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Cardiology > Coronary Heart Disease > Flashcards

Coronary Heart Disease Flashcards

1
Q

What is coronary heart disease?

A

Mismatch between myocardial oxygen supply and demand

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2
Q

What is the cardinal symptom of CAD?

A

retrosternal chest pain

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3
Q

T or F: ischemia in CAD can result in MI

A

T

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4
Q

T or F: coronary blood flow increases by 4-fold during exertion

A

T

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5
Q

What are some factors that can reduce oxygen supply?

A

Coronary atherosclerosis and sequelae:

  • Rupture of an unstable atherosclerotic plaque (most common cause)
  • Stenosis
  • Thromboembolisms

Vasospasms:

↑ HR (lower perfusion to coronaries)

Anemia

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6
Q

Why does a higher HR decreases perfusion to the coronaries?

A

Perfusion of the coronaries occurs during diastole. Therefore, higher heart rates reduce perfusion by shortening diastole.

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7
Q

List factors that increase O2 demand?

A

↑ HR

↑ Afterload

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8
Q

Whats the effect of higher HR on O2 demand and supply?

A

Increases in heart rate (e.g., during physical exertion) both reduce oxygen supply and increase oxygen demand!

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9
Q

When does myocardial ischemia occur in coronary atherosclerosis ?

A

Depending on the extent of stenoses (and the corresponding ischemia), patients remain asymptomatic or develop angina and other symptoms. Symptoms usually develop if stenosis is ≥ 70%. If ischemia is severe enough, myocardial infarction can occur.

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10
Q

What happens to blood flow in coronary stenosis?

A

The greater the stenosis, the higher the resistance to blood flow through the blood vessel, provided the length of the vessel and viscosity of blood remain constant.

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11
Q

List the clinical features of CAD:

A

Typically retrosternal chest pain or pressure:

  • Pain can also radiate to left arm, neck, jaw, epigastric region, or back.
  • Pain does not depend on body position or respiration
  • No chest wall tenderness
  • Angina may be absent, particularly in younger patients
  • Often gradual progression
  • Can also present as gastrointestinal discomfort

Dyspnea

Dizziness, palpitations

Restlessness, anxiety

Autonomic symptoms (e.g., diaphoresis, nausea, vomiting, syncope)

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12
Q

What is the difference between stable and unstable angina?

A

Stable:

  • reproducible/predictable
  • chest pain usually subsides within minutes of exercise (due to release of vasodilators like adenosine), with rest or administration of nitroglycerine
  • common triggers mental/physical stress or exposure to cold

Unstable:

  • occurs at rest, doesnt go away with nitro
  • severe, worsening angina (crescendo angina)
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13
Q

What is nitroglycerin?

A

A peripheral vasodilator that decreases preload through venous dilation (venous pooling), which can reduce myocardial wall tension and improve myocardial perfusion. It is used to treat angina due to coronary syndrome.

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14
Q

True or False: Unstable angina can progress to MI

A

True:
Unstable angina is a form of acute coronary syndrome and may progress to myocardial infarction. Most patients with CAD first become symptomatic with acute myocardial infarction or sudden cardiac death!

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15
Q

What is vasospatic angina?

A

Angina caused by transient coronary spasms (usually occurring close to areas of coronary stenosis)

Unrelated to exertion and may even occur at rest (classically at night)

Caused by cigarette smoking, use of stimulants (e.g., cocaine, amphetamines) or sumatriptan, alcohol, stress, hyperventilation, exposure to cold

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16
Q

How to diagnose vasospastic angina?

A
  • Reversible ST elevation on ECG
  • No troponin I or T level elevations on serial measurements
  • Coronary spasms on angiography confirm the diagnosis
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17
Q

What are some atherosclerotic signs that can be used for CAD?

A
  • lack of foot pulse, carotid bruit
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18
Q

What are some resting ECG features for CAD?

A

Usually normal in stable angina

Treat as unstable angina if abnormalities (of the ST segment or the T wave) occur during an episode of chest pain

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19
Q

What is the best initial test for angina?

A

Resting ECG –> Best initial test for both types of angina (and other types of chest pain)

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20
Q

When is a Cardiac Stress used?

A

Cardiac stress tests are generally most useful in patients with an intermediate pretest probability of coronary artery disease.

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21
Q

What kind of stress test is used for those unable to exercise (ie aortic dissection)?

A

pharmacologic stress test (ie. adrenaline-type drug)

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22
Q

What type of detection methods are used in stress test and when are they used?

A

ECG and imaging (echocardiogram or scintigraphy [radionucleotide scan]) –> echo better for women

ECG used if resting ECG can be interpreted
Imaging if cannot (ie atrial fibrillation)

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23
Q

How long does a patient exercise in a cardiac exercise stress test?

A

The patient exercises until the target heart rate is achieved (e.g., on a treadmill).

Maximum heart rate = 220 – age (in years)
Target heart rate = 85% of the maximum heart rate
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24
Q

What are some contraindications for cardiac exercise stress test?

A
  • Acute myocardial infarction with elevated troponin levels and/or ST elevations (in the past 2 days)
  • Unstable angina pectoris or ST depressions at rest
  • Decompensated heart failure or severe symptomatic stenosis of one or more heart valves
  • Acute endocarditis, myocarditis, or pericarditis
    - Hemodynamically significant arrhythmias
    - Acute thromboembolic disease
    - Acute aortic dissection
    - Mental or physical impairment to exercise
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25
Q

What kind of agents are used in a Cardiac pharmacological stress test?

A

IV administration of positive inotropic/chronotropic substances (e.g., dobutamine) or vasodilators (e.g., dipyridamole or adenosine) to simulate the effect of exercise on the myocardium

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26
Q

What is a chronotropic agent?

A

An agent with the ability to influence heart rate. Positively chronotropic drugs (e.g., adrenaline) increase heart rate, while negatively chronotropic drugs (e.g., beta blockers) decrease heart rate.

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27
Q

Which patients should undergo cardiac catherization?

A

Patients with new-onset chest pain, ST segment depression, hypotension or arrhythmias should undergo cardiac catheterization!

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28
Q

What ECG findings in a stress test may indicate CAD?

A
  • Downsloping or horizontal ST depressions of ≥ 0.1 mV in the limb leads and ≥ 0.2 mV in the precordial leads
  • ST elevations ≥ 0.1 mV (requires immediate test termination!)
  • Excessive or delayed increase in heart rate
  • New onset ventricular arrhythmia
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29
Q

What is the purpose of imaging in stress test?

A

The goal is to distinguish between:
Irreversible ischemia: necrosis (myocardial scars)
Reversible ischemia: tissue that is ischemic (but not yet irreversibly dead) and therefore still potentially salvageable
–> myocardial stunning or hibernating myocardium

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30
Q

What is the treatment approach of CAD?

A
  • -> All patients: risk factor reduction and antiplatelet drugs
  • -> Mild CHD: pharmacologic therapy
  • -> Moderate CHD: consider coronary angiography and percutaneous transluminal coronary angioplasty (PTCA)/percutaneous coronary intervention (PCI)
  • -> Severe CHD: coronary angiography and revascularization or coronary artery bypass grafting
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31
Q

What is coronary angiography?

A

A procedure that uses contrast dye and radiography to take images of the coronary arteries. Performed via cardiac catheterization by inserting a catheter into an artery of the arm or groin and guiding it to the coronary arteries. –> INVASIVE but GOLD STD

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32
Q

What is percutaneous transluminal coronary angioplasty (PTCA)/percutaneous coronary intervention (PCI)?

A

An endovascular procedure in which an inflatable balloon is passed over a wire into a narrowed or obstructed artery. Upon inflation, the balloon widens the arterial lumen, which improves perfusion.

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33
Q

What is coronary artery bypass grafting?

A

A surgical cardiac revascularization technique used to treat patients with significant, symptomatic stenosis of a coronary artery or its branches. The stenosed segment is bypassed using an arterial (e.g., internal thoracic artery) or venous (e.g., great saphenous vein) autograft, re-establishing blood flow to the ischemic areas of the myocardium.

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34
Q

What are the first line agents used for angina?

A

Beta-blockers (except in vasospastic angina): can reduce the frequency of coronary events [reduces HR and extends diastole]
Nitrates (venous dilator):
Can prevent exertional angina
Suitable for relief of acute angina or for long-term treatment

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35
Q

What are the second line treatment for angina?

A
  • Calcium channel blockers (CCBs): indicated if there are contraindications to beta-blockers or in addition to beta-blockers (if angina or hypertension persist)
  • Ranolazine: indicated in stable angina that is refractory to first-line treatment
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36
Q

What are the indications for revascularization techniques (ie. PCI or bypass graft)?

A
  • -> In stable angina: activity-limiting symptoms despite optimal medical treatment, contraindications to medical therapy, stenosis of critical (e.g., LCA) or multiple coronary arteries
  • -> Acute coronary syndrome
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37
Q

What are special considerations that need to be taken with treatment in the context of CAD?

A

1) Antiplatelet drugs indicated in all patients: aspirin or clopidogrel (if aspirin/ASA is contraindicated) → ↓ risk of infarction, ↓ morbidity

2) Treating arterial hypertension
- -> Reduce blood pressure to < 140/90 mm Hg in cases of low/moderate risk and to < 130/80 mm Hg in high-risk patients
a) Beta-blockers are the first-line therapy for CHD combined with arterial hypertension.
b) ACE-inhibitors patients post-MI, especially those with left ventricular systolic dysfunction.
3) HbA1c of 6.5–7%
4) Risk-adjusted LDL levels (ie. statins)

38
Q

What is the pathophysiology of CAD?

A

Minor endothelial damage –> LDL deposits –> macrophage eat up –> foam cells –> fatty streak –> cells die –> cholesterol sealed off by fibrous cap –> vessels tries to dilate

39
Q

What happens if cholesterol pool in plaque is too high?

A

bulges into lumen –> stenosis –> downstream ischemia

40
Q

How is acute coronary syndrome produced?

A

Vulnerable plaques have inflammation eating away fibrous cap –> Plaque ruptures –> blood contact with cholesterol initiates intense thrombogenic response –> clots occlude lumen of vessel

41
Q

What factors are considered to calclulare a 10 year coronary death risk score?

A 
Age in years
Total cholesterol
Smoking status
High-density lipoprotein (HDL) level
Systolic blood pressure (SBP)
42
Q

What are some risk factors for CAD?

A

Age
Gender (men 10 years sooner than women)
Family History (M<55 y.o., F<65 y.o.)—2 x risk if in immediate family
Smoking (almost adds 10 years of aging to risk)
Hypertension
Diabetes (1/3 risk coronary events in 10 y if NIDDM)
Dyslipidemia (+‘good’ HDL, ­‘bad’ LDL)
Obesity (especially central) / sedentary lifestyle

43
Q

What are some novel cardiac risk factors?

A 
Elevated prothrombotic markers
     ↑ Fibrinogen; ↑ t-PA 
Elevated atherogenic markers
     ↑ Lipoprotein (a)
     ↑ Plasminogen-activator-inhibitor-1
     ↑ Homocysteine
     ↑ Small, dense LDL particles
     ↑ Apolipoprotein-B to AI ratio
     ↑ Small HDL particle size
     ↓ Large HDL particle size
Elevated inflammation markers
     ↑ C-reactive protein
44
Q

What is the primary prevention of CAD?

A

–>start screening lipids in men ≥40 yeas of age and women ≥50 years of age or postmenopausal (Framingham Risk Score [FRS])

Smoking, diabetes, hypertension, hyperlipidemia, family history, age, sex —> treat risk factors

2+ major risk factors National Cholesterol Education Program 10 year CAD risk score calculation

Educate patients regarding signs and symptoms of STEMI, and emergency response

Consider statin espically if high risk (FRS ≥20%) +/- ASA if at increased risk

45
Q

What percentage of stenosis is characteristic of CAD?

A

> 70% reduction in lumen diameter, then can start getting lack of sufficient blood flow downstream for high demand states (e.g. exercise)

If stenosis > 90%, can start to get too little flow even at rest

46
Q

What are some compensatory processes in CAD to prevent ischemia?

A

1) downstream vasodilation

2) collateral perfusion

47
Q

How to calculate Coronary Artery Supply?

A

Coronary Perfusion Pressure = Aortic Pressure - Left Ventricular Pressure (in diastole)
–> transmyocardial gradient

48
Q

T or F: STEMI or NSTEMI are a result of longstanding ischemia

A

T

49
Q

T or F: Angina (aka chest pain) is caused by myocardial ischemia with necrosis

A

F: without necrosis

50
Q

What is the sensation associated with angina?

A

pressure, squeezing over pain and burning (sometimes can be dyspnea or nausea)

51
Q

Describe each stages of stable angina

A

Grade I –> Ordinary physical activity does not cause angina, such as walking and climbing stairs. Angina with strenuous or rapid or prolonged exertion at work or recreation

Grade II –> Slight limitation of ordinary activity. Walking more than two blocks on the level and climbing more than one flight of ordinary stairs at a normal pace and in normal conditions

Grade III –> Marked limitation of ordinary physical activity. Walking one or two blocks on the level and climbing one flight of stairs in normal conditions and at normal pace

Grade IV –> Inability to carry on any physical activity without discomfort, anginal syndrome may be present at rest

52
Q

What are big five causes of chest pain?

A 
Acute coronary syndrome
Aortic dissection
Pulmonary Embolism
Tension Pneumothorax
Esophageal Rupture
53
Q

What are the characteristics of typical angina?

A
  1. Substernal/radiating to the left arm, neck
  2. Exertional/emotional stress
  3. Relieved with rest/NTG
54
Q

In a stress test, what are some features of a high risk group?

A

Drop in BP response (normal: should not successive with each stage)
Poor exercise capacity (even if not just the heart)
Early positive ST changes
> 2 mm ST depression within the first 6 minutes of the protocol
ST depression in multiple leads
ST elevation (implies critically blocked artery)
Ventricular arrhythmias

55
Q

With patients that cannot do the stress test, what is the alternative and how does it work?

A

Myocardial Perfusion Imaging MIBI or PET

Can give an intravenous radioactive tracer that follows blood flow to heart. -> Then scan the heart with a gamma camera to get 3-D reconstruction of heart (mostly see the LV)

In pet both rest and stressed images are taken:
If an area doesn’t ‘light up’, then there’s a coronary blockage in that territory = perfusion defect:
if seen on BOTH stress & rest = scar = infarct
If defect with stress, OK rest = reversible = ischemia

56
Q

Which imaging is good at ruling out CAD?

A

CT scans

57
Q

What does a CT scan detect in relation to CAD?

A

degree of coronary calcification (ie a calcium score)

58
Q

What are the indications for invasive testing ie. angiography?

A

High risk EST
High clinical suspicion with equivocal non-invasive testing
Unresponsive to maximal medical therapy
Heart failure with ischemia
Multiple ischemic areas on myocardial perfusion scanning

59
Q

What are some problems with bare metal stents?

A

1% / mm of stent length chance of scar tissue –> in-stent restenosis

Average patient ~8-12% chance of re-stenosis by ~ ½ year

Sometimes restenosis –> clots –> acute coronary syndromes (not just progressive worsening angina)

60
Q

What is the standard of care for stents now?

A

Second Generation Drug-Eluting Stents (ie. anti-inflammatory drugs) –> reduced stent thrombosis and re-stenosis

61
Q

What happens in coronary bypass surgery (aka coronary artery bypass grafting ‘CABG’, aorto-coronary bypass ‘ACB’)

A

Take a section of a new blood vessel…Attach to aorta and

attach down-stream to blockage –> blood detours around blockage!

62
Q

T or F: CABG increases survival rate

A 
F:
only in 
Left main blockages >50% (old data)
3-vessel blockages with poor LV function (old data)
Proximal LAD + another coronary blockage

But 8-10 years after a heart bypass operation, mortality increases by 60-80 per cent.

63
Q

T or F: CABG does not have major effect on Heart Attack rate

A

T

64
Q

What preventative management of CAD?

A

Antiplatelet agents

  • Stable CAD Aspirin (ASA) 81mg forever (Clopidogrel 75 mg if intolerant of ASA)
  • Unstable CAD = acute coronary syndromes –> add P2Y12 receptor antagonist (eg Clopidogrel, Ticagrelor (irreversible), Prasugrel) for 1 year if not longer.
    • -> Coined dual anti-platelet therapy (DAPT)

ACE inhibitors or Angiotensin blockers (ARB’s)

  • for all patients
  • Aldosterone receptor blockade if Systolic heart failure with CAD

Blood pressure control [decrease afterload]

  • <140/90 mm Hg or <130/80 mm Hg (perhaps lower) if patient has diabetes or chronic kidney disease
  • lifestyle control initially and if fails then ACEI/ARB + BetaB + thiazide
Beta blockers (or other anti-anginals) [decrease HR]
- for all (not indefinitely)

Cholesterol management

  • LDL-C ≤ 2.0 mM (or at least 50% decrease in LDL)
  • -> very high risk, <1.8 is a reasonable therapeutic option
  • consider statin

Diet / Nutrition / Weight management

  • Target BMI between 19 and 25 kg/m2.
  • ≥ 89cm in women ; ≥ 102cm in men,

Diabetes management

  • require statin (LDL goal less than 2 nM)
  • HbA1C less than 7%

Exercise
- 30-60 minutes of moderate intensity aerobic activity on 5-7 days per week; resistance training 2 days

End Smoking

End Pain(-killers)
- discontinue all COX-2 inhibitors and NSAIDs, EXCEPT aspirin or Acetaminophen

Immunization

  • Influenza vaccination annually (inactivated, injectable)
  • Pneumococcal polysaccharide vaccine
65
Q

What illness is co-morbid with CAD?

A

Depression

66
Q

What the difference post-surgical care among DES and BMS?

A

BARE METAL STENT for Stable Ischemic Heart Disease:
ASA 81mg + Clopidogrel 75 –> 1 month
then ASA 81mg forever after

DRUG-ELUTING STENT for Stable Ischemic Heart Disease:
ASA 81mg + Clopidogrel 75 –> At least 6 months
then ASA 81mg forever after

67
Q

When can antiplatelet therapy be stopped after stenting?

A

Completion of full course or else high risk of massive heart attack (even if undergoing another surgery following a recent stent)

68
Q

What is angina?

A

symptom of inadequate coronary supply vs. demands, often exercise related, usually requires 70% stenosis to occur

69
Q

T or F: many plaque rupture occurs at stenosis rates lower than those that causes angina (ie above 70%)

A

T: 40-60% stenotic plaques rupture

70
Q

Once a plaque ruptures, what may happen?

A

obstructive –> severe ischemia –> MI
non-obstructive –> worse angina
–> may eventually heal over, no symptoms

71
Q

What is unstable angina?

A

a spectrum of symptoms of ischemia between stable angina and myocardial infarction
–> A pattern of accelerating angina, not always
predictable and reproducible with same workload
–> NO myocardial damage ie. necrosis (no rise in blood enzymes)

72
Q

T or F: unstable angina is seen in acute coronary syndrome

A

True

73
Q

What are some signs of ACS?

A
  • Hypotension (sBP ≤ 80 mmHg)
  • 3rd / 4th Heart sounds
  • Pulmonary crackles
  • Chest pain not reproduced with palpation
74
Q

What are some symptoms of ACS?

A

Chest pain radiating to right shoulder, left/right/both arms,history of MI, nausea/vomiting, diaphoresis,

75
Q

What some symptoms that may help rule out ACS?

A

pleuritic chest pain, chest pain (stabbing, sharp), positional chest pain, chest pain produced with palpation

76
Q

What is the name of variant angina?

A

Prinzmetal

77
Q

What happens in Prinzmetal?

A

Non-exertional, often early morning angina, from spontaneous, severe coronary vasospasm –> major drop in O2 supply

78
Q

What are some features of Prinzmetal?

A

Classically without major coronary plaques
- Maybe associated with other arterial spasm
(migraines / Raynaud’s peripheral arteries)
- Sometimes can be severe enough to cause heart attack
- Treatment = very high dose anti-spasm drugs

79
Q

T or F: in NSTEMI there is severe mismatch between myocardial supply and demand of O2

A

T –> tissue necrosis

80
Q

Which MI has absence of ST elevation?

A

NSTEMI (subendocardial - coronary artery partially occluded so that distal myocardium below endocardium not receiving perfusion)

81
Q

Why is there a ST elevation in STEMI?

A

usually transmural ischemia (entire three layers)

82
Q

How many of coronary occlusion is required for full thickness necrosis?

A

6 hours

83
Q

How to diagnose Acute MI?

A

2 of the 3:
Typical Chest Pain (>20-30min.)
Blood Enzymes of Myocardial Damage
Typical EKG Changes

84
Q

What increases probability of AMI with chest pain?

A 
ST elevation (ie. STEMI)
new conduction defect
new ST elevation
new Q wave 
new T wave
85
Q

What is the best blood marker of myocardial damage?

A

–> Troponins
Initial kinetics similar to CK
However remain elevated several days (up to 14) [CK only 18 hrs)
Very specific for myocardial damage
Ultra-sensitive-“Minor Myocardial Damage”
Use increasing

TROPONIN DOES NOT = ACUTE MYOCARDIAL INFARCT

86
Q

T or F: troponins only released in MI

A

F:
Troponin is released from myocardium in response to many stressors:

Volume overload / CHF
Pulmonary embolism
Tachycardias (especially prolonged)
Post-defibrillation
Sepsis
AND …any major hemodynamic stressor that’s severe / prolonged (called a Type II Myocardial infarct = high Demand infarct, + /-  coronary disease contributing to reduced Supply)
87
Q

How to manage STEMI?

A

Minimize the time to reperfusion of the heart with either fibrinolysis or PCI

25% less risk of death with aspirin…160 mg to chew

88
Q

What are contraindications?

A
  1. prior intracranial hemorrhage
  2. known structural cerebral vascular lesion
  3. known malignant intracranial neoplasm
  4. ischemic stroke < 3 months
    except acute ischemic stroke < 3 hours
  5. significant closed head or facial trauma < 3 months
  6. active bleeding (except menses) or bleeding diathesis
  7. suspected aortic dissection
89
Q

Is PCI or fibrinolytics preferred for early presentation of STEMI?

A

Fribrinolytics AND if PCI not rapidly available

invasive strategy not an option

90
Q

How to manage ACS?

A

…all the same drugs / life-style treatments as for stable angina, but expanded:

A—2 anti-platelets: ASA + P2Y12 Receptor Antagonist (Ticagrelor, Prasugrel, Clopidogrel)

A—anti-coagulants: Unfractionated Heparin, Exoxaparin (LMWH), Bivalirudin (direct thrombin inhibitor), Fondaparinux (Xa inhibitor)

A—ACE inhibitors / ARB’s much more important—cautious use if low BP!

B—B-blockers & BP control more important, but cautious use if low BP!

C—Cholesterol lowering crucial, aim for very low LDL <1.8mM - Statins

D—Diet may cut risk of future heart attacks substantially

D—Diabetes control important to keep Glucose < 10mM (MI stress –> ↑glucose)

E—End smoking! Maybe best chance while in hospital, 2 x risk if don’t quit

E—Exercise: Live longer / better if start supervised cardiac rehab program

91
Q

What can result from post-MI?

A

MECHANICAL = myocardium turned to mush
too much gone –> CHF
too much gone –> shock
mush weakens wall –> bulges out = aneurysm / clots
mush –> tear LV:
- leak into pericardium –> usually instant death!
- leak in septum = Ventricular septal defect

ELECTRICAL
Tachyarrhythmias, especially ventricular –> sudden death
Bradyarrhythmias (heart blocks, some risk sudden death)

ARTERIAL = risk of more clot, more damage
Re-infarction
Post-MI unstable angina

Cardiology (29 decks)

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