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Cardiovascular & Respiratory Pharmacology (Karen) > Treatment of Ischaemic Heart Disease (IHD) > Flashcards

Treatment of Ischaemic Heart Disease (IHD) Flashcards

1
Q

What is variant or vasospastic angina?

A

Coronary spasm at rest, unpredictable

Unknown mediator, difficult to treat

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2
Q

What is the concern in crescendo angina?

A

Thrombus formation leading to MI

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3
Q

What happens to arterioles when there is arterial occlusion?

A

They are maximally dilated even at rest;

tf very little coronary reserve to respond to increased O2 demands of cardiac muscle –> angina, MI

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4
Q

What are the aims in treating stable angina?

A
  • prevent attacks and progression to MI
  • relieve symptoms by
    • increasing O2 (-HR = more time in diastole = more coronary filling)
    • reduce O2 demand (-CO, -SV, -HR, -preload through venous dilation, -afterload through arteriole dilation and -resistance)
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5
Q

What is the mechanism of nitrates in angina tx?

A

target: preload; prophylactic and symptom-relieving

  • biotransformation
  • release NO from endothelium into vascular SM
  • stimulates guanylate cyclase:
    • CTP –> cGMP
  • cGMP dephosphorylates myosin light chain (can’t int w/actin)
  • vascular relaxation
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6
Q

cGMP causes

A

relaxation of all vessels

major effect on veins (tf -preload)

minor effect on large arteries (-afterload), coronary arteries (no effects if stenosed)

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7
Q

what is coronary steal?

A

dilation of coronaries causes increased blood supply to already perfused areas, away from poorly perfused areas

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8
Q

glyceryl trinitrate (GTN, nitroglycerin)

A
  • angina
  • short acting
  • 1st-pass metabolism (i.e. broken down by liver)
    • tf admin sublingual in acute attack, anticipation of effort
    • transdermal for prophylaxis
    • i.v. for emerge
  • absorbed by plastic, unstable, light-sensitive
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9
Q

isosorbide dinitrate

A
  • angina: prophylactic, anticipation of exertion
  • longer acting
  • 1st pass metabolism
    • taken orally –> active compound isosorbide-5-mononitrate
  • dilates veins
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10
Q

What are the adverse effects of nitrates in angina tx?

A
  • cGMP –> non-significant SM relaxation in gut, airways
  • postural hypotension
  • venous pooling
  • reflex tachycardia to drop in BP (tf co-Rx w/b-blockers or cardiac-selective Ca2+ channel blocker to -HR)
  • headache, flushing (cerebral, head, neck, arterial dilation)
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11
Q

why is GTN/nitroglycerin contraindicated with viagra?

A
  • viagra is a phosphodiesterase inhibitor
    • inh the breakdown of cGMP, cAMP
  • GTN ++cGMP
  • viagra –breakdown cGMP
  • +++relaxation in SM
  • fatal decrease in BP
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12
Q

What is the mechanism of GTN tolerance in angina tx?

A

classic:

  • -tissue thiols req’d for NO production from GTN
    • prevented by co-Rx w/N-acetyl cysteine

new:

  • increased sensitivity to vasoconstrictors (ANGII, catecholamines) making it harder to dilate
  • increase in endothelial ROS, scavening NO
  • reduced/abnormal activity in ALDHS (mitochondrial enzyme) leading to -NO and +ROS
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13
Q

verapamil

A
  • Ca2+ channel blocker
  • equally selective for vascular and cardiac Ca2+ channels
  • contraindicated in heart failure
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14
Q

nifedipine

A
  • Ca2+ channel blocker
  • selective for vascular Ca2+ channels
  • can be used for hypertension, angina treatment
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15
Q

What is the mechanism of cardioselective Ca2+ channel blockers in angina tx?

A
  • -Ca2+ entry to heart (SA, AV, muscle) through L-type channels
  • -HR (+O2 supply)
  • -SV, -CO, -O2 demand
  • mostly verapamil and diltiazem
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16
Q

What is the mechanism of vascular-selective Ca2+ channel blockers in angina tx?

A
  • block Ca2+ entry into vessels via L-type & receptor-operated channels
  • +arterial dilation
  • -afterload
  • -O2 demand
  • e.g. nifedipine, felodipine
17
Q

What are the adverse effects of Ca2+ blockers in angina tx?

A
  • prophylactic use
  • verapamil:
    • flushing, headache, oedema
      • oedema bc CCB’s only target arterial SM and cause dilation; don’t get accommodating venodilation
    • bradycardia, AV block
      • **contraindicated w/B-blockers
  • nifedipine:
    • flushing, headache, oedema ^^
    • hypotension
    • reflex tachycardia
      • **co-Rx w/B-blockers
18
Q

What is the mechanism of beta-blockers in angina tx?

A

prophylactic use

  • block effects of SNS on cardiac B1-aRs
    • -HR @ SA, AV
    • -contractility, SV @ muscle
    • +diastole
    • +coronary perfusion
    • +O2 supply
    • -CO
    • -O2 demand
19
Q

What are the adverse effects of beta-blocker use in angina tx?

A
  • first-line therapy for prophylaxis is atenolol and propranolol
    • atenolol is cardio-B1 selective
    • propranolol is non-selective (B1, B2)
      • tf get effects of bronchoconstriction and fatigue in skeletal muscle
20
Q

How does ivabradine function to decrease HR?

A
  • blocks the Ifunny current at the leaky Na+-in K+-out channel in the SA node
  • reduces the slope of the diastolic depolarization
  • increases time to threshold
  • increased time between beat
  • increased dialstolic coronary filling time
  • tf -myocardial O2 demand, +O2 supply
21
Q

What is the benfit of ivabradine?

A
  • decreases HR without affecting:
    • myocardial contractility and relaxation
    • AV conduction
    • ventriular repolarization
  • tf cardiac function and BP are maintained
    • compared to atenolol (blocks all B1-mediated cardiac effects, and verapamil which -contractility and rate)
  • preserves endothelium-mediated vasodilation at rest and exercise
    • +exercise toleramce +coronary blood flow
    • compared to atenolol which can cause reflex vasoconstriction in coronary arteries at the A1-aRs due to a drop in BP
22
Q

What additional benefit does ivabradine offer that other angina tx do not?

A

has been shown to decrease risk of MI and need for revascularization in pt with IHD and LV dysfunction

(if bpm > 70)

23
Q

What are the adverse effects of ivabradine?

A
  • If current in retina tf get birghtness in visual field
  • conduction abnormalities
24
Q
A
25
Q

What is the treatment for variant angina?

A
  • short-acting nitrates (GTN) for acute coronary spasm
  • prophylaxis w/dihydropyridine Ca2+ channel blocker
    • contraindicates B-blocker use
      • vasospasm via a-adrenoceptor may be worsened if B2-mediated coronary dilation is blocked
26
Q

What is the tx for unstable angina?

A
  • same as classic
  • plus aspirin to prevent thrombosis
27
Q

What are the revascularisation tx for angina?

A
  • PCI - percutaneous coronary intervention
  • CABG - coronary artery bypass graft

Cardiovascular & Respiratory Pharmacology (Karen) (15 decks)

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