Drugs for Angina and Ischemic Heart Disease Flashcards Preview

Cardiovascular II > Drugs for Angina and Ischemic Heart Disease > Flashcards

Flashcards in Drugs for Angina and Ischemic Heart Disease Deck (48)
Loading flashcards...


-Ca2+ mediates smooth muscle contraction; enters cells via voltage dependent calcium channels

-CCBs block Ca2+ entry to relax vascular smooth muscle

-vasculature does NOT have troponin so acts on Myosin-light chain kinase system (Ca2+-calmodulin sensitive)


Anti-anginal mechanisms of CCBs

-Decreased myocardial O2 demand (Classic angina)

-Dilation of peripheral arterioles

-Decreased PVR and after load, decreased BP

-Arterioles more affected than veins (less orthostatic hypotension)

-DHPs are more potent vasodilaters

-Decreased cardiac contractility and heart rate (seen with non-DHPs)

-increased blood supply (operates in variant angina)--dilation of coronary arteries relieves local spasm


Major adverse effects of CCBs

-cardiac depression, cardiac arrest, and acute heart failure (cardioactive CCBs)

-bradyarrythmias, AV block (cardioactive CCBs)

-short acting DHP CCBs--vasodilation triggers reflex sympathetic activation


Nifedipine adverse effects

-immediate release

-increases risk of MI in patients with HTN--slow-release and long-acting DHPs are better tolerated

-causes tachycardia due to hypotension and associated baroreflex


Minor adverse effects of CCBs

-flushing, headache, anorexia, dizziness

-peripheral edema



Beta-blockers indicated in angina






MOA of B-blockers in angina

-decreased myocardial O2 demand

-decrease HR leads to improved myocardial perfusion and reduced O2 demand at rest and during excercise

-Decrease in contractility

-Decrease in BP leads to reduced afterload


B-blockers adverse effects

-reduced CO


-impaired liver glucose mobilization

-produce and unfavorable blood lipoprotein profile (increase VLDL and decrease HDL)

-sedation, depression

-withdrawl syndrome associated with sympathetic hyperresponsiveness


B-blocker contraindications


-peripheral vascular disease

-Raynaud's syndrome

-Type 1 diabetics on insulin

-bradyarrhthmias and AV conduction abnormalities

-severe depression of cardiac function


Effects of Nitrates alone in treatment of angina pectoris

-reflex increase in HR

-decrease in arterial pressure

-decrease EDV

-reflex increase contractility

-decrease in ejection time


Effects of B-blockers or CCBs alone in treatment of angina pectoris

-decreases HR, arterial pressure, contractility

-increases EDV and ejection time


Effects of combined nitrates with B-blockers or CCBs in treatment of angina pectoris

-decrease HR, arterial pressure

-no change or decrease in EDV

-no change in contractility, ejection time


Ranolazine MOA

-inhibits late Na+ currents in cardiomyocytes

-ischemic myocardium is often partially depolarized

-Na+ channel in cardiomyocytes is voltage-gated

-Late Na+ current is enhanced in ischemic myocardium and brings about Ca2+ overload and depolarization abnormalities

-Ranolazine normalizes repolarization of cardiac myocytes and reduces mechanical dysfunction

-reduce diastolic tension and compression of coronary vessels in diastole and reduces cardiac contractility and O2 demand


Ranolazine may reduce

-diastolic tension and compression of coronary vessels in diastole

-may reduce cardiac contractility and oxygen demand


Ranalozaine does not affect

-heart rate

-general ionotropic state of myocardium

-coronary blood flow

-peripheral hemodynamics


Ranolazine clinical use

-stable angina which is refractory to standard medications

-decreases angina episodes and improves exercise tolerance in patients taking nitrates, or amlodipine, or atenolol


Ranolazine adverse effects

-QT interval prolongation--may trigger polymorphic ventricular arrhythmias






Ranolazine drug interactions

-metabolized by CYP3A4/5--interaction with drugs that modulate the activity of these enzymes

-do not combine with strong CYP3A inhibitors: anti fungal azaleas, verapamil

-inhibits CYP2D6--increases half life of Amitriptyline, Fluoxetine, metoprolol, opioid drugs

-drugs that prolong QT interval--certain anti arrhythmic (Quinidine) and antipsychotic drugs (Thioridazine)--may trigger ventricular arrhythmias