Drugs Used in Chronic IHD - Lecture Flashcards Preview

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chronic ischemic heart disease

Characterized by partial occlusion of coronary artery


Classic angina (angina of effort, stable angina)

occlusion of coronary arteries resulting from formation of atherosclerotic plaque

-most common form of angina

-symptoms occur during exertion or stress


Variant (Prinzmetal) angina

episodes of vasoconstriction of coronary arteries

-likely genetic in origin
-symptoms occur at rest
-much less common than classic angina



imbalance between oxygen demand of the heart and oxygen supply via the coronary arteries

balanced at rest - no symptoms

During exertion (exercise or stress): oxygen demand on the heart >> supply of oxygen through partially blocked coronary artery --> chest pain


Treatments to increase (or restore) coronary blood flow - surgical and non-surgical revascularization approaches

Coronary artery bypass grafting

Percutaneous transluminal coronary angioplasty (PTCA)

Atherectomy - tip of catheter shears off the plaque

Stent - expandable tube used as scaffolding to keep vessel open
-drug-eluting stents (anti proliferative drugs)


Vasodilator clinical use in vasospastic (Prinzmetal) angina

relieve coronary spasm
restore blood flow into ischemic area


vasodilators in atherosclerotic (classic) angina

not useful!


Coronary Steal Phenomenon

redistribution of blood to non-ischemic areas

associated with dilation of small arterioles (ex. potent arteriolar vasodilators - dipyridamole)


Endothelium dependent vascular relaxation

Release of endothelium-derived relaxation factor (EDRF) by ACh


Vascular effects of NO


Platelet aggregation
monocyte adhesion
smooth muscle cell proliferation
Superoxide radical
LDL oxidation


NO mechanism to vasodilation

NO binds to guanylyl cyclase, which converts GTP to cGMP

cGMP activates protein kinase G which
1) leads to Myosin-LC Dephosphorylation and leads to smooth muscle relaxation
2) opens potassium channel which leads to hyper polarization and reduced calcium entry


Mechanism of action of nitrates

Nitrates donate NO via ADH2 Thiols

NO --> Vascular smooth muscle relaxation leads to:
1) venous dilations, reduced preload, decreased O2 demand - treats Angina of effort
2) coronary artery dilation, coronary spasm relief - treats variant angina


Anti-Anginal mechanisms of CCBs

Decreased myocardial O2 demand - operates in atherosclerotic angina

- Dilation of peripheral arterioles: decreased PVR and after load, decreased BP
-arterioles more affected than veins - less orthostatic hypotension
-Dihydropyridines more potent vasodilator

-Decreased cardiac contractility and HR (observed with cardioactive CCBs)

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


Beta-blocker MOA in angina

decreased myocardial oxygen demand

-Decrease in HR leads to improved myocardial perfusion and reduced oxygen demand at rest and during exercise
-decrease in contractility
-decrease in BP leads to reduced afterload


Ischemic myocardium membrane potential abnormalities

Ischemic myocardium 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 MOA in angina

normalizes depolarization of cardiac myocytes and reduced mechanical dysfunction
-may reduce diastolic tension and compression of coronary vessel in diastole
-may reduce cardiac contractility and oxygen demand