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Flashcards in Angina Tx Deck (31):
1

nitrate

release NO -> GC ->increase cGMP -> relax vascular sm. muscle -> venodilation and coronary vasodilation
CO and pulmonary vascular resistance reduced
HR and BP same
AE: hypotension, tachycardia (may worsen angina), dizzy, syncope, headache (tolerance develops), loss of efficacy with continuous exposure (nitrate free interval at night)
CI: sildenifil (PDE5 inhibitors)

2

How does venodilation reduce angina?

decrease preload: reduce wall stress and MvO2
subendocardial blood flow increased

3

How does coronary vasodilation reduce angina?

prevents/reverses coronary vasospasm
redistribution of blood flow to area of ischemia; selective dilation of epicardial and collateral coronary vessels

4

sublingual tablet nitrate

fast onset, short duration
small dose

5

buccal nitrate

aerosol: fast onset, short duration
small dose
tablet: med. duration

6

isosorbide dinitrate

oral nitrate
med. onset and duration

7

Nitro-SR capsule

oral nitrate
med. onset, 8-12 hours

8

isosorbide mononitrate

oral nitrate
med. onset, 8-12 hours
use eccentric dosing

9

transderm nitro

patch: MUST remove at night
med. onset, duration: 24 hrs
small dose
AE: rash

10

nitrol 2% ointment

med. onset and duration

11

IV nitrate

immediate onset
titrate dose up to maintain effect
do NOT suddenly interrupt in unstable angina: can get coronary vasospasm (overlap with other forms)

12

How does nitrate tolerance occur?

volume expansion, neurohumoral activation, depletion of cysteine stores needed to release NO

13

Dihydropyridine

voltage-dependent binding: selective vasodilators: reduce after load
AE: GI, edema, coronary steal (decreased with slow release), increase HR, contractility and O2 demand
CI: hypotension, advanced CHF
ONLY use with B-blocker
Use in angina when patients (with B-block) with valvular insufficiency, bradycardia, SA/AV block

14

Non-dihydropyridine

Use-dependent binding: equipotent for cardiac tissue and vasculature
use: a. fib, PSVT, prevent/reverse VASOSPASM
AE: bradycardia, systole, AV block
CI: B-blocker, CHF
cross placenta/breast milk
Use in angina when patients have asthma, COPD, severe PVD, DM

15

verapamil

non-dihydropyridine
metabolized by and inhibits CYP3A4

16

diltiazem

non-dihydropyridine
metabolized by and inhibits CYP3A4

17

nifedipine

dihydropyridine

18

amlodipine

dihydropyridine

19

felodipine

dihydropyridine
long T1/2

20

nicardipine

dihydropyridine

21

isradipine

dihydropyridine
long T1/2

22

Ca effects on
1. cardiac muscle
2. sm. muscle (arterial)

1. intracellular Ca binds troponin C removing tropomyosin: actin-myosin can contract
2. bind calmodulin to activate MLCK which phosphorylates myosin triggering contraction

23

Ca channel blockers

inhibit L-type Ca channel
other Ca channels (neural N and P-type) insensitive
extensive first pass metabolism
short T1/2: now have slow release formulas
USE: exertional and vasospastic angina
add on to B-blockers or for patients unable to tolerate B-blockers
concerns: HTN: higher rates of MI and CHF, inhibit apoptosis (cancer)

24

ranazoline

metabolic modulator: MOA unknown
partial FA oxidase inhibitor (increase glucose oxidation and efficiency of O2 utilization)
use: chronic stable angina in combo with amlodapine, B-block, nitrate
NOT for acute angina
expensive
AE: dizzy, headache, constipation, nausea, increased BUN/creatine, syncope, asthenia
CI: CYP3A4 inhibitors, prolonged QT, class IA or III, tricyclic antidepressants, increase digoxin concentrations (inhibit p-gp), hepatic or renal impairment
no improvement for mortality

25

B-blockers

first choice in angina
reduce mortality (MI and CHD)
reduce after load, HR, inotropy
does NOT: prevent vasospasm or reduce preload
combine with nitrates: reduce LVEDP, LV volume, dilate coronary artery
CCB (dihydropyridine): prevent vasospasm, reduce vascular resistance
*block reflex tachycardia and inotropy of nitrates and CCB
Unstable: with nitrates, ASA, heparin
Exertional: reduce HR, contractility
MI

26

prinzmetal's angina

variant
vasospasm blocks flow
normal coronary angiograms, excellent prognosis

27

unstable angina

atherosclerosis or thrombosis blocks flow
recurrent with minimal exertion, prolonged and frequent
HIGH correlation with myocardial infarction

28

exertional angina

coronary circulation can meet oxygen demands on myocardium at rest, but now when heart work is increased by exercise due to atherosclerosis
usually due to fixed coronary vascular obstruction
Tx: surgical revascularization or angioplasty

29

Ways to Tx angina

1. increase coronary flow
2. reduce MvO2 (decrease HR, contractility, work load (preload/afterload)
3. prevent platelet deposition and atherosclerosis (aspirin and statins)

30

When does perfusion of the heart occur?

diastole
slow HR increases time spent in diastole for heart perfusion

31

Preventing MI and CHD in patients with angina

1. B-blockers
2. aspirin
3. ACE I
4. revascularization (angioplasty, CABG, atherectomy)
5. thrombolytics
6. LDL reduction/HDL increase