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CV Pharmacology > IHD Treatment > Flashcards

IHD Treatment Flashcards

1
Q

What are the dihydropyridine CCBs?

A

Nifedipine, Amlodipine, Felodipine, Nicardipine, Isradipine

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2
Q

What are the non-dihydropyridine CCBs?

A

Verapamil, Diltiazem

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3
Q

How are CCBs cardioselective?

A

They work on L-type voltage-dependent Ca2+ channels that are responsible for phase 2 of the cardiac & pacemaker action potential. They have large conductance and slow inactivation.

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4
Q

What is the mechanism of action of CCBs?

A
  • increased time that channels are closed, which reduces the magnitude of the current and therefore contraction
  • induce relaxation of arterial smooth muscle to reduce afterload
  • non-DHPs reduce inotropy, slow AV conduction, and slow pacemakers
    • slow recovery of the Ca2+ channel
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5
Q

What are the differences between the two classes of CCBs?

A
  • Dihydropyridines: selective vasodilators in periphery and heart
    • can cause reflex tachycardia
      • Must use with beta-blockers
    • voltage-dependent binding - bind to channels responding to slow changes in voltage (smooth muscle cells)
  • Non-DHPs: equal effects on cardiac tissue & vasculature
    • use-dependent binding - bind to channels constantly opening & closing (cardiac cells)
    • Never use with beta-blockers
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6
Q

How are CCBs metabolized?

A
  • absorbed from GI tract
    • extensive first-pass metabolism
  • eliminated via hepatic metabolism
    • reduce dose in hepatic disease
    • metabolized by & inhibit CYP3A4
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7
Q

Why are CCBs formulated for slow release?

A
  • most have short plasma half-life
  • absence of bolus effect that causes reflex tach, headache, & coronary steal
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8
Q

What are the adverse effects of dihydropyridines?

A
  • pregnancy category C, crosses placenta & breast milk
  • excessive vasodilation → dizziness, hypotension, headache
  • GI irritation
  • peripheral edema
  • coronary steal worsening angina
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9
Q

What are the adverse effects of non-dihydropyridines?

A
  • bradycardia, asystole, AV block
    • NEVER GIVE WITH BETA-BLOCKERS
  • CHF
  • constipation
  • pregnancy category C
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10
Q

What are the drug interactions of non-DHPs?

A
  • metabolized and inhibit CYP3A4
    • can increase plasma levels of statins
    • rifampin will decrease levels
  • verapamil reduces clearance of digoxin
  • beta-blockers cause increased risk of SA or AV block
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11
Q

What is the molecular mechanism of action for nitrates?

A
  • Organic nitrate ester reductase induces denitration and releases NO
  • NO activates guanylate cyclase to cause an increase in cGMP
  • cGMP activates PKG
  • PKG induces smooth muscle relaxation by reducing [Ca2+]
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12
Q

What are the CV effects of nitrates?

A
  • venodilation decreases preload
    • decreased pressure in diastole improves coronary a perfusion
  • coronary vasodilation
    • reverses/prevents vasospasm
  • hemodynamic changes
    • BP unchanged or slight decrease
    • HR unchanged or slight increase
    • pulmonary vascular resistance decreased
    • cardiac output slightly reduced
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13
Q

What are the adverse effects of nitrates?

A
  • hypotension
    • reflex tachycardia that worsens angina
    • dizziness, orthostatic hypotension, syncope
  • headache (transient)
  • drug rash (with long-lasting and cutaneous)
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14
Q

Why should nitrates never be taken with Sildenifil (Viagra)?

A
  • Sildenifil is type V PDE inhibitor
    • increases cGMP by preventing breakdown
  • exaggerated cGMP response can cause profound hypotension and MI from blood pooling
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15
Q

What is the mechanism of nitrate tolerance?

A
  • depletion of tissue cystein required for conversion to NO
  • volume expansion, neurohumoral activation
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16
Q

What drugs are used to treat angina?

A

Nitrates (drug of choice), beta-blockers, CCBs, & Ranazoline (Ranexa)

17
Q

How do you treat angina?

A
  • increase coronary blood flow
  • reduce myocardial O2 consumption
    • decrease chronotropy
    • decrease inotropy
    • decrease preload (venodilation) or afterload (vasodilation)
  • prevent platelet aggregation with aspirin
18
Q

What are the indications for using dihydropyridine CCBs in angina?

A
  • when combined with a beta-blocker
  • with sinus bradycardia, SA/AV block
  • valvular insufficiency due to reduction of aftelroad)
19
Q

What are the indications for using non-dihydropyridine CCBs in angina?

A
  • asthma or COPD
  • insulin-dependent diabetes
  • severe peripheral vascular disease
  • depression
  • must have good LV function
20
Q

Why are CCBs reserved for treating angina when beta-blockers can’t be administered or aren’t fully effective?

A
  • fail to reduce reinfarction or death in pts with CHD
  • increase morbidity & mortality in patients with LV dysfunction
  • significantly higher rates of MI & CHF when used for hypertension
21
Q

How do beta-blockers treat angina?

A
  • decrease oxygen demand by reducing HR and contractility with exercise
    • also increases coronary artery perfusion
  • decrease afterload
  • do not prevent vasospasm
  • combined with nitrates or dihydropyridine CCBs to prevent reflex tachycardia and increases in inotropy
22
Q

When are beta-blockers contraindicated with acute MI/unstable angina?

A

with CHF, hypotension, sinus bradycardia, heart block

23
Q

What is the mechanism of action of Ranolazine?

A
  • FA oxidase inhibitor - increases glucose oxidation and O2 utilization efficiency
  • late Na+ current inhibitor - prevents Ca2+ overload and reduces diastolic wall stress
  • no effect on HR and BP
24
Q

What are the indications fo Ranolazine use?

A
  • chronic stable angina with amlodapine, beta-blockers, or nitrates
  • not for acute angina
25
Q

What are the adverse effects of Ranolazine?

A
  • dizziness, headache, constipation, nausea
  • <1% syncope and asthenia
  • small, reversible elevations in serum creatinine and BUN
26
Q

What are the contraindications for Ranolazine use?

A
  • use of CYP3A4 inhibitors (like verapamil, diltiazem, amiodarone)
  • long QT
  • Digoxin due to p-gp inhibition
  • hepatic impairment
27
Q

How effective is Ranolazine in treating IHD?

A
  • modest benefit for increasing time to onset of anginal pain
  • no improvement in mortality or recurrent MI
  • pair with beta-blockers, nitrates, and amlodapine
28
Q

What therapies are used to prevent events or death from MI or CHD?

A
  • beta-blockers
  • aspirin
  • ACEI with LV dysfunction
  • revascularization
  • thrombolytic therapy
  • LDL reduction with statin
  • HDL raising

CV Pharmacology (5 decks)

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