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CRRAB Pharmacology > Antianginal Drugs > Flashcards

Antianginal Drugs Flashcards

1
Q

What is angina?

A

Chest pain caused by an accumulation of metabolites as a result of myocardial ischemia

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2
Q

What are symptoms of angina?

*Remember it is a SYMPTOM and NOT a disease.

A

Squeezing, pressure, heaviness, tightness, or pain in the chest.

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3
Q

What is the most common cause of angina?

A

Atheromatous obstruction of the large coronary vessels (CAD)

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4
Q

What is the primary cause of angina pectoris?

A

An imbalance b/t the O2 requirement of the heart and the O2 supplies to it via the coronary vessels. (Basically, supply vs. demand)

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5
Q

What are the 3 types of angina?

A
  1. Classic Angina (a.k.a. Effort Agina)
  2. Prinzmetal Angina (a.k.a. Vasospastic or Variant Angina)
  3. Unstable Angina (a.k.a. Acute Coronary Syndrome)
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6
Q

What is the mechanism of Classic Angina?

A

Inadequate blood flow in the presence of CAD; myocardial O2 requirement increases and coronary blood flow does not increase proportionally (especially during exercise)–> ischemia –> pain

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7
Q

What is the cause of Prinzmetal Angina?

A

Transient spasm of localized portions of the coronary vessels –> decreased O2 delivery to tissue –> significant myocardial ischemia and pain

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8
Q

What underlying problem is Variant Angina usually associated with?

A

Atheromas

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9
Q

Why does Variant Angina result in nocturnal episodes?

A

Recumbent increase in venous return triggers neurogenic alpha-adrenergic coronary vasospasm.

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10
Q

How can coronary flow reserve become impaired?

A

Endothelial dysfunction –> impaired vasodilation–> inability to alter flow –> inadequate flow to the heart

Ischemia occurs at lower levels of demand

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11
Q

What are the signs and symptoms of Unstable Angina?

A

Episodes of angina occurring at rest

Increased severity, frequency, duration of chest pain in patients with previously stable angina

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12
Q

What is the mechanism of Unstable Angina?

A

Partially occlusive thrombi (small platelet clot) at a site of a fissured or ulcerated plaque –> increased epicardial coronary artery resistance –> reduced blood flow –> reduced blood flow to heart

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13
Q

What is the prognosis of Unstable Angina?

A

It’s variable although typically associated with high risk of MI and death (emergency!)

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14
Q

What is the theory behind treating angina?

A

Treat the imbalance between supply and demand of myocardial O2.

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15
Q

What is the theory behind treating CLASSIC Angina?

A
  1. Decrease cardiac work

2. Shift myocardial metabolism

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16
Q

What is the theory behind treating VARIANT Angina?

A
  1. Reverse spasm

2. Treat the atherosclerosis

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17
Q

What is the theory behind treating UNSTABLE Angina?

A
  1. Decrease cardiac work
  2. Shift myocardial metabolism
  3. Reverse spasm
    AND
  4. Treat the atherosclerosis
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18
Q

What are the determinants of myocardial O2 demand?

A

Ventricular Wall Stress
HR
Contractility
Basal Metabolism

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19
Q

What is ventricular wall stress?

A

The tangible force acting on the myocardial fibers, tending to pull them apart.

20
Q

When is energy expended when considering ventricular wall stress?

A

Energy is expended when OPPOSING the ventricular wall stress.

21
Q

Ventricular wall stress is related to what variables?

A

Intraventricular pressure (P )
Radius of the ventricle (r )
Ventricular wall thickness (h)

Ventricular wall stress = (P x r) / 2h

*Basically, as cells are stretched apart they must use more energy to contract and bring them back to baseline.

22
Q

What does the ventricular wall stress equation mean?

A

Increase pressure –> increase wall stress and O2 consumption

Increase radius (LV filling) –> increase wall stress and O2 consumption

Increase wall thickness –> decrease wall stress and decrease O2 consumption

23
Q

Why does an increase in wall thickness result in a decrease in O2 consumption?

A

The force is spread out over a greater muscle mass.

Hypertrophied hearts have lower wall stress and O2 consumption per gram tissue (compensatory role in reducing O2 consumption).

24
Q

How does an increase in HR cause an increase in O2 demand?

A

More contractions per minute and more ATP consumed per minute

25
Q

How does an increase in contractility cause an increase in O2 demand?

A

Greater force requires greater O2 consumption

26
Q

What normally causes an increase in coronary blood flow?

A

An increase in O2 demand

27
Q

Coronary flow is inversely or directly proportional to coronary vascular resistance? What causes an increase in this resistance?

A

Inversely proportional.

Damage to the endothelium of coronary vessels alters ability to dilate causing an increase in resistance.

28
Q

Arteriorlar tone directly controls _____________.

Venous tone determines capacity of ____________.

Systolic or diastolic wall stress?

A
  1. vascular resistance and arterial blood pressure (systolic wall stress)
  2. venous circulation and location of blood sequestration (diastolic wall stress)
29
Q

What are the 3 categories of drugs traditionally used to treat angina?

A
  1. Organic nitrates
  2. Ca2+ channel blockers
  3. beta-adrenoceptor antagonists (blockers)
30
Q

Organic Nitrates

MOA
Effects
Therapeutic Uses
Pharm
Toxicity
Interactions
A

MOA: release NO in smooth muscle –> activates guanylyl cyclase –> increases cGMP –> dephosphorylation of MLC –> relaxation!

Effects: Smooth muscle relaxation (esp. vessels)
Vasodilation (veins&raquo_space; arteries)
Decrease in venous return –> DECREASE PRELOAD –> DECREASE LVEDP –> redistribution of blood flow to endocardium
Decrease pulmonary vascular resistance
Decrease heart size
May increase coronary flow in some areas (min. changes)
**Increase HR and contractility

Therapeutic Uses: Angina

           - acute --> sublingual
           - prophylaxis --> oral and transdurmal
           - acute coronary syndrome --> IV

Pharm: 1st pass met; high lipid solubility –> rapid absorption

Toxicity: orthostatic hypotension, reflex tachycardia, HA

Interactions: synergistic hypotension w/ phosphodiesterase type 5 inhibitors (Viagra, Cialis, Levitra)

31
Q

What are some examples of organic nitrates?

A

Nitroglycerin (most common)
Isosorbide dinitrate- longer direction of action than nitro
Isosorbide mononitrate- active metabolite of denigrate, used orally for prophylaxis

32
Q

What are some examples of Ca2+ channel blockers?

A

Verapamil
Diltiazem
Nifedipine

33
Q

What is the pneumonic to remember the Ca2+ channel blockers?

A

“Very Nice Drugs!” = Verapamil, Nifedipine, and Diltiazem

34
Q

Verapamil and Diltiazem (Ca2+ channel blockers)

MOA
Effects
Therapeutic Uses
Pharm
Toxicity
Interactions
A

MOA: non-selectively block L-type Ca2+ channels in vessels and the heart –> muscle relaxation

Effects: DECREASE HEART RATE AND CONTRACTILITY –> decrease O2 demand
INCREASE CORONARY BLOOD FLOW (DECREASE AORTIC DIASTOLIC PRESSURE) –> increase O2 supply
**Decrease LVEDP

Therapeutic Uses: prophylaxis of angina and HTN

Pharm: oral, IV, duration of 4-8 hr

Toxicity: AV block, acute HF, constipation and edema

Interactions: additive effects with other depressants and hypotensive medications

35
Q

Nifedipine

MOA
Effects
Therapeutic Uses
Pharm
Toxicity
Interactions
A

A Dihydropyridine

MOA: blocks vascular L-type Ca2+ channels MORE

Effects: LESS cardiac effect

Therapeutic Uses: prophylaxis of angina and HTN

Pharm: oral, duration of 4-6 hr

Toxicity: excessive hypotension, baroreceptor reflex tachycardia

Interactions: additive effects w/ vasodilators

36
Q

What are some examples of beta-adrenoceptor blockers?

A

Propanolol, Atenolol, and Metoprolol

37
Q

Propanolol (beta-adrenoceptor blocker)

MOA
Effects
Therapeutic Uses
Pharm
Toxicity
Interactions
A

MOA: non-selective competitive antagonist at beta-adrenoceptors

Effects: DECREASE HR and CONTRACTILITY
DECREASE AORTIC PRESSURE
**decrease total coronary blood flow
**increase coronary artery R and increase LVEDP

Therapeutic Uses: prophylaxis for angina (esp. classic and maybe “silent” angina)

Pharm: oral and perenteral, duration of 4-6 hr

Toxicity: asthma, AV block, acute heart failure, sedation

Interactions: additive effects with all cardiac depressants

38
Q

What type of blockers are Atenolol, Metoprolol, etc.? What is concerning about using them?

A

beta1-selective blockers

less risk of bronchspasm but still significant!

39
Q

What are possible major benefits from using beta-adrenoceptor blockers?

A

DECREASE in mortality of patients with recent MI

IMPROVE survival and prevent stroke in patients with HTN

40
Q

What is the MOA of Ranolazine?

A

New Drug

MOA: decrease late Na+ current that facilitates Ca2+ entry via Na+/Ca2+ exchanger –> results in reduction in intracellular Ca2+ concentration –> decrease heart contractility and work

41
Q

What is the MOA of Trimetazidine?

A

New Drug

MOA: metabolic modulator –> pFOX inhibitor

Partially inhibitors fatty acid oxidation pathway in myocardium –> metabolism shifts to FA oxidation in ischemic myocardium

*NOT approved in the USA

42
Q

What is the MOA of Ivabradine?

A

New Drug (bradycardic)

MOA: relatively selective If Na+ channel blocker –> decrease HR by inhibiting the hyper polarization activated Na+ channel in SA node

Use: decrease anginal attacks with similar efficacy to that of Ca2+ and beta blockers

*NOT approved in the USA (close!)

43
Q

What is the MOA of Fasudil?

A

New Drug

MOA: inhibits smooth muscle Rho kinase –> reduces coronary vasospasm in experimental animals

*In clinical trials in CAD

44
Q

What risk factors can contribute to the worsening of athersclerosis? Any prophylactic treatment?

A 
Smoking
HTN
Hyperlipidemia
Obesity
Clinical depression

Tx: Aspirin and statins

45
Q

Look at the table on slide 46 of her powerpoint “Antianginal Drugs”!!

A

Know it well.

CRRAB Pharmacology (3 decks)

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