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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
How does an increase in contractility cause an increase in O2 demand?
Greater force requires greater O2 consumption
26
What normally causes an increase in coronary blood flow?
An increase in O2 demand
27
Coronary flow is inversely or directly proportional to coronary vascular resistance? What causes an increase in this resistance?
Inversely proportional. Damage to the endothelium of coronary vessels alters ability to dilate causing an increase in resistance.
28
Arteriorlar tone directly controls _____________. Venous tone determines capacity of ____________. Systolic or diastolic wall stress?
1. vascular resistance and arterial blood pressure (systolic wall stress) 2. venous circulation and location of blood sequestration (diastolic wall stress)
29
What are the 3 categories of drugs traditionally used to treat angina?
1. Organic nitrates 2. Ca2+ channel blockers 3. beta-adrenoceptor antagonists (blockers)
30
Organic Nitrates ``` MOA Effects Therapeutic Uses Pharm Toxicity Interactions ```
MOA: release NO in smooth muscle --> activates guanylyl cyclase --> increases cGMP --> dephosphorylation of MLC --> relaxation! Effects: Smooth muscle relaxation (esp. vessels) Vasodilation (veins >> 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
What are some examples of organic nitrates?
Nitroglycerin (most common) Isosorbide dinitrate- longer direction of action than nitro Isosorbide mononitrate- active metabolite of denigrate, used orally for prophylaxis
32
What are some examples of Ca2+ channel blockers?
Verapamil Diltiazem Nifedipine
33
What is the pneumonic to remember the Ca2+ channel blockers?
"Very Nice Drugs!" = Verapamil, Nifedipine, and Diltiazem
34
Verapamil and Diltiazem (Ca2+ channel blockers) ``` MOA Effects Therapeutic Uses Pharm Toxicity Interactions ```
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
Nifedipine ``` MOA Effects Therapeutic Uses Pharm Toxicity Interactions ```
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
What are some examples of beta-adrenoceptor blockers?
Propanolol, Atenolol, and Metoprolol
37
Propanolol (beta-adrenoceptor blocker) ``` MOA Effects Therapeutic Uses Pharm Toxicity Interactions ```
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
What type of blockers are Atenolol, Metoprolol, etc.? What is concerning about using them?
beta1-selective blockers less risk of bronchspasm but still significant!
39
What are possible major benefits from using beta-adrenoceptor blockers?
DECREASE in mortality of patients with recent MI IMPROVE survival and prevent stroke in patients with HTN
40
What is the MOA of Ranolazine?
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
What is the MOA of Trimetazidine?
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
What is the MOA of Ivabradine?
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
What is the MOA of Fasudil?
New Drug MOA: inhibits smooth muscle Rho kinase --> reduces coronary vasospasm in experimental animals *In clinical trials in CAD
44
What risk factors can contribute to the worsening of athersclerosis? Any prophylactic treatment?
``` Smoking HTN Hyperlipidemia Obesity Clinical depression ``` Tx: Aspirin and statins
45
Look at the table on slide 46 of her powerpoint "Antianginal Drugs"!!
Know it well.

CRRAB Pharmacology (3 decks)

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