar to verapamil
-slow AV conduction and decreases firing rate of the sinus node pacemaker, reduces HR and decreases BP
indications: relieve coronary artery spasms in patients with variant angina
pharmokinetics: extensively metabolized by the liver
adverse effects: same as other Ca2+ blockers
What is the MOA, indications, pharmokinetics and adverse effects of Na+ blocker Ranolazine?
MOA: inhibits late phase of Na+ current which improves O2 supply and demand
-reduces Na+ and Ca2+ overload which improves diastolic function
indications: treatment of patients with chronic angina in combination therapy or alone; mostly used in patients who have failed all other antianginal therapies
- do not use in acute attack of angina
