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cardio week 3 > Treatment of Angina > Flashcards

Treatment of Angina Flashcards

1
Q

What is angina?

A

lack of sufficient oxygen (ischemia) to the heart which causes chest pain

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2
Q

What is the main mechanism of angina?

A

coronary artery obstruction limiting blood supply to part of the myocardium

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3
Q

What are the three main mechanisms of angina?

A
  • atherosclerosis and thrombosis block blood flow (unstable angina)
  • Prinzmetal angina
  • exertional angina, where oxygen demands can be met at rest but not upon exertion
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4
Q

Describe unstable anginas

A

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

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5
Q

Describe Prinzmetal (variant) anginas

A

a direct result of reduction in coronary flow due to vasospasm, not an increase in myocardial oxygen demand that carries an excellent prognosis

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6
Q

T or F. Angiograms with Prinzmetal (variant) anginas are abnormal

A

F. They will be normal usually

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7
Q

What is the end-stage of exertion angina?

A

typically need surgical re-vascularization or angioplasty

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8
Q

What are some of the approaches for treating angina?

A
  • increase coronary blood flow
  • reduce myocardial oxygen consumption
  • prevent platelet deposit/aggregation (aspirin)
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9
Q

How can we reduce myocardial oxygen consumption?

A
  • reduce HR
  • reduce contractility
  • reduce ventricular work by decreasing after load or preload
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10
Q

When does perfusion of the heart occur?

A

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

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11
Q

Briefly describe the anatomy of blood vessels in the myocardial wall (not the coronary arteries and its branches but lower level).

A

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

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12
Q

Why would slowing the HR be good for angina?

A

because it allows the heart to spend more time in diastole

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13
Q

What do nitrates do?

A

cause:

  • veno/vasodilation resulting in decreased preload AND afterload
  • coronary vasodilation (can prevent or reverse prinzmetal)
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14
Q

What are the overall effects on hemodynamics of nitrates at usual doses?

A
  • unchanged or slight decrease in BP
  • unchanged or slight increase in HR (due to reflex)
  • PVR decreased
  • CO reduced slightly
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15
Q

What are the major effects of non-dyhydropyridine CCBs?

A

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

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16
Q

What are the major effects of dyhydropyridine CCBs?

A

potent vasodilator, reduces afterload and increase coronary vasodilation

17
Q

What is the reflex effect of dyhydropyridine CCBs?

A

reflex tachycardia via increased HR and contractility, AV node unaffected

18
Q

So how are dyhydropyridine CCBs in angina given?

A

only in combo with a BB

19
Q

Which anginas are CCBs best for?

A

exertional and Prinzmetal

20
Q

Are CCBs effective in patients with coronary heart disease? BBs?

A

they fail to consistently reduce re-infarction or CHD death and are associated with INCREASED morbidity and mortality in those with impaired LV function

In contrast, BBs are very effective

21
Q

What is another source of concern with CCBs in angina?

A

they may inhibit apoptosis, promoting cancer cell growth

22
Q

So what is the 1st line for angina?

A

BBs, and CCBs are reserved for those unable to tolerate BBs or as adjunctive therapy

23
Q

What are the main effects of BBs?

A
  • reduce HR and inotropy
  • reduce after load

do not reduce preload or coronary vasospasm

24
Q

What is the rationale for combining BBs with nitrates?

A

-reduce LVEDP, LV volume, and cause dilation of coronary arteries

25
Q

What is the rationale for combining BBs with dihydropyridine CCBs?

A

prevents coronary vasospasm and reduces systemic vascular resistance

26
Q

How should BBs be used for unstable angina?

A

use with nitrates, ASA, and Heparin

27
Q

How do BBs affect exertional angina?

A

reduce HR and inotropy

28
Q

How do BBs affect Prinzmetal angina?

A

not effective because they can block B2 which have a vasodilator effect

29
Q

Can BBs be used in MI?

A

yes, they reduce chest pain, ST elevation, ventricular fib, re-infarction rates during hospitalization, and overall mortality during 2-3 yrs post MI

30
Q

What is the recommended therapy for acute MI/unstable angina?

A

give BB IV followed by PO therapy provided no CHF, hypotension, or sinus bradycardia/heart block

31
Q

What is Ranolazine?

A

heart metabolic demand reducer that may be a late sodium current inhibitor (no hemodynamic effect- no changes on HR or BP) used in chronic stable angina in combo with amlodapine, BBs, or nitrates

will not relieve acute angina attack

32
Q

Contraindications of Ranolazine?

A
  • pregnancy
  • CYP3A4 inhibitor (avoid others-verapamil, diltiazem, cyclosporine, AZOLES, grapefruit)
  • existing prolonged QT
  • concurrent use of class Ia or II anti-arrhythmics
  • tricyclic antidepressants
  • hepatic impairment
33
Q

Adverse effects of Ranolazine?

A
  • dizziness, headache
  • constipation, N/V
  • increase in creatinine, BUN
34
Q

What does Ranolazine do do digoxin?

A

increases concentration 40-60% via P-gp inhibition

35
Q

Benefits of Ranolazine?

A

increasing exercise tolerance and decreasing time to onset of angina. No improvement on CV death or recurrent MI

36
Q

What agents are used in CHD?

A
  • all should receive aspirin (85-325 mg/day) unless contraindicated
  • BBs reduce CHD events (nitrates don’t, CCBs variable)
  • thrombolytic therapy post MI
  • LDL reducers and HDL raising/TAH lowering also prevent CHD/MI death up to 35%

cardio week 3 (16 decks)

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