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MBBS IV - Junior Clerkship WCS > JC 06 (Medicine) - Ischaemic heart disease, Angina pectoris > Flashcards

JC 06 (Medicine) - Ischaemic heart disease, Angina pectoris Flashcards

1
Q

6 pathophysiological processes that cause MI

A
  1. Critical coronary stenosis
  2. Vascular Inflammation
  3. Coagulopathies
  4. Vasospasm
  5. Microvascular dysfunction
  6. Endothelial dysfunction
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2
Q

Explain the pathophysiological changes in epicardial coronary arteries that lead to myocardial ischemia

A

Insufficient oxygen supply to myocardial tissue by 2 mechanisms:

  1. Atherosclerotic disease
    - Stable plaque > Reduction in CFR > Demand ischaemia +/- angina
    - Vulnerable plaque > Plaque rupture > Thrombosis > Acute coronary syndrome/ Infarction
  2. Vasospastic disease
    - Focal/ transient vasospasm > Prinzmetal angina
    - Persistent vasospasm > Myocardial infarction
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3
Q

Explain the pathophysiological changes in coronary microcirculation that lead to myocardial ischemia

A

Microvascular dysfunction

> impairs coronary physiology and myocardial blood flow

> myocardial ischaemia in CAD and Cardiomyopathies

> Severe acute ischaemia

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4
Q

Mechanism of ischemic chest pain (referred pain)

A

Ischemic episodes
> excite chemosensitive and mechanosensitive receptors in heart
> Release adenosin, bradykinin, cytokines
> Excite sensory sympathetic and vagal afferent fibers
> Upper thoracic sympathetic ganglia and thoracic roots of spinal cord
> cardiac sympathetic afferents impulses converge with somatic thoracic structures
> Chest pain

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5
Q

Mechanism of silent myocardial ischaemia

A

Long term diabetes
> Reduced nerve growth factor
> failed development of cardiac sensory system
> failed afferent signal to thoracic ganglia and impulse convergence with somatic nerve fibers
> no chest pain

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6
Q

Prevalence of angina

Typical presentations

A

> 60 years old = 25-37% men and 16-23% women

50% present with angina pectoris
50% with acute coronary syndrome

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7
Q

Primary cardiac causes of IHD

A
  1. Coronary artery abnormalities:
    - Spasm, arteritis, dissection, malformation, myocardail bridging
  2. Valvular
    - Aortic stenosis
  3. Structural
    - Hypertrophic cardiomyopathy, Dilated cardiomyopathy
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8
Q

Primary non-cardiac causes of IHD

A
  1. Decrease oxygen delivery - hypoxemia
    - Anemia, Sickle cell disease, carbon monoxide poisoning
  2. Endocrine
    - Hyperthyroidism (thyrotoxic AF), Pheochromocytoma
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9
Q

Effect of LDL levels on onset of IHD

A

Reduce LDL cholesterol = delay onset of IHD

Familial hypercholesterolemia greatly decreases age of IHD onset

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10
Q

Pathogenesis of atherosclerotic plaque formation

A
  1. Atherophil (modified smooth muscle cells or macrophages) proliferate
    > Atherocyte phagocytizes lipids
    > Lipid-laden atherocytes die and release lipids
    > Other atherocytes engulf lipid content under sufficient oxygen
    > Increasing platelet and fibrin blocks O2 diffusion and astrocytes cannot engulf lipid content
    > extra-cellular lipid accumulates, internal elastic membrane fractures and stiffens
    > Pathological intimal thickening
  2. Fibrophils (modified fibroblasts or histocytes) produce fibrous tissue and accelerate calcium deposition
    > Fibroatheroma formation

> > Formation of atherosclerotic plaque in intima layer

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11
Q

Define risk factors of coronary artery disease

A

□ Modifiable: abdominal obesity, BP, cholesterol, cigarette smoking, alcohol, diet, DM, lack of exercise, cocaine abuse

□ Non-modifiable: family Hx of CVD, male gender, advanced age

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12
Q

Define stable, unstable angina

Define myocardial infarction

A

□ Stable angina: ischaemia due to fixed stenosis
□ Unstable angina: ischaemia due to dynamic obstruction (e.g. ruptured atherosclerotic plaque, acute thrombosis)
□ Myocardial infarction: myocardial necrosis due to acute occlusion

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13
Q

Typical presentation of stable angina (ESC Guidelines)

Provoking and relieving factors

A

Retrosternal chest discomfort with typical quality (dull, constricting) and duration (<30min)
→ ± radiation to arms, shoulder, jaw

Provoked by exertion or emotion

Relieved by rest or sublingual nitrate ≤5min

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14
Q

Clinical grading of angina pectoralis

A 
CCS grading of angina pectoralis
0 – asymptomatic
I – angina with strenuous exertion
II – angina with moderate exertion
(slight limitation of ordinary activities)
III – angina with mild exertion
(great limitation) → indicated for Tx
IV – angina at rest
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15
Q

Patterns of pain radiation in angina pectoris

A 
Neck/ throat tightness
Lower jaw 
Left shoulder or arm in ulnar distribution 
Interscapular 
Epigastrium 
Back

Sometimes to right arm

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16
Q

Associated non-chest pain manifestations of myocardial ischemia

A

Dyspnea:

  • rest or exertional
  • Paroxysmal nocturnal dyspnea

Abdomen:

  • Atypical, sharp pain
  • RUQ pain (mimic pancreatitis or gallbladder disease)
  • Nausea and vomiting

Psychologial:
- Intense Fear

Diaphoresis

Weakness, syncope, coma

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17
Q

Signs of risk factors of coronary artery disease

A
  1. BP: >15mmHg arm BP disparity
  2. > 30 BMI
  3. Lipid
    - Cutaneous xanthomas, xanthelesma, corneal arcus
  4. DM:
    - acathosis nigricans, skin tags
  5. Others:
    - Franks sing (ear lobe crease)
    - Tar stains, teeth stains
    - Wheezing, prolonged expiration (COPD)
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18
Q

Signs of coronary artery disease complications

A
  1. CHF:
    - Increase JVP
    - Abnormal heart sounds
    - Displaced apex
    - Low-output cardiac failure
  2. Arrhythmia
  3. PAD:
    - Peripheral pulse absence
    - Carotid bruit
    - Trophic signs
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19
Q

Baseline investigations for suspected coronary artery disease (4 tests)

A

Blood tests

12-lead ECG:
- Evidence of MI, myocardial damage

Echocardiogram:

  • LVEF (prognostic)
  • Structural heart diseases
  • Regional wall motion abnormalities

CXR:
- Pulmonary cause or complications

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20
Q

Outline full spread of blood test metrics for suspected coronary artery disease

A

Blood:

  • CBC
  • Thyroid function test
  • Fasting glucose, HbA1c, OGTT > DM
  • Fasting lipid profile > Hyperlipidaemia
  • RFT/ Creatinine (prognostic)
  • LFT, CK (statin)

Markers:

  • High-sensitivity C-reactive proteins
  • Brain natriuretic peptide (BNP)
  • hs- TNT
21
Q

List diagnostic investigations for suspected coronary artery disease

A

→ Anatomical test: CT coronary angiography
→ Functional test: exercise tolerance test (ETT), stress echo
→ Myocardial perfusion scintigraphy
→ Cardiac MRI

22
Q

Modalities of cardiac stress tests (3)

A

□ Exercise: bicycle ergometer, treadmill test

□ Vasodilators, eg. adenosine, dipyridamole → based on ‘coronary steal phenomenon’

□ Inotropes, eg. dobutamine

Conducted with 12-lead ECG, BP, ECHO
Positive = horizontal or down-sloping ST depression of >0.1mm
Positive ECHO = regional wall motion abnormality, LV dysfunction

23
Q

Outline the selection process of diagnostic investigations for suspected coronary artery disease

A
  1. Contraindicated for stress testing / Clinical findings warrant coronary imaging&raquo_space; CT Coronary angiography
  2. No contraindication for stress testing + unable to exercise&raquo_space; Pharmacological stress test
  3. No contraindication for stress test + able to exercise&raquo_space; Exercise stress test
  4. No contraindication for stress test + able to exercise + no previous revascularization/ resting ECG normal&raquo_space; Exercise tolerance test with ECG

2,3,4 may require follow-up coronary imaging if high risk or inadequate information for diagnosis

24
Q

Direct indications for coronary angiogram

A
  1. Unacceptable angina despite medical therapy
  2. Non-invasive test results with high-risk features
  3. Angina or risk of CAF with depressed LVEF
  4. Unclear non-invasive test results and prognosis
25
Q

5 principles of management of IHD

A

Patient education and decision making

Manage comorbid conditions

Aggressive modification of preventable risk factors

Pharmacological management

Revascularization surgery: PCI, CABG

26
Q

Lifestyle changes for management of IHD

A

□ Lifestyle: stop smoking, regular exercise

□ Treat precipitating factors: thyrotoxicosis, anaemia

□ Manage risk factors:
→ DM: aim HbA1c <7%, consider SGLT2i or GLP-1a
→ HTN: aim <140/90, use BB if indicated
→ Lipids: ↓LDL to <1.8mmol/L with lifestyle and drug

27
Q

CVD prevention in patients with diagnosed atherosclerotic cardiovascular disease (4)

A

LDL-C >50% reduction and <1.8mmol/L

SBP <140 - 130 mmHg

Antithrombotic therapy

Stop smoking and lifestyle recommendations

28
Q

Outline 6 classes of lipid modifying therapies proven to reduce CVD

A

Statins (1st line)

Cholesterol absorption inhibitors e.g. Ezetimibe (2nd line)

PCSK9 inhibitors (3rd line)

Bile acid sequestrants

Long-chain omega-3 fatty acids

antisense oligonucleotide inhibitor of apolipoprotein B (for familial hypercholesterolemia ONLY)

29
Q

Which lipid modifying therapy is most effective in lowering LDL-C and non-HDL-C?

A

PCSK9 inhibitors

30
Q

List classes of drugs for prognostic improvement of IHD

A
  1. Antiplatelets/ anticoagulants
  2. Statins/ lipid modifying drugs: in all patients regardless of LDL, first line
  3. ± ACEI only in those with HTN, LVEF ≤40%, DM/CKD
  4. ± ARB only in those with SIHD, HTN, DM, Poor LVEF and refractory to ACEI
31
Q

List specific antiplatelet/ anticoagulant combinations for prognostic improvement of IHD

A
  1. Aspirin (1st line)
  2. Clopidogrel (2nd line, refractory/ CO to aspirin, post MI)
  3. Aspirin + P2Y12 blocker (Ticagrelor/ Prasugrel): after PCI/ Mutli-vessel CAD/ Post-MI
  4. Aspirin + Rivaroxaban: High risk CAD/ PAD, Post-MI
32
Q

List specific drugs for angina relief (standard first line treatment)

A

Symptomatic → relieve ischaemia during
angina episodes

□ 1st-line:
Urgent: PRN sublingual nitrates
Long-term: Long-acting nitrates + Beta-blocker or CCB/ Beta-blocker + DHP- CCB if severe

□ 2nd-line: long-acting nitrates, ivabradine,
trimetazidine, ranolazine, nicorandil

33
Q

Contraindications for ACEI/ ARB use in IHD patients

A

Bilateral renal artery stenosis

34
Q

Indications for CABG over PCI

A

Two vessel disease and proximal LAD lesion

Triple vessel disease

Unprotected left main coronary artery disease

35
Q

Indication for B-blocker use in IHD

A
  • First-line monotherapy or combination with CCB or nitrate to decrease angina
  • Systolic LV failure (LVEF < 40%) and past-MI
  • Ventricular rate control in A-fib
36
Q

Side effects and contraindications of B-blocker use in IHD

A

Side effects:
- Bradycardia, syncope, hypotension, bronchial spasm

Contraindications: (electrical and veqssel problems)

  • AV block, sinus node dysfunction
  • Bronchial asthma (vasocontriction)
  • Vasospasm angina, PAD, Raynaud’s phenomenon
  • Depression
37
Q

Indication for CCB use in IHD

A

Monotherapy if refractory/ intolerant to B-blocker

Combination with B-blocker or nitrates to decrease angina

Vasospasm angina ** (B-blocker C/O)

Ventricular rate control in A-fib

38
Q

Side effects and contraindications of CCBs

A

Side effects:
Bradycardia (non-DHP CCBs)
syncope, hypotension, peripheral edema, headache, dizziness, constipation

C/O:
AV block, Heart failure, sinus node dysfunction

39
Q

Differences and similarities between Amlodipine, Nifedipine, Diltiazem and Verapamil action on heart (different CCBs)

A

Amlodipine and Nifedipine: (for low basal HR)

  • Increase HR
  • No effects on SA and AV node conduction

Diltiazem and Verapamil: (for tachycardia)

  • Decrease HR
  • Decrease SA and AV node conduction

ALL:

  • Decrease myocardial contractility
  • Increase neurohormonal activation
  • Increase vascular dilation
  • Increase coronary flow
40
Q

Indications of nitrate use for IHD

A

Releive acute anginal pain

Prophylaxis to increase exercise tolerance and prevent exercise-induced ischaemia

Long-acting nitrate to decrease angina

41
Q

Side effects and C/O of nitrate use in IHD

A

Side effects:
- Hypotension, syncope, tachycardia, headache

C/O:

  • HOCM
  • Same-day use with Selective Phosphodiesterase Inhibitors (PDE-5) e.g. Sildenafil
  • SBP <90mmHg/ Severe hypotension
42
Q

List 4 novel agents for use in IHD

A

Ivabradine (funny current blocker, decrease HR and myocardial oxygen consumption)

Ranolazine (reduce Ca overload, anti-arrhythmic)

Trimetazidine (Increase energy for myocardial contraction)

Nicorandil (dilation of coronary resistance arterioles and vasodilation)

43
Q

Side effects of Ivabradine

A

Phosphenes (seeing ring of light)

Bradycardia and AFib

Headache, dizziness

Ventricular extrasystoles, 1st degree heart block

44
Q

Side effects of Ranolazine

A

Long QT

headache, dizziness, syncope, postural hypotension

nausea, constipation

C/O liver or renal failure

45
Q

Side effects of Trimetazidine

A

Nausea vomiting fatigue dizziness myalgia

Induce Parkinsonism symptoms

46
Q

Side effects of Nicorandil

A
  1. c/o corticosteroids - GI perforation

2. c/o sulphonylureas - antagonizing effect

47
Q

Explain INOCA and first line treatment

A

Microvascular dysfunction > angina and ischemia without occlusion

INOCA = Ischemia with no-obstructive CAD

First line:
Antiplatelet, anti-ischemic, nitrates

48
Q

Characterize Prizmetal angina

A

Vasospastic disease
- Focal/ transient vasospasm > Prinzmetal angina

Cyclical Occurs at rest
Common after cold exposure
Risk of Ventricular arrhythmia

MBBS IV - Junior Clerkship WCS (131 decks)

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