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Cardiovascular Medicine Midterm > Chronic IHD Drugs - Konorev > Flashcards

Chronic IHD Drugs - Konorev Flashcards

1
Q

Chronic ischemic heart disease is characterized by partial occlusion of coronary artery. What are some common types?

A
  1. Classic angina (angina of effort, stable angina): occlusion of coronary arteries resulting from formation of atherosclerotic plaque.
  2. Variant (prinzematal) angina: episodes of vasoconstriction of coronary arteries.
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2
Q

Which form of chronic IHD is most common and angina may occur with exertion or stress? which one is likely to have a genetic origin and symptoms occur even at rest.

A

Classic angina is most common and symptoms may occur during exertion or stress. Variant angina is less common and likely to have a genetic origin with symptoms that occur even at rest.

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3
Q

The approaches available today to treat angina pectoris is to balance heart’s O2 supply and demand. What are some general approaches this can be done?

A
  1. Increase (or restore) coronary blood flow - surgical and non-surgical revascularization approaches.
  2. increase coronary blood flow using vasodilators (useful in prinzemetal angina, NOT useful in classic angina, in fact may even exacerbate)
  3. Reduce myocardial oxygen demand
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4
Q

What are some examples of surgical and non-surgical revascularization methods as used in treating angina pectoris?

A
  1. coronary artery bypass grafting,
  2. PTCA,
  3. atherectomy,
  4. stent,
  5. Drug-eluting stents (antiproliferative drugs)
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5
Q

Explain the coronary steal phenomenon

A

redistribution of blood to non-ischemic areas - associated with the dilation of small arterioles (example - potent arteriolar vasodilators, such as dipyridamole). The idea is that with partial block of one coronary artery, if you dilate the adjacent coronary artery, this will create a higher perfusion pressure on the non-plaque artery and this will cause blood to go with the higher pressure route and thus stealing blood away from the partial blocked artery, and decreasing collateral blood flow to the ischemic area.

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6
Q

What are some determinants of myocardial oxygen demand?

A
  1. HR
  2. Contractility
  3. Preload
  4. Afterload
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7
Q

Complete the following: Coronary blood flow is unique in that, flow is dependent on 1. During the initial phase of contractility (isovolumetric contraction), coronary blood flow drops to almost 2 and remains at 3 throughout systole. During 4, there is a dramatic increase in coronary blood flow due to 5.

A
  1. phase of cardiac cycle
  2. zero
  3. remains very low
  4. Diastole
  5. Compression of coronary artery, and also cuz of the ostia of the coronary arteries are right behind aortic valves that are open during systole which hinders flow from aorta into the coronary arteries, and during diastole when aortic valves are closed, blood flow to the coronary flow is free flowing.
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8
Q

Explain how tachycardia is harmful for coronary blood flow.

A

During tachycardia, there will be a increase O2 demand. Tachycardia does not change the duration of systole by much, however, duration of diastole is dramatically reduced. Thus with tachycardia, there will decreased length of diastole and thus coronary blood flow is impeded. this is why tachycardia is so harmful in IHD patients.

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9
Q

What drug is a vasodilator that lacks a direct effect on autonomic receptors but may provoke angina attacks?

A

Hydralazine

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10
Q

what are the four classes of drugs use in chronic IHD?

A
  1. Nitrates (nitrovasodilators)
  2. CCB
  3. beta blockers
  4. Newer agent: Ranolazine
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11
Q

Organic nitrates (such as nitroglycerin) is metabolically activated to Nitric oxide by what enzyme?

A

Aldehyde dehydrogenase 2 (ADH2). Thiol compounds are needed to release NO from nitrates.

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12
Q

List the stepwise pathway how organic nitrates (nitroglycerin) leads to smooth muscle relaxation.

A
  1. Organic nitrates are metabolic activated to NO.
  2. NO enters vascular smooth muscle cells.
  3. NO binds to Guanylyl Cyclase and converts GTP into cGMP.
  4. cGMP activates Protein kinase G which has two effects: 1) myosin light chain dephosphorylation leading to smooth muscle relaxation; and 2) acts on K channels and hyperpolarize cell and reduce Calcium entry into cell.
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13
Q

NO acts on vascular smooth muscle and cause relaxation, but the most sensitive vessel to actions of NO are __ which leads to reduced preload and thus decrease O2 demand.

A

large veins. The order of sensitivity is Veins > large arteries > small arteries and arterioles

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14
Q

Because NO works generally on vascular smooth muscle and thus can act on arteries and veins, it has been used to treat which forms of angina?

A
  1. Variant angina by dilating coronary artery and thus relieve coronary spasm
  2. Angina of effort by venous dilation, reducing preload and thus reducing O2 demand
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15
Q

Besides vasodilation, what other actions does NO known to have?

A

NO is a very good all around protector of vasculature.

  1. Prevent LDL oxidation (prevents against atherosclerosis)
  2. Prevent Superoxide radical formation ((prevent oxidative damage of vasculatures)
  3. Prevent smooth muscle cell proliferation (prevent intimal changes and thus prevent occlusion)
  4. Prevent monocyte adhesion (prevents inflammatory changes in vasculature)
  5. Prevent platelet aggregation (protects against thrombosis)
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16
Q

Explain how nitrates tolerance is developed.

A
  1. Depletion of thiol compounds which is needed for the activation of nitrates to NO.
  2. Increased generation of O2 radicals such as superoxide radical which depletes tissues of NO
  3. Reflex activation of sympathetic nervous system (tachycardia, decreased coronary blood supply)
  4. Retention of salt and water.
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17
Q

which noncardioactive CCB has a half life of about 2-4 hours? about 4hrs? about 30-50hours?

A

2-4 hrs = Nicardipine
4 hrs = Nifedipine
30-50 hrs = amlodipine

18
Q

CCB mainly uses which type of Ca channels to have it’s action?

A

L-type Ca2+channel

19
Q

Generally speaking, the physiology of skeletal and cardiac muscle contraction is different from the way smooth muscle cause contraction. As a result, smooth muscle contraction is slower. Explain why.

A

Ca2+ when it enters smooth muscle cells binds to Calmodulin and then the Ca2+ and Calmodulin complex activates myosin-LC kinase (MLCK). MLCK then phosphorylates a residue on the myosin light chain (Myosin-LC-PO4). Only after it has been phosphorylated it is able to interact with actin to produce contraction. Because these addition steps of phosphorylation is required, contraction in smooth muscle is slower.

20
Q

Explain how CCB works on different forms of angina.

A
  1. Atherosclerotic angina (exertion angina) - decrease myocardial O2 demand by dilation of peripheral arterioles which decrease PVR and afterload and thus decrease BP.
  2. Variant angina: Increase blood supply by dilating coronary arteries to relieve local spasm
21
Q

Which beta blockers are indicated for angina

A

Ones are that have no partial agonist or intrinsic sympathomimetic activity. They include: 1. Propranolol

  1. Nadolol
  2. Metaprolol
  3. Atenolol
22
Q

what is the MOA of beta blockers that which are used for angina?

A

Decrease myocardial O2 demand 1. decreasing HR which leads to improved myocardial perfusion and reduced O2 demand at rest and during exercise; 2. decrease in contractility; and 3. decrease BP which leads to reduced afterload

23
Q

What is the MOA of Ranolazine?

A

Inhibits late Na current in cardiomyocytes. In an ischemic myocardium there is partial depolarization and the late Na current is enhanced and thus brings about Ca2+ overload and depolarization abnormalities. With the use of Ranolazine, it normalizes repolarization of cardiac myocytes and reduces mechanical dysfunction

24
Q

A 61 year old man is about go on a day long fishing trip in a remote lake. Which nitrovasodilators can he take to ease his mind from getting any angina attacks?

A

Isosorbide mononitrate orally. It has a half life of about 6- 10 hours.

25
Q

What adverse effects are associated with nitrates?

A
  • Headache cuz of meningeal vasodilation
  • Orthostatic hypotension
  • increased sympathetic discharge (tachycardia, increased cardiac contractility)
  • increased renal Na and H20 reabsorption.
26
Q

What is the single biggest drug interaction associated with nitrate? what product builds up that which gives it severe affects?

A
  • interaction of nitrates with drugs used for tx of ED such as sildenafil, vardenafil, and tadalafil
    Combination causes severe increase in cGMP and dramatic drop in BP. MI have been reported
27
Q

What adverse affects are associated with CCB’s?

A

Major ones are:

  • cardiac depression, cardiac arrest, and acute HF.
  • Bradyarrhythmias, AV block
  • Short acting DHP cause vasodilation triggered reflex sympathetic activation
  • Nifedipine increase the risk of MI in pts with HTN cuz it’s fast release. Slow and long acting DHP are better tolerated.
28
Q

What adverse effects are associated with use of beta blockers for angina pectoris?

A
  • reduced CO
  • Bronchoconstriction
  • Impaired liver glucose mobilization
  • produce an unfavorable blood lipoprotein profile (increase VLDL and decrease HDL)
  • Sedation, depression
  • Withdrawal syndrome (sympathetic hyperresponsiveness
29
Q

What are some contraindications for Beta blockers?

A
  • asthma
  • peripheral vascular disease
  • Raynaud’s syndrome
  • Type 1 DM
  • Bradyarrhythmias an AV conduction abnormalities
  • severe depression of cardiac function
30
Q

If you want to decrease LV ejection time what combination or solo use of Nitrates, CCB and betablockers would you NOT want to use?

A

Nitrates alone is the best option. If beta blockers or CCB is used alone it was shown to increase Ejection time. Combo therapy has no effect on ejection time

31
Q

If you want to decrease end-diastolic volume which solo or combo of nitrates, CCB and beta blockers would you NOT want to use?

A

Nitrates alone is the best option. If beta blockers or CCB is used alone it was shown to increase End-diastolic volume. Combo therapy has shown to have little effect in decreasing or no effect.

32
Q

What is the clinical indication of ranolazine?

A

2nd line therapy for stable angina which is refractory to standard meds. Decreases angina episodes and improves exercise tolerance in patients taking nitrates, amlodipine or atenolol.

33
Q

What adverse effects are associated with Ranolazine?

A
  • QT interval prolongation (may trigger polymorphic ventricular arrhythmias)
  • Constipation
  • Nausea
  • Dizziness/Headache
34
Q

What drug interactions are associated with Ranolazine?

A
  • Metabolized by CYP3A4/5 cuz should not be used with CYP3A inhibitors such as antifungal azoles, or verapamil
  • Ranolazine inhibits CYP2D6 and thus increase half life of amitriptyline, fluoxetine, metoprolol, opioid drugs
  • Drugs that prolong QT interval such as quinidine, antipscyhotic drugs like thioridazine. These can trigger ventricular arrhythmias.
35
Q

What adverse effects are associated with cardioactive CCBs?

A
  • cardiac depression, cardiac arrest, and acute HF.
  • Bradyarrhythmias
  • AV block
  • Flushing, headache, anorexia, dizzines
  • peripheral edema
  • constipation
36
Q

what combination of drugs should be avoided in treating atherosclerotic angina cuz it’s known to cause inapprorpiate decrease in heart rate?

A

Beta blockers and cardioactive CCB

37
Q

What is a good option for prevention/long term therapy for variant angina?

A

Diltiazem (CCB - a vasodilator)

38
Q

Which drug is makes coronary vasospam associated ischemia worse, but is a good tool for using ischemia due to coronary thrombosis?

A

Propranolol.

39
Q

When drugs are used in combo for tx of angina, which combo has additive effects?

A

Non-DHP CCBs and beta blockers on cardiac force.

40
Q

Beta blockers (e.g. propranolol) helps chronic stable angina by decreasing _

A

myocardial O2 demand

41
Q

A potential detrimental effect of nitrates in the prophylactic treatment of exertional angina includes:

A

Increase cardiac rate. While nitrates decrease myocardial demand for O2, it does this by increasing capacitance of systemic veins but it can also decrease arterial pressure and as a reflex sympathetic activity is increased and thus increases cardiac rate. this normally okay for most patients, but NOT in patients with atherosclortic angina.

Cardiovascular Medicine Midterm (6 decks)

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