Tx of Angina Flashcards
What is angina?
lack of sufficient oxygen (ischemia) to the heart which causes chest pain
What is the main mechanism of angina?
coronary artery obstruction limiting blood supply to part of the myocardium
What are the three main mechanisms of angina?
-atherosclerosis and thrombosis block blood flow (unstable angina)-Prinzmetal angina-exertional angina, where oxygen demands can be met at rest but not upon exertion
Describe unstable anginas
These are recurrent anginas associated with minimal exertion, prolonged and frequent pain, and are though to be due to fissuring of atherosclerotic plaque and subsequent platelet aggregation.These have a high correlation with myocardial infarction
Describe Prinzmetal (variant) anginas
a direct result of reduction in coronary flow due to vasospasm, not an increase in myocardial oxygen demand that carries an excellent prognosis
T or F. Angiograms with Prinzmetal (variant) anginas are abnormal
F. They will be normal usually
What is the end-stage of exertion angina?
typically need surgical re-vascularization or angioplasty
What are some of the approaches for treating angina?
-increase coronary blood flow-reduce myocardial oxygen consumption-prevent platelet deposit/aggregation (aspirin)
How can we reduce myocardial oxygen consumption?
- reduce HR- reduce contractility- reduce ventricular work by decreasing after load or preload
When does perfusion of the heart occur?
diastole- only during diastole are the vessels that extend down into the myocardial wall open to provide perfusion to the myocardium- so any therapy that reduces contractility will increase perfusion
Briefly describe the anatomy of blood vessels in the myocardial wall (not the coronary arteries and its branches but lower level).
epicardial arteries (coronary, etc.) on the surface of the heart give rise to perpendicularly extendedly intramural arteries that extend down into the myocardium and then connect to a large sub-endothelial plexus near the most inner portion of the wall. Arterioles brand from the intramural arteries at various depths
Why would slowing the HR be good for angina?
because it allows the heart to spend more time in diastole
What do nitrates do?
cause:- veno/vasodilation resulting in decreased preload AND afterload- coronary vasodilation (can prevent or reverse prinzmetal)
What are the overall effects on hemodynamics of nitrates at usual doses?
-unchanged or slight decrease in BP-unchanged or slight increase in HR (due to reflex)-PVR decreased-CO reduced slightly
What are the major effects of non-dyhydropyridine CCBs?
direct effect on heart to reduce heart work (demand)- reduce chrono, dromo, and ino, increases coronary vasodilation (good for prinzmetal), reduce after load (not preload)better for angina than the dihydropyridines and should never be combined with a BB
What are the major effects of dyhydropyridine CCBs?
potent vasodilator, reduces afterload and increase coronary vasodilation
What is the reflex effect of dyhydropyridine CCBs?
reflex tachycardia via increased HR and contractility, AV node unaffected
So how are dyhydropyridine CCBs in angina given?
only in combo with a BB
Which anginas are CCBs best for?
exertional and Prinzmetal
Are CCBs effective in patients with coronary heart disease? BBs?
they fail to consistently reduce re-infarction or CHD death and are associated with INCREASED morbidity and mortality in those with impaired LV functionIn contrast, BBs are very effective
What is another source of concern with CCBs in angina?
they may inhibit apoptosis, promoting cancer cell growth
So what is the 1st line for angina?
BBs, and CCBs are reserved for those unable to tolerate BBs or as adjunctive therapy
What are the main effects of BBs?
-reduce HR and inotropy-reduce after loaddo not reduce preload or coronary vasospasm
What is the rationale for combining BBs with nitrates?
-reduce LVEDP, LV volume, and cause dilation of coronary arteries
