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Cardiovascular Therapeutics > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

Ischemic Heart Disease Definition

A

narrowing of one or more coronary arteries due to atherosclerosis

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2
Q

Ischemic heart disease names

A

Coronary artery disease (CAD); coronary heart disease (CHD), Atherosclerotic cardiovascular disease (ASCVD)

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3
Q

What is the most known outcome of ischemic heart disease?

A

Heart attack (or myocardial infarction)

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4
Q

What is the leading cause of premature mortality and hospitalization?

A

Ischemic Heart Disease
2nd leading cause of death after cancer
Leading cause of hopsitilization

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5
Q

What are the main types of cardiovascular disease?

A

Ischemic heart disease (IHD)
Cerebrovascular disease (CVD)
Peripheral arterial disease (PAD)
Venous thromboembolic disease (VTE)
Heart failure
Arrhythmia

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6
Q

What diseases are due to artherosclerosis?

A

Ischemic heart disease (IHD)
Cerebrovascular disease (CVD)
Peripheral arterial disease (PAD)

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7
Q

The major cause of myocardial infarction is….

A

Artherosclerosis in coronary artery –> Coronary artery disease

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8
Q

One cause of cerebrovascular Accident (CVA) or stroke is….

A

Artherosclerosis in cerebral arteries –> Cerebrovascular disease

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9
Q

Peripheral Arterial Disease (PAD) is due to….. and can cause…

A

Artherosclerosis in arteries of the limb and can cause poor circulation, pain, numbness, etc.

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10
Q

A heart attack is a result of conditions that have been present for…

A

Many Years

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11
Q

Symptoms of Coronary artherosclerosis can present as….

A

Silent (asymptomatic) disease –> most patients!!

Chronic, stable (exertional) angina

Acute coronary syndromes (ACS)

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12
Q

Acute Coronary Syndrome includes…..

A

Unstable angina, NSTEMI, STEMI

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13
Q

Angina Sx

A

Dull, retrosternal discomfort/ache/heaviness

May or may not radiate to jaw, neck, shoulders, arms

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14
Q

What are the two types of angina? What are they a result of?

A

Stable angina is a problem of “demand exceeding supply”

Unstable angina is a result of inadequate “supply regardless of demand

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15
Q

Fixed Obstruction Angina (stable angina) is defined as…

A

An increase in demand that cannot be accommodated with increased supply.

“Demand” for oxygen increases when cardiac myocytes increase energy expenditure

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16
Q

Is stable angina pain associated with plaque rupture?

A

NO

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17
Q

What happens if we increase pre-load?

A

Increase workload

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18
Q

An increase in demand means an increase in these body functions…

A

Heart rate (HR)
Venous return
Blood pressure (BP)
Contractility
(exertion, emotion, mental stress)

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19
Q

What are some triggers of stable angina?

A

SNS activity: Physical exertion, Emotion, Mental stress
Exertion after a heavy meal (SNS and metabolic demands)
Metabolic demands imposed by:
chills, fever, hyperthyroidism, tachycardia, exposure to cold, and hypoglycemia
Anemia (low oxygen content in blood)

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20
Q

An important factor to consider in unstable angina is….

A

Rate of increase of myocardial work (quick onset) can be very important

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21
Q

When are coronary arteries supplied with blood?

A

Diastole

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22
Q

In response to metabolic demnds, small endocardial vessels do wht?

A

Under normal conditions, small endocardial vessels can constrict or dilate according to metabolic demands

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23
Q

At what % do epicardial vessels need to be obstructed at to be fully dilated? What is the result?

A

If epicardial vessels are obstructed over 70-75%, endocardial vessels will be fully dilated under resting conditions

Increases in demand will not be accompanied by increased flow –> further dilation is not possible

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24
Q

In fixed obstruction, what other vascular problems may present?

A

Endothelial dysfunction (↓ N.O. production)

Microvascular dysfunction (poor response to N.O.)

The role of vasospasm

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25
Q

What is the role of vasospasm in fixed obstruction angina?

A

Can be the sole cause of angina (rare! - Prinzmetal’s angina or variant angina)
Can also play a role in patients with ACVD

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26
Q

Stable angina can be relived by….

A

Rest and Nitroglycerin

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27
Q

Nitrates cause….

A

Vasodilation

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28
Q

All nitrates are….

A

Pro-drugs

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29
Q

Nitrates are converted to….

A

Nitric Oxide

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30
Q

What is Nitric Oxide? What does it do?

A

NO is a paracrine hormone synthesized by endothelial cells to signal smooth muscle cells ‘next door’

Relaxes smooth muscle in blood vessel walls (vasodilation)

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31
Q

Do Nitrates drop arterial blood pressure?

A

NO

Targets veins

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32
Q

How does NTG treat stable angina?

A

Primary effect is by reducing pre-load. Blood pools in the veins. Reduce workload of the heart.

High pre-load, greater venous return, frank-starling law, increase workload of heart

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33
Q

Pre-load Definition

A

Preload is the degree to which the myocardium is stretched before it contracts

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34
Q

What is the Frank Starling Law?

A

The energy (force) of contraction is proportional to the initial length of the cardiac muscle fiber”

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35
Q

An increase preload equals

A

Increased workload of the heart

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36
Q

Class I Angina

A
  • Ordinary physical activity does not cause angina. Occurs with strenous, rapid or prolonged exertion
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37
Q

Class II Angina

A

Slight limitation or ordinary activity. Walking, climbing stairs rapidly

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38
Q

Class III ANgina

A

Marked limitations of ordinary physical activity

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39
Q

Class IV Angina

A

Inability to carry on physical activity w/t discomfort –> angina sx present at rest

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40
Q

Exercise Stress Testing occurs on

A

On treadmill or stationary bike

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41
Q

In an exercise stress test, what is the process?

A

ECG, heart rate and BP monitor
Exercise is initiated slowly and slowly builds
It is stopped if chest pain, ST changes, decrease in BP >/=10mmhg

42
Q

During an exercise stress test, what is observed on the ECG if cardiac ischemia is occuring?

A
  • Depression of S-T segment
  • Angina Pain
43
Q

S-T Depression is indicative of…

A

S-T depression is a classic sign of cardiac ischemia

44
Q

What is a common way to notice stable angina?

A

S-T Depression

45
Q

Does S-T depression indicate if myocardial cell death has occured?

A

Does NOT indicate if myocardial cell death has occurred (i.e., myocardial infarction)

46
Q

ST depression indicates…

A

ischemia) – does not tell you if any cardiac myocytes have died

47
Q

ST elevation indicates…..

A

Infarction

48
Q

If the QT interval is delayed, greater the risk for…

A

Time for ventricular depolarization and repolarization
If process is delayed ↑’s risk for ventricular arrhythmias

49
Q

Is stable angina a medical emergency?

A

NO

50
Q

Cardiac Catheterization and Angiography are used to…..

A

Commonly performed to evaluate coronary artery blood flow and identify locations of narrowed vessels due to atherosclerosis

51
Q

What is the Core Medication Therapy for patients with cornary artery disease?

A

ABCDEK

Antiplatelets
Blood pressure medications (not necessarily for BP)
Cholesterol-lowering medications
K-CKD (CKD often present with CAD so always check!)
Diabetes medications
Exercise/diet/ lifestyle changes (stress, alcohol, tobacco)

52
Q

Beta-blockers can be used to help prevent…..

A

Angina

53
Q

ACE Inhibitors in CAD???

A

“Consider” in all patients with stable IHD

54
Q

ACE inhibitors should be used in CAD when…..

A

Prescribe” in all patients with the following indications:
Ejection fraction < 40% (i.e., LVSD) *one exception- if they take valsartan/saccubitril
Hypertension
Chronic kidney dz

55
Q

if a patient has an intolerance to an ACE, what drug can be used?

A

ARB’s

56
Q

In regards to angina, goals of tx should include?

A

goals of therapy must include BOTH symptom relief AND protection against disease progression and disease outcomes

57
Q

Anti-angina therapy alternatives include….

A

The following drugs have an indication to prevent or reduce the frequency/intensity of stable angina episodes

Beta-blockers
DHP CCBs
Non-DHP CCBs
Nitrates
Ranolazine (CorzynaTM) (secondary therapy)

58
Q

Are beta-blockers useful in angina? Why?

A

Prevents angina through↓ demand

59
Q

When are beta-blockers used first line in stable-angina?

A

Should be used first-line for stable angina in people with another indication for BB:
Post MI (indication for BB)
Systolic HF (indication for BB)

Typically used first-line for other patients due to evidence in conditions above.

60
Q

Beta-Blockers Dose in Stable Angina?

A

Dose titrated to a resting HR of 55 to 60 bpm

61
Q

What beta-blockers should be used to prevent angina? Which are preferred? Why?

A

All BB are effective equally to prevent angina

B1 selective agents preferred due to lower risk of:
Erectile dysfunction (B2-blockade)
Peripheral circulation problems (esp pts with PAD)
Interaction with B-2 agonists (i.e., Ventolin)

62
Q

Which Beta-blockers should be avoided?

A

Avoid BB with ISA (e.g., acebutolol)

63
Q

Beta Blockers should be monitored for…..

A

↓Heart Rate and BP AV block or low HR

Signs of poor cardiac output  Exercise tolerance or ↓ Renal perfusion (RAAS / edema etc)

Reduced circulation  Caution in Raynaud’s / PAD (esp B2)

Respiratory disease (Asthma)  generally safe

Diabetes  Can mask hypoglycemia; Blood sugar ↑?

64
Q

Non-slective beta and alpha blockers examples. BP Effect, useful in stable angina?

A

Carvedilol (Coreg) and Labetalol (Trandate)
Non-selective (B1 and B2 inhibition) AND
Alpha1-receptor inhibition (vasodilatory effect)

Greater fall in BP expected compared to other beta-blockers

Not typically used for stable angina (unless complications exist)

65
Q

Non-DHP CCB’s Examples

A

Diltiazem and Verapamil

No DVD’s

66
Q

Non-DHP CCB’s tx effect compared to BB’s

A

Same therapeutic effect as BBs - Main difference is intensity of action (reducing cardiac workload, peak HR does not get as high, prevent heart attack)

67
Q

Non-DHP CCB Adverse Effect

A

Constipation can occur in 1/10 patients

68
Q

Non-DHP CCB’s inhibit….

A

Inhibits 3A4 (also a substrate)

69
Q

Avoid Non-DHP CCB’s in….

A

systolic dysfunction (low EF/systolic HF)  Can increase the risk of HF exacerbation (One key difference between BB and Non-DHP CCBs)
Already using BB (not an ideal combination)
Bradycardia or AV block

70
Q

Heart Block/AV Block is diagnosed by….

A

AN ECG

71
Q

1st Degree AV Block ECG

A

-P-R interval Delay –> Time from atrial contraction to ventricular contraction is delayed

72
Q

2nd Degree AV Block

A

Intermittently dropped QRS

73
Q

3rd Degree AV Block

A

P and QRS are independent

74
Q

What types of AV Block are C.I. to beta-blockers and/or Non-DHP CCB?

A

2nd or 3rd degree AV block is a contraindication to beta-blockers and/or non-DHP Calcium channel blockers

**UNLESS a ventricular pacemaker is present
75
Q

What can occur in a pt from Non-DHP CCB’s and/or BB’s?

A

Bradycardia or first degree heart block can occur from Non-DHP CCB or BB

76
Q

DHP CCB’s for stable angina?

A

Vasodilator

Good tolerability

77
Q

BB and DHP CCB’s Interaction with each Other

A

Can be safely combined with BB if symptoms persist (notwithstanding BP lowering effects)

78
Q

DHP CCB’s over BB’s are a good alternative for…

A

Good alternative as monotherapy for patients with bradycardia or intolerance to BB

79
Q

Nitrates can be used….

A

Can be used as:
treatment (prn use – spray/s/l tablets) or prevention (typically with NTG patch*)

Nitrate-free interval required to maintain efficacy

80
Q

Why is a nitrate-free interval required?

A

Tolerance is possible - Varies from patient to patient (not predictable)

Nitrate-free interval of 10-14 hours every day appears to prevent tolerance from occurring

81
Q

How long does it take for NTG to work? When should it be taken?

A

PRN NTG can be used BEFORE activities that are known to cause angina (take 2-5 min before – should last 30 min)

82
Q

S/e of NTG

A

Headache most common s/e – quite common. Tolerance to headache usually occurs within 2 weeks (acetaminophen may be used)
Low blood pressure/orth hypotension possible but not common
Patches may cause skin irritation, redness, etc. Rotate site every day.

83
Q

C.I. of Nitrates

A

PDE5 inhibitors 24hrs for sildenafil/vardenafil; 48hrs for tadalafil)
Caution with BP lowering drugs

84
Q

Combo Options to consider for help if angina pain persists

A

Metoprolol + NTG patch

Metoprolol + Amlodipine

Increase Metoprolol dose (Reasonable approach not like HTN)

Switch metoprolol to monotherapy of another agent

Ranolazine…. Add on

BB + NTG
BB + DHP-CCB
Increase BB

85
Q

If blood pressure is low, DOC

A

Nitro

86
Q

If blood pressure is high, DOC

A

Amlodipine

87
Q

Ranozoline Indication, MOA, impact on BP or HR

A

Not used commonly - Indicated as “add-on therapy” for people inadequately controlled or intolerant of first-line agents

Inhibits the late sodium current (INa)
Leads to  Ca in cardiac cell and possibly lower diastolic tone

No impact on BP or HR

88
Q

Ranazoline should be used in caution with (drugs/conditions)….

A

Cautions: 3A4 inhibitors, QT prolongation, renal dysfunction, others

89
Q

What are the common options to treat coronary artherosclerosis?

A

Medical therapy
Continue with drugs

Revascularization

90
Q

What are the types of revascularization?

A

Coronary artery bypass grafting (CABG)
Percutaneous Coronary Intervention (angioplasty/stent implantation)
Fibrinolytic medications (only for acute emergencies such as myocardial infarction – used much less frequently currently)

91
Q

CABG

A

Invasive  Requires open heart surgery

92
Q

PCI is

A

percutaneous coronary intervention

93
Q

What is the most common tx for stable angina? What does it treat?

A

PCI

Very effective  Increasing supply  Will cure the angina but not the the coronary artery disease

94
Q

DAPT stands for and is….

A

Dual Antiplatelet Therapy

Refers to the use of ASA + a P2Y12 inhibitor (ADP inhibitor)

95
Q

What is the difference between BMS and DES?

A

Originally, only bare metal stents were used (BMS)

Stents often elute drug now (Drug Eluting Stents - DES)

Drug coating (in DES) is usually an immunosuppresant to ↓ inflammatory cytokines and cell proliferation following stent implantation

96
Q

What is thr risks associated with longer and shorter DAPT durations?

A

Longer DAPT = ↑ risk of bleeding

Shorter DAPT = ↑ risk of events

97
Q

How long do people often get DAPT for?

A

1 Year

98
Q

In the setting of SIHD (stable ischemic heart disease) DAPT ise recommended….

A

In the setting of SIHD, DAPT is recommended after PCI

99
Q

All DAPT evidence is based on….

A

clopidogrel + ASA

100
Q

Monitoring DAPT includes….

A

Clinical signs of bleeding
Bloody stools, melena (dark stools), hematemesis, bruising**, oozing from injuries

General tolerability
GI upset

Laboratory testing
RBC, Hb, Hct, platelet count (q6 months)

Cardiovascular Therapeutics (5 decks)

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