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Week 7 Flashcards

1
Q

What is myocardial ischaemia?

A

An acute or chronic state where the supply of oxygenated blood to myocardium falls below metabolic demand, leading to disturbances; sustained ischaemia may progress to infarction.

It is framed as an imbalance between coronary oxygen supply and oxygen demand.

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2
Q

What are the three principal determinants of myocardial O₂ demand (MVO₂)?

A
  • Heart rate
  • Myocardial contractility (inotropic state)
  • Ventricular wall stress (LaPlace law)

Therapies that lower these variables can relieve ischaemia.

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3
Q

What are common coronary causes of myocardial ischaemia?

A
  • Atherosclerotic fixed stenosis
  • Acute thrombotic occlusion (Type 1 MI)
  • Plaque erosion with in-situ thrombosis
  • Vasospasm (Prinzmetal)
  • Spontaneous coronary artery dissection (SCAD)
  • Embolism
  • Anomalous coronary origin/compression

Type 2 MI involves non-coronary supply-demand mismatch.

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4
Q

What are the causes of non-coronary supply-demand mismatch (Type 2 MI)?

A
  • Severe anemia
  • Hypoxemia
  • Shock/hypotension
  • Severe hypertension or LVH
  • Rapid SVT/brady-arrhythmia
  • Severe aortic stenosis
  • Thyrotoxicosis
  • Sepsis

Other causes include microvascular dysfunction and inflammatory vasculitides.

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5
Q

What characterizes Prinzmetal/Variant angina?

A

Episodic rest pain from focal coronary spasm, transient ST-segment elevation during pain, responsive to nitrates/CCBs.

β-blockers may aggravate this condition.

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6
Q

What is chronic stable angina?

A

Exertional, reproducible chest pressure lasting <10 min, relieved by rest/nitroglycerin due to fixed ≥70% atherosclerotic stenosis.

It limits flow reserve.

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7
Q

What distinguishes unstable angina from stable angina?

A

Crescendo pattern, pain at rest >20 min, or new-onset severe class III angina; no biomarker rise.

It is associated with plaque rupture/erosion.

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8
Q

What ECG changes are seen in stable/unstable angina?

A

Transient horizontal/down-sloping ST-segment depression and/or symmetric T-wave inversion in ischemic territory.

These changes usually resolve ≤20 min post-pain.

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9
Q

What ECG changes are associated with Prinzmetal angina?

A

Transient convex ST-elevation in leads overlying spasm territory, with reciprocal depressions; normalizes after nitrate relief.

Often ≥1 mm elevation is noted.

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10
Q

What are key aspects of management for myocardial ischaemia?

A
  • Risk-factor modification (e.g., LDL <55 mg/dL, BP <130/80)
  • Symptom control with nitrates and β-blockers
  • Event prevention with high-intensity statins and antiplatelets
  • Revascularisation for severe cases

European Society of Cardiology guidelines recommend these strategies.

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11
Q

Fill in the blank: The formula for ventricular wall stress is _______.

A

Pressure × radius / 2·wall-thickness

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12
Q

What are the non-modifiable risk factors for atherosclerosis?

A

Age, male sex, family history of premature ASCVD, monogenic disorders (e.g., FH)

ASCVD: Atherosclerotic Cardiovascular Disease; FH: Familial Hypercholesterolemia.

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13
Q

List the modifiable major risk factors for atherosclerosis.

A
  • Dyslipidaemia (↑LDL‑C, ↓HDL‑C, ↑Lp(a))
  • Hypertension
  • Diabetes/metabolic syndrome
  • Cigarette smoking
  • Chronic kidney disease
  • Obesity
  • Physical inactivity
  • Diet high in saturated/trans-fats
  • Psychosocial stress

LDL-C: Low-Density Lipoprotein Cholesterol; HDL-C: High-Density Lipoprotein Cholesterol; Lp(a): Lipoprotein(a).

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14
Q

What are some emerging risk factors for atherosclerosis?

A
  • Chronic inflammatory disorders
  • Air pollution
  • Clonal haematopoiesis
  • HIV
  • Sleep apnoea

Clonal haematopoiesis refers to the presence of blood cells derived from a single mutated stem cell.

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15
Q

What is the current paradigm for the pathogenesis of atherosclerosis?

A

Response-to-injury & lipid retention paradigm: endothelial dysfunction → increased permeability + expression of VCAM‑1/ICAM‑1 → LDL infiltration & oxidation → monocyte adhesion and transformation to foam cells → cytokine-driven smooth-muscle migration/proliferation → extracellular-matrix deposition forming fibrofatty plaque → possible calcification

VCAM-1: Vascular Cell Adhesion Molecule 1; ICAM-1: Intercellular Adhesion Molecule 1.

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16
Q

What are the key drivers of atherosclerosis?

A
  • Modified lipoproteins
  • Innate/adaptive immunity (TLRs, T-cells)
  • Defective efferocytosis
  • Neovascularization
  • Outward (positive) remodelling

TLRs: Toll-like Receptors; Efferocytosis: the process of clearing apoptotic cells.

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17
Q

Describe the microscopy findings in early fatty streak.

A

Foam-cell–laden intima, minimal matrix

Foam cells are lipid-laden macrophages found in the early stages of atherosclerosis.

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18
Q

What characterizes a fibro-atheroma?

A
  • Lipid-rich necrotic core with cholesterol clefts
  • Necrotic debris
  • Overlying fibrous cap of smooth muscle cells and collagen
  • Shoulder region rich in T-cells/macrophages
  • Vasa-vasorum neovascularisation

Vasa-vasorum are small blood vessels that supply the walls of larger blood vessels.

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19
Q

What are the features of a complicated plaque?

A
  • Surface ulceration
  • Intraplaque haemorrhage
  • Calcification
  • Thrombosis

Complicated plaques are associated with acute cardiovascular events.

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20
Q

True or False: Plaque rupture accounts for approximately 60% of STEMI and NSTEMI.

A

True

STEMI: ST-Elevation Myocardial Infarction; NSTEMI: Non-ST-Elevation Myocardial Infarction.

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21
Q

What is the main difference between plaque rupture and plaque erosion?

A

Plaque rupture features a large lipid core and thin inflamed cap; plaque erosion has an intact cap and produces a platelet-rich thrombus

Plaque erosion is particularly noted in younger females and smokers.

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22
Q

Fill in the blank: A Mediterranean/plant-forward diet is recommended to reduce _______ in atherosclerosis.

A

[saturated fats]

This diet emphasizes the reduction of saturated fats and processed meats while increasing polyunsaturated fatty acids and fiber.

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23
Q

What lifestyle changes are recommended for atherosclerosis management?

A
  • Mediterranean/plant-forward diet
  • ≥150 min/wk moderate exercise
  • Weight optimisation (BMI <25 kg/m²)
  • Smoking cessation
  • Limited alcohol
  • Stress reduction
  • Good sleep hygiene

BMI: Body Mass Index.

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24
Q

What pharmacologic treatment is recommended for high-risk patients with LDL ≥ 70 mg/dL?

A

Add ezetimibe

Ezetimibe is a medication that lowers cholesterol levels.

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25
List some emerging therapies for atherosclerosis.
* Anti-inflammatories (colchicine 0.5 mg, IL-1β inhibitors) * Lp(a)-lowering RNA therapeutics ## Footnote Lp(a): Lipoprotein(a); IL-1β: Interleukin-1 beta.
26
What are Triacylglycerols (TG)?
Glycerol + 3 fatty acids; energy storage. ## Footnote Triacylglycerols are the main form of stored fat in the body.
27
What are the components of Phospholipids?
Glycerol, 2 fatty acids, phosphate head; membrane bilayers. ## Footnote Phospholipids are essential for forming cellular membranes.
28
What is the role of Cholesterol in the body?
Modulates membrane fluidity, precursor of bile acids & steroids; stored/transported as cholesterol-esters. ## Footnote Cholesterol is vital for cell membrane structure and hormone production.
29
List the classes of Lipoproteins.
* Chylomicrons * VLDL * IDL * LDL * HDL * Lp(a) ## Footnote Lipoproteins are classified by their density and apolipoprotein content.
30
What is the structure of LDL?
Core triglycerides + cholesterol esters; surface phospholipid monolayer with apoB-100. ## Footnote LDL delivers cholesterol to peripheral tissues.
31
What is the role of apoB-100 in LDL?
Structural ligand for LDL receptor. ## Footnote ApoB-100 is crucial for the uptake of LDL by cells.
32
What happens when there is excess LDL?
Undergoes sub-endothelial oxidation → foam-cell formation. ## Footnote Foam cells are a key component in atherosclerosis.
33
What is the function of Apolipoprotein A-I?
Facilitates HDL-cholesterol efflux. ## Footnote Apolipoproteins are proteins that bind lipids to form lipoproteins.
34
What is the association between LDL and Atherosclerosis?
Causal through Mendelian, epidemiologic, interventional evidence. ## Footnote High levels of LDL cholesterol are linked to cardiovascular diseases.
35
How does oxidised LDL affect the body?
Activates endothelium, fuels foam-cell formation, provokes inflammation. ## Footnote Inflammation from oxidised LDL contributes to atherosclerosis progression.
36
What do lipid-lowering agents like Statins do?
HMG-CoA-reductase inhibition increases LDL receptor expression; decreases LDL 30–55%. ## Footnote Statins also have anti-inflammatory effects.
37
What is the mechanism of Ezetimibe?
NPC1L1 blockade; synergistic with statin. ## Footnote Ezetimibe reduces cholesterol absorption in the intestine.
38
What are PCSK9 inhibitors and their effect?
Prevent LDL receptor degradation; decrease LDL 50–60%. ## Footnote Examples include evolocumab and alirocumab.
39
What role does HDL play in heart disease?
Facilitates reverse cholesterol transport, antioxidant, anti-inflammatory, endothelial-protective. ## Footnote Raising HDL levels pharmacologically has shown limited success.
40
What does Hypertriglyceridemia predict?
Residual ASCVD and pancreatitis. ## Footnote Management includes lifestyle changes and medications.
41
Fill in the blank: HDL is known for its role in _______.
Reverse cholesterol transport. ## Footnote HDL helps to remove cholesterol from cells and transport it to the liver.
42
What is the global leading single cause of death?
Ischaemic Heart Disease ## Footnote Myocardial infarction (MI) is the leading cause of death worldwide.
43
Approximately how many myocardial infarctions occur annually in the US as of 2023?
≈805,000 MIs/yr ## Footnote This statistic indicates the high prevalence of myocardial infarctions in the US.
44
What is the median age for males and females experiencing myocardial infarctions in the US?
Median age 65 ♂, 72 ♀ ## Footnote This reflects the age distribution among individuals affected by MI.
45
What proportion of myocardial infarctions are STEMI?
~27% ## Footnote This indicates the percentage of MIs that are classified as ST-Elevation Myocardial Infarctions.
46
What are common risk factors for Ischaemic Heart Disease?
Overlaps with atherosclerosis; acute triggers such as: * Cocaine * Intense exertion in sedentary individuals * Emotional stress ## Footnote These factors contribute to the risk of developing Ischaemic Heart Disease.
47
What is the pathophysiological mechanism of myocardial infarction?
Abrupt occlusive thrombosis on vulnerable plaque leading to transmural wavefront necrosis ## Footnote This process occurs from sub-endocardium to epicardium within 30–40 minutes.
48
What factors dictate the size of the infarct in myocardial infarction?
Collateral flow, ischaemic pre-conditioning, and reperfusion time ## Footnote These factors influence the extent of damage during a myocardial infarction.
49
What are common clinical manifestations of myocardial infarction?
Prolonged crushing retrosternal chest pain ± radiation, diaphoresis, nausea, dyspnoea; atypical symptoms in elderly/diabetics ## Footnote Symptoms may vary based on demographics and individual health conditions.
50
What are the sympathetic and vagal responses during myocardial infarction?
Sympathetic surge: tachycardia, hypertension; Vagal response: hypotension, bradycardia ## Footnote These responses reflect the body's reaction to stress during an MI.
51
What characterizes the ECG findings in STEMI?
New ST-elevation at the J-point ≥1 mm in contiguous leads (V2-V3 sex-specific), reciprocal depressions; later Q-waves, T-wave inversion ## Footnote These are critical indicators for diagnosing STEMI on an ECG.
52
What are the ECG findings associated with NSTEMI?
ST-depression, T-wave inversion, or non-diagnostic; loss of R-wave amplitude/evolution ## Footnote These changes differ from those seen in STEMI and are important for diagnosis.
53
What are the dynamic ECG changes associated with myocardial infarction (MI)?
Dynamic ST‑T changes, new LBBB, posterior infarction by V1‑V3 ST‑depression, hyperacute T‑waves, ventricular arrhythmias. ## Footnote LBBB refers to Left Bundle Branch Block, indicating a delay in the electrical conduction in the heart.
54
What cardiac biomarker is used to fulfill the 4th Universal MI definition?
High‑sensitivity cardiac troponin I/T: rise/fall with ≥1 value > 99ᵗʰ percentile + evidence of ischaemia. ## Footnote CK‑MB is reserved for reinfarction timing and BNP is useful prognostically.
55
What imaging techniques are used for ischemia and viability assessment?
Coronary CTA, stress echo, nuclear MPI, stress CMR, invasive coronary angiography ± OCT/IVUS, CMR T2‑mapping, LGE. ## Footnote OCT refers to Optical Coherence Tomography, and IVUS refers to Intravascular Ultrasound.
56
What is the morphology of an infarct at 0–30 minutes?
Reversible. ## Footnote This indicates that changes during this time frame may not lead to permanent damage.
57
What changes occur in myocardial morphology at 0.5–4 hours post-infarction?
Wavy fibres, oedema. ## Footnote Oedema refers to swelling due to excess fluid in the tissues.
58
What histological changes occur in the heart between 4–24 hours after an infarct?
Coagulative necrosis, neutrophils. ## Footnote Coagulative necrosis is a form of tissue death that occurs due to loss of blood supply.
59
What is observed in the heart from 1 to 3 days after an infarct?
Dense neutrophils. ## Footnote Neutrophils are a type of white blood cell that plays a key role in the inflammatory response.
60
What changes are seen in the heart from 3 to 7 days after an infarct?
Macrophages, granulation. ## Footnote Macrophages are immune cells that help clear dead cells and debris from the site of injury.
61
What morphological changes occur in the heart from 7 to 10 days after an infarct?
Soft, yellow. ## Footnote This indicates the transition towards scar formation.
62
What is the morphology of the heart tissue after more than 2 weeks post-infarct?
Collagen scar. ## Footnote This represents the final stage of healing where a fibrous scar replaces the necrotic tissue.
63
What initial investigations should be conducted for suspected IHD?
Initial 12‑lead ECG & hs‑cTn at 0/1‑h algorithms. ## Footnote hs‑cTn refers to high-sensitivity cardiac troponin.
64
How should stress versus anatomic imaging be selected in IHD diagnosis?
By pre‑test probability; avoid stress testing in high‑risk ACS—proceed to angiography. ## Footnote ACS refers to Acute Coronary Syndrome.
65
What factors should be considered when choosing the modality for imaging in IHD?
Renal function, pregnancy, arrhythmia. ## Footnote These factors can influence the safety and efficacy of certain imaging modalities.
66
What does MONA-B stand for in the management of myocardial infarction?
Morphine for analgesia, Oxygen if SpO₂ < 90%, Sublingual then IV nitrates, Aspirin 162–325 mg chewed, P2Y₁₂ inhibitor loading, β-blocker within 24 h, Anticoagulation, high-intensity statin ASAP, ACE-I/ARB by 24 h, Aldosterone antagonist if EF ≤ 40% & HF/DM ## Footnote MONA-B is a protocol for the acute management of myocardial infarction, emphasizing immediate treatment options.
67
What is the role of aspirin in the management of myocardial infarction?
Aspirin irreversibly acetylates platelet COX-1, blocking TxA₂ ## Footnote This action helps to prevent platelet aggregation.
68
What do P2Y₁₂ inhibitors do?
Prevent ADP-mediated aggregation ## Footnote Examples include ticagrelor and prasugrel.
69
How do nitrates function in myocardial infarction treatment?
NO-donors ↑cGMP → venodilation ↓pre-load & wall stress ## Footnote Nitrates also relieve spasm.
70
What is the effect of β-blockers in myocardial infarction management?
↓HR, contractility, BP lowering MVO₂ and arrhythmias ## Footnote β-blockers are competitive β-adrenergic antagonists.
71
What is the mechanism of action of morphine in myocardial infarction?
μ-agonist analgesia & venodilation via histamine ## Footnote Morphine provides pain relief and reduces venous return.
72
What do anticoagulants do in the context of myocardial infarction?
Heparins potentiate antithrombin III (factor Xa & IIa inhibition); bivalirudin is a direct IIa inhibitor ## Footnote Anticoagulants help prevent further clotting.
73
What is the goal time for primary PCI in STEMI management?
≤90 min FMC ## Footnote FMC stands for First Medical Contact.
74
What should be done if primary PCI is not available within 120 minutes for STEMI?
Fibrinolysis (tenecteplase) within 30 min then rescue PCI ## Footnote This is a backup strategy to restore blood flow.
75
What is recommended for NSTEMI/UA patients at high risk?
Early invasive (<24 h) intervention ## Footnote Criteria include GRACE > 140, troponin-positive, dynamic ST-T changes.
76
What adjunct treatments may be used in cases of cardiogenic shock?
Intracoronary imaging, thrombus aspiration, mechanical circulatory support (IABP, Impella) ## Footnote These interventions can support circulation during critical events.
77
When is surgical CABG indicated in myocardial infarction management?
For multi-vessel/L-main unsuitable for PCI ## Footnote CABG is a surgical option for patients who cannot undergo PCI.
78
What are early complications of cardiac events?
Arrhythmias (VT/VF), acute LV failure, pulmonary oedema, cardiogenic shock, papillary-muscle rupture, severe MR, IV-septal rupture, free-wall rupture, tamponade, pericarditis (fibrinous) ## Footnote VT stands for ventricular tachycardia, VF for ventricular fibrillation, MR for mitral regurgitation, IV for interventricular.
79
What are late complications of cardiac events?
Ventricular aneurysm, mural thrombus/embolism, Dressler (auto-immune) pericarditis, chronic HF, electrical remodelling-arrhythmias ## Footnote HF stands for heart failure.
80
What is the most common cause of death in early complications?
Arrhythmias (VT/VF) ## Footnote VT and VF are types of heart arrhythmias that can lead to sudden cardiac death.
81
What does secondary prevention lifestyle include?
Smoking cessation, heart-healthy diet, structured CR exercise, weight/BMI optimisation, BP management, LDL management, HbA1c management, limited alcohol, vaccination, psychosocial stress management, adherence monitoring ## Footnote CR stands for cardiac rehabilitation.
82
What are the components of a heart-healthy diet?
DASH and Mediterranean diets ## Footnote DASH stands for Dietary Approaches to Stop Hypertension.
83
Fill in the blank: Blood pressure should be maintained at _______ mm Hg.
< 130/80
84
What is the target LDL level for secondary prevention?
< 55 mg/dL ## Footnote Statins or non-statins may be used to achieve this target.
85
What is the target HbA1c level for diabetic patients?
< 7% ## Footnote HbA1c is a measure of average blood glucose levels over the past 2-3 months.
86
True or False: Vaccination is part of secondary prevention lifestyle modifications.
True
87
What are the 5 A's related to smoking cessation?
Ask, Advise, Assess, Assist, Arrange ## Footnote These are steps in a framework for helping patients quit smoking.
88
What is the recommended frequency of structured CR exercise?
5–7 days per week
89
Fill in the blank: Psychosocial stress management is important for _______ prevention.
secondary
90
What type of disease is atherosclerosis?
An inflammatory lipid-driven disease ## Footnote Atherosclerosis involves the accumulation of lipids and inflammatory processes in arterial walls.
91
What are the fundamental factors in atherosclerosis?
Cumulative LDL-exposure and endothelial dysfunction ## Footnote LDL stands for low-density lipoprotein, known as 'bad cholesterol'.
92
What is the primary focus for symptom relief in stable angina?
MVO₂ reduction ## Footnote MVO₂ stands for myocardial oxygen consumption.
93
What is crucial for the prognosis of stable angina?
Risk-factor control and antithrombotics ## Footnote Antithrombotics are medications that prevent blood clots.
94
What does acute MI require for effective treatment?
Rapid reperfusion plus intensive antithrombotic and secondary-prevention therapy ## Footnote MI stands for myocardial infarction, commonly known as a heart attack.
95
According to the 2025 ACC/AHA multisociety ACS guideline, what is essential for treating acute MI?
Rapid reperfusion ## Footnote ACS stands for acute coronary syndrome.
96
What is increasingly recognized in acute coronary syndrome (ACS)?
Plaque erosion ## Footnote Plaque erosion may lead to different therapeutic approaches compared to plaque rupture.
97
What may plaque erosion indicate in terms of treatment?
A different therapeutic nuance compared with classic rupture ## Footnote Classic rupture refers to the breaking of atherosclerotic plaque, leading to clot formation.
98
What contributes to durable patient benefit in cardiovascular health?
Life-long lifestyle optimisation alongside evidence-based pharmacology ## Footnote Lifestyle optimisation includes diet, exercise, and smoking cessation.

Cardiovascular (13 decks)

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