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IC 1.0 > Treating Angina > Flashcards

Treating Angina Flashcards

1
Q

What is the principle type of heart disease?

A

CAD

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2
Q

What are the primary risk factors for CAD? How common are these risk factors?

A

half of Americans have at least one:

  • hypertension
  • high LDL
  • smoking
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3
Q

What is angina? What is the underlying event that elicits it?

A
  • it is chest pain or discomfort

- occurs when the amount of blood delivered to the heart by the coronaries isn’t sufficient

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4
Q

What is the primary symptom of heart disease?

A

angina pectoris

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5
Q

What is angina pectoris?

A
  • the primary symptom of heart disease

- it refers to chest pain result from myocardial ischemia

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6
Q

What drug class is used for immediate relief of angina? What about for prophylaxis?

A
  • organic nitrates for immediate relief

- calcium channel blockers and beta blockers for prophylaxis

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7
Q

How is angina often described by patients?

A

as a strangling, vise-like, constricting, or crushing chest pain

  • retrosternal, often radiating down the left arm
  • usually relieved within minutes of rest or administration of nitroglycerin
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8
Q

Where do most patients localize their angina to?

A

retrosternal, often radiating down the left arm

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9
Q

What are the two general types of angina? How do they differ in etiology?

A
  • classic (aka atherosclerotic): atheromatous obstruction of large coronaries, often presenting during exercise
  • variant (aka angiospastic): spasm or constriction of atherosclerotic coronary vessels, often not in the setting of exercise
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10
Q

How does the treatment of classic angina differ from that of variant angina?

A
  • variant is relieved by nitrates or calcium channel blockers
  • classic may be uncontrolled by drugs and require coronary bypass or angioplasty
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11
Q

The oxygen demand of cardiac tissue depends on what?

A

cardiac workload as determined by inotropy, heart rate, and wall stress

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12
Q

Why does angina often present during times of stress or during physical activity?

A

because both increase sympathetic tone and increase the workload of the heart

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13
Q

What is the main energy source in cardiac myocytes? How does this affect it’s oxygen demand?

A

these cells use primarily fatty acid oxidation, which requires more oxygen than glycolysis

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14
Q

How is trimetazidine used in the treatment of angina?

A

it is a pFOX inhibitor which partially inhibits fatty acid oxidation and shifts the heart’s metabolism toward more glycolysis, reducing it’s oxygen demand

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15
Q

What are pFOX inhibitors?

A

drugs that reduce the hearts oxygen demand by inhibiting fatty acid oxidation and shifting the hearts metabolism towards glycolysis

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16
Q

Coronary blood flow is directly related to what two factors?

A
  • perfusion pressure

- duration of diastole

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17
Q

Through what second messenger does NO induce vasodilation?

A

it stimulates GC to produce more cGMP

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18
Q

Through what mechanism does Ranolazine treat angina?

A

its reduces intracellular calcium concentration to reduce cardiac contractility and oxygen demand

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19
Q

Through what mechanism does allopurinol treat angina?

A

it preserves coronary blood flow by inhibiting xanthine oxidase, thereby reducing oxidative stress and endothelial dysfunction

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20
Q

List the short acting nitrates used for treating angina.

A
  • amyl nitrite
  • nitroglycerin
  • isosorbide dinitrate
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21
Q

What are the beneficial effects of nitrates?

A
  • pronounced dilation of large veins, reducing preload
  • reduced ventricular diastolic pressure, improving subendocardial perfusion
  • redistribution of regional coronary blood flow from normal to ischemic areas
  • mild arteriolar dilation, reducing afterload
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22
Q

Are nitrates balanced vasodilators or not?

A

no, they preferentially dilate large veins

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23
Q

What is sildenafil?

A

an inhibitor of PDE-5, an enzyme that normally metabolizes cGMP, and serves to potentiate the effects of nitrate therapy

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24
Q

When using a nitrate with sildenafil, what must you be careful of?

A

sildenafil will potentiate the effects of nitric oxide and could induce severe hypotension leading to myocardial ischemia and infarction

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25
Q

How does cGMP affect platelets?

A

it inhibits aggregation

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26
Q

Nitrates

A
  • a class of drugs used in the treatment of angina
  • function to increase NO release and the downstream effects of cGMP
  • benefits arise from pronounced dilation of large veins reducing preload, redistribution of regional coronary blood flow to ischemic areas, and mild arteriolar dilation which reduces afterload
  • adverse effects include reflex tachycardia and increased inotropy, which increase O2 demand while shortening diastole and cardiac blood supply
  • acute nitrate toxicity can cause strong vasodilation leading to orthostatic hypotension, tachycardia, and throbbing headaches (“Monday disease”)
  • often given sublingual for rapid administration without first pass effect
  • fastest preparations are inhaled amyl nitrite and IV sodium nitroprusside
  • subject to a strong first pass effect by hepatic reductase
  • minimize tolerance, which builds quickly, in those receiving chronic treatment by using the lowest effective dose with nitrate-free intervals of 10-12 hours daily
27
Q

What is the preferred route of administration for nitroglycerin and isosorbide dinitrate? Why?

A

they are given sublingual, which allows for rapid absorption and avoiding hepatic destruction

28
Q

Which oral route of administration isn’t subject to first pass effect?

A

sublingual

29
Q

Oral nitrates are subject to a strong first pass effect by which enzyme?

A

hepatic reductase

30
Q

What is unique about sodium nitroprusside compared to the other nitrates?

A

it dilates arteries and veins equally

31
Q

What are the two fastest acting preparations of nitrate therapy?

A
  • inhaled amyl nitrite

- IV sodium nitroprusside

32
Q

Describe the pharmacokinetics of sublingual nitroglycerin.

A
  • used for immediate anginal relief
  • rapid onset
  • short duration although they avoid first pass effect
33
Q

How is tolerance minimized in those receiving nitrate therapy?

A

in those receiving chronic treatment, the lowest effective dose is administered in addition to nitrate-free intervals of 10-12 hours daily

34
Q

What is “Monday disease”?

A

headache and dizziness experienced by explosives manufactures on Mondays as their tolerance diminishes over weekends

35
Q

What are the two major types of calcium channels in the heart?

A

L-channel (long lasting) and T-channel (transient)

36
Q

What are the two important cardiovascular actions of calcium current?

A
  • triggers contraction of myocardium and vascular smooth muscles
  • required for pacemaker activity of the SA node and conduction through the AV node
37
Q

Calcium channel blockers typically block which specific channel type?

A

L-type channels in the myocardium and vascular smooth muscles

38
Q

Do CCBs induce a balanced vasodilation or not?

A

no, arterioles are more sensitive to the effects than veins

39
Q

Which smooth muscles in the body are most sensitive to the effects of CCBs?

A
  • vascular smooth muscles are most sensitive (arterioles > veins)
  • followed by bronchiolar, GI, and uterine smooth muscle
40
Q

What are 1A, 1B, and 1C CCBs?

A

refer to CCBs that act on different binding sites on the L-type calcium channel

41
Q

What controls the tissue selectivity of calcium channel blockers?

A

the binding site (1A, 1B, or 1C) to which they bind on the L-type calcium channels

42
Q

CCBs work on which calcium channel?

A

L-type

43
Q

What are the three classes of CCBs? How do they differ in action and tissue selectivity?

A
  • dihydropyridines (nifedipine): binds 1A and has vascular selectivity
  • benzothiazepines (diltiazem): binds 1B and has balanced action between the vasculature and heart
  • phenylalkylamine (verapamil): binds 1C and preferentially acts in the myocardium
44
Q

What are the major cardiac effects of CCBs like verapamil?

A
  • decrease contractility
  • reduce SA node impulse generation
  • slow AV node conduction
45
Q

A balanced CCB like diltiazem has what effects?

A
  • preferential dilation of arterioles
  • decreased inotropy
  • slowed SA node impulse generation (low HR)
  • slowed AV node conduction
46
Q

How does the CCB nifedipine affect the heart?

A
  • it has vascular selectivity and causes arteriolar dilation

- because it doesn’t also inhibit calcium channels in the heart, there is a reflex tachycardia

47
Q

Which CCB is most and least likely to elicit reflex tachycardia?

A
  • nifedipine is has vascular selectivity and therefore is most likely
  • verapamil has a strong myocardial depressive effect and is least likely
48
Q

Dihydropyridine CCBs

A
  • 1A CCBs with vascular selectivity
  • act by blocking L-type calcium channels
  • induce coronary and systemic vasodilation, thereby increasing myocardial oxygen delivery and reducing afterload
  • risk of MI due to reflex tachycardia
  • side effects include flushing, edema, dizziness, nausea, and constipation (smooth muscle outside the CV system)
  • also interfere with platelet aggregation and insulin secretion
49
Q

Non-dihydropyridine CCBs

A
  • 1B and 1C CCBs that act on L-type calcium channels
  • 1B are balanced while 1C have more cardiac effects than vascular
  • function to reduce SA automaticity, AV conduction, and inotropy
  • both inhibit reflex tachycardia, in contrast to the dihydropyridines
  • but serious cardiac depression could cause cardiac arrest, CHF, or AV heart block
  • side effects include flushing, edema, dizziness, nausea, and constipation (smooth muscle outside the CV system)
  • also interfere with insulin secretion and platelet aggregation
  • may reduce renal clearance of digoxin and enhance toxicity
  • contraindicated in patients with SA or AV node disturbances
50
Q

What are the side effects of calcium channel blockers?

A
  • inhibition of insulin secretion
  • interference with platelet aggregation
  • flushing, edema
  • dizziness
  • nausea
  • constipation
51
Q

Beta-Blockers in the treatment of angina

A
  • atenolol, metoprolol, and propranolol are the most commonly used for angina
  • act by decreasing sympathetic tone, reducing inotropy, heart rate (prolonged diastole), and afterload (inhibit constriction and some directly induce dilation), without dilating coronary arteries
  • produce better outcomes and symptomatic relief than CCBs, improve mortality in patients with MI, reduce incidence of stroke in patients with HTN, effective in those with silent/ambulatory ischemia
  • most useful for management of angina associated with effort
  • may induce or worsen CHF in patients with acute MI or decompensated heart failure and reduce exercise tolerance in these patients
  • potentially harmful in variant angina
  • may increase plasma triglycerides and decrease HDL, promoting atherogenesis; inhibit the hyperglycemic response of epinephrine, delaying normoglycemia
  • use with caution in patients with reduced myocardial reserve, asthma, peripheral vascular insufficiency, or diabetes
  • minor SE: GI or CNS disturbance
52
Q

How does the efficacy of beta blockers compare to CCBs?

A

beta blockers are associated with better outcomes and greater symptomatic relief than CCBs

53
Q

Beta blockers are especially useful for what kind of angina?

A

that associated with exercise

54
Q

Beta blockers have been shown to have what beneficial long-term outcomes?

A
  • reduced mortality in patients with MI
  • improved survival and prevention of stroke in patients with hypertension
  • better outcomes and symptomatic relief than CCB in those with angina
  • reduce ischemic time per day in those with ambulatory or silent myocardial ischemia
55
Q

What is ambulatory ischemia? How is it best treated?

A
  • myocardial ischemia which is only detected by the appearance of ECG signs
  • beta blockers are particularly useful in treating these cases because they reduce total amount of ischemic time per day
56
Q

Through what mechanism do beta blockers reduce afterload?

A

some inhibit vasoconstriction and some also induce vasodilation directly

57
Q

What are the adverse effects associated with beta blocker use in angina?

A
  • may induce or worsen CHF and reduce exercise tolerance in these patients
  • may promote atherogenesis by increasing plasma triglycerides and decreasing HDL
  • may be harmful in those with variant angina
  • inhibits hyperglycemic responses mediated by epinephrine and delays recovery of normoglycemia
58
Q

Why are beta blockers harmful for patients with variant angina?

A
  • because beta blockers slow heart rate and prolong ejection time
  • this increases LV EDV and increases the myocardial oxygen requirement
59
Q

Why is it beneficial to combine nitrates with a beta blocker or non-dihydropyridine CCB?

A

because beta blockers and these CCBs will inhibit the reflex tachycardia that accompanies nitrate use

60
Q

Effective anti-anginal therapy will achieve what two goals?

A
  • increase exercise tolerance

- decrease frequency and duration of myocardial ischemia

61
Q

What are the preferred drugs for variant angina? Why?

A

nitrates and CCBs which both dilate spastic coronary blood vessels

62
Q

What is first-line therapy for angina?

A
  • modify risk factors
  • add an anti-platelet drug like aspirin
  • recommend a statin plus weight loss
  • treat the underlying cause of atherosclerosis
63
Q

What are the two most effective drug combinations for the treatment of angina?

A
  • beta blocker + CCB

- a dihydropyridine CCB and verapamil

64
Q

What mono therapy for angina is recommended in patients hypertension? Normotensive?

A
  • hypertensive patients: slow release CCB or beta blocker

- normotensive: long-acting nitrate

IC 1.0 (24 decks)

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