Acute Coronary Syndromes and Sudden Death Flashcards

1
Q

What is the term for a blood clot formation in the coronary arteries?

A

Coronary thrombosis

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2
Q

What is the term used to describe the rupture of a plaque in the arterial wall?

A

Plaque rupture

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3
Q

What type of plaque is considered “vulnerable” due to its thin cap?

A

Thin cap = ‘vulnerable’ plaque

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4
Q

What components are exposed when a plaque ruptures?

A

Collagen/lipid

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5
Q

What is the term for the strong tendency of a substance to promote blood clot formation?

A

Thrombogenic +++

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6
Q

What is the initial step in the formation of a blood clot in coronary thrombosis?

A

Platelet adhesion

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7
Q

What is the term for a mass of platelets that form at the site of plaque rupture?

A

Platelet thrombus

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8
Q

What happens to the clotting system when plaque rupture occurs?

A

Clotting system activated

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9
Q

What type of thrombus is formed as a result of coronary thrombosis?

A

Red thrombus

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10
Q

What can result from partial or intermittent occlusion of a coronary artery or embolism?

A

Occlusion (?partial/intermittent) or embolism

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11
Q

What are some diagnostic factors for acute coronary syndrome (ACS)?

A

History, typical cardiac pain, atypical pain, shortness of breath, collapse, pale, sweaty, complications (e.g., arrhythmia, heart failure), ECG changes (ST elevation/depression, T wave inversion), elevated cardiac markers (cardiac troponin)

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12
Q

Where does cross-bridging between thick and thin filaments occur?

A

Troponin complex

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13
Q

What does Tn-T bind to in the troponin complex?

A

Tropomyosin

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14
Q

What does Tn-C bind to during excitation-contraction coupling?

A

Calcium (Ca2+)

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15
Q

Which components of the troponin complex are specific to cardiac muscle?

A

Tn-T and Tn-I

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16
Q

What is the role of creatine kinase (CK)?

A

Moves high-energy phosphate from ATP in the mitochondria to ADP in the cytoplasm

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17
Q

Which form of creatine kinase is more specific to cardiac muscle?

A

CK-MB

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18
Q

What are some markers used for diagnosing myocardial damage?

A

Cardiac specific markers (troponin T or I), cardiac selective enzymes (creatine kinase MB), myoglobin, non-specific enzymes (AST, LDH)

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19
Q

What does STEMI stand for, and which region of the heart does it typically affect?

A

STEMI stands for ST-segment elevation myocardial infarction. It typically affects the anterior region of the heart.

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20
Q

What ECG finding is commonly observed in widespread myocardial ischemia?

A

ST depression

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21
Q

What does NSTEMI stand for, and which region of the heart does it typically affect?

A

NSTEMI stands for non-ST-segment elevation myocardial infarction. It can affect the anterior region of the heart.

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22
Q

What are some key components of acute management for acute coronary syndrome (ACS)?

A

Aspirin, LMW heparin (e.g., enoxaparin), anti-anginal medication, nitrate (e.g., GTN), revascularization (timing may vary).

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23
Q

What is the recommended anti-thrombotic treatment for ACS?

A

The recommended anti-thrombotic treatment for ACS includes aspirin, P2Y12 inhibitors (such as clopidogrel or ticagrelor), and anticoagulants (such as heparin or low-molecular-weight heparin).

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24
Q

What are some common presentations of acute coronary syndrome (ACS)?

A

Common presentations of ACS include unstable angina, NSTEMI, and STEMI.

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25
Q

What is the term used to describe the sequence of events that occur during myocardial ischemia?

A

Ischemic cascade

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26
Q

What factors influence the severity of ischemia?

A

Time and metabolic disturbance

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27
Q

What type of cardiac dysfunction can occur as a result of ischemia?

A

Diastolic dysfunction and systolic dysfunction

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28
Q

What are some ECG changes that can be observed during ischemia?

A

ECG changes such as ST-segment depression or elevation

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29
Q

What is a common symptom experienced during myocardial ischemia?

A

Chest pain

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30
Q

What is the consequence of prolonged ischemia on myocytes?

A

Myocyte necrosis

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31
Q

What can result from inadequate blood supply during ischemia?

A

Hypoperfusion, arrhythmia, acute heart failure

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32
Q

How long does it take for myocardial necrosis to be detectable after the onset of acute ST-segment elevation myocardial infarction (STEMI)?

A

Necrosis is detectable after 15 minutes.

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33
Q

Which part of the myocardium is more sensitive to ischemia?

A

Sub-endocardial myocardium

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34
Q

Up to how many hours after coronary occlusion can myocardium be salvaged?

A

Myocardium can be salvaged up to 12 hours after coronary occlusion.

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35
Q

What is the primary treatment option for acute reperfusion in STEMI?

A

Thrombolysis with “clot-buster” drugs (fibrinolytic agents).

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36
Q

What was the significant finding of the ISIS-2 trial regarding thrombolysis for acute myocardial infarction (MI)?

A

The trial showed a 39% reduction in mortality with streptokinase and aspirin compared to placebo.

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37
Q

What is the alternative treatment option for acute reperfusion in STEMI, as shown by the PAMI trial?

A

Primary percutaneous coronary intervention (PCI)

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38
Q

What was the mortality rate observed in the PAMI trial for patients who underwent primary PCI?

A

The mortality rate for patients who underwent primary PCI was 2.6%.

39
Q

What was the mortality rate observed in the Stent-PAMI trial for patients who underwent primary PCI with stent placement?

A

The mortality rate for patients who underwent primary PCI with stent placement was 0.8%.

40
Q

What is the recommended intervention for NSTEMI within 72 hours?

A

Angiography (+/-) percutaneous coronary intervention (PCI) within 72 hours, unless there are complications.

41
Q

What is the recommended intervention for unstable angina within 72 hours?

A

Angiography (+/-) percutaneous coronary intervention (PCI) within 72 hours, unless the patient is at very low risk. In such cases, they can be discharged on medical therapy and scheduled for elective investigation.

42
Q

What are the usual medications prescribed for patients after acute myocardial infarction (MI)?

A

The usual discharge cocktail includes dual antiplatelet therapy (e.g., aspirin and clopidogrel for 12 months), high-dose statin (e.g., atorvastatin), ACE inhibitor (e.g., ramipril), and beta-blocker (e.g., bisoprolol).

43
Q

What are some complications that can occur after MI?

A

Complications can include poor ventricular function, acute pulmonary edema, shock, arrhythmias, mechanical complications (cardiac rupture, ventricular septal defect, mitral valve dysfunction), reinfarction, and stent thrombosis.

44
Q

What is the specific complication that can occur after MI involving a ruptured papillary muscle?

A

Post MI - Ruptured papillary muscle.

45
Q

What is the specific complication that can occur after MI involving a ventricular septal defect (VSD)?

A

Post MI - Ventricular septal defect.

46
Q

What are some examples of secondary preventive medications after myocardial infarction (MI)?

A

Dual antiplatelet therapy, ACE inhibitors, beta-blockers, and statins.

47
Q

What is the purpose of dual antiplatelet therapy in secondary prevention?

A

Dual antiplatelet therapy helps prevent stent thrombosis and reduces further coronary events.

48
Q

What is the purpose of ACE inhibitors in secondary prevention?

A

ACE inhibitors help prevent adverse left ventricular remodeling and also reduce further coronary events.

49
Q

What is the purpose of beta-blockers in secondary prevention?

A

Beta-blockers help prevent recurrent ischemia and arrhythmias and improve prognosis if there is impaired left ventricular function.

50
Q

What is the purpose of statins in secondary prevention?

A

Statins help prevent atheroma progression and reduce vascular inflammation.

51
Q

How is sudden cardiac death (SCD) defined?

A

Sudden cardiac death is defined as unexpected death due to cardiac causes occurring in a short time period (<1 hour of onset). Most cases are due to (severe ventricular) arrhythmias.

52
Q

What is ventricular fibrillation (VF)?

A

Ventricular fibrillation is a chaotic, disorganized rhythm of the heart’s ventricles, resulting in ineffective pumping of blood.

53
Q

What is the purpose of cardiac defibrillators?

A

Cardiac defibrillators deliver an electric shock to depolarize all of the myocardium, aiming to restart the heart in a normal rhythm.

54
Q

What is the most common cause of sudden cardiac death (SCD) in individuals over the age of 30?

A

Ischemic heart disease (IHD) is the most common cause of SCD in individuals over the age of 30.

55
Q

What are some causes of SCD related to cardiomyopathies?

A

Causes include hypertrophic cardiomyopathy (commonest if <30 yrs), dilated cardiomyopathy, and right ventricular cardiomyopathy.

56
Q

What are some ion channelopathies that can lead to SCD?

A

Long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia (VT) are examples of ion channelopathies that can cause SCD.

57
Q

What are some other causes of SCD?

A

Other causes include aortic stenosis, commotio cordis (blow to the chest), and coronary artery anomalies.

58
Q

How many deaths per year occur due to sudden cardiac death in the UK?

A

Approximately 60,000 deaths per year occur due to sudden cardiac death in the UK.

59
Q

What percentage of all cardiac deaths does sudden cardiac death account for?

A

Sudden cardiac death accounts for approximately 50% of all cardiac deaths.

60
Q

What is the male-to-female ratio of sudden cardiac death cases?

A

The male-to-female ratio is approximately 3:1.

61
Q

At what age does sudden cardiac death typically peak?

A

Sudden cardiac death typically peaks between the ages of 45 and 75.

62
Q

What is the common cause of sudden cardiac death in the majority of cases?

A

The majority of sudden cardiac death cases are related to coronary disease, including acute myocardial infarction and chronic ischemic heart disease.

63
Q

What is the most common cause of sudden cardiac death in individuals under the age of 30?

A

Hypertrophic cardiomyopathy (HCM) is the most common cause of sudden cardiac death in individuals aged under 30.

64
Q

What are some characteristics of hypertrophic cardiomyopathy (HCM)?

A

HCM is an autosomal dominant condition with inappropriate left ventricular hypertrophy (LVH) and no other causes such as hypertension or aortic stenosis. The LV septum is often thicker than the posterior wall (asymmetrical LVH), and there may be left ventricular outflow tract obstruction and mitral regurgitation (systolic anterior motion).

65
Q

What are some common presentations of hypertrophic cardiomyopathy (HCM)?

A

Chest pain, breathlessness, palpitations, dizziness, syncope, murmur (due to left ventricular outflow tract obstruction or mitral regurgitation), abnormal screening ECG. In family screening, there is a 2-4% risk of sudden cardiac death (SCD) per year in adults and a 4-6% risk of SCD per year in children.

66
Q

What can be observed on an ECG in hypertrophic cardiomyopathy (HCM)?

A

ECG may show left ventricular hypertrophy (big complexes) and marked T-wave changes. It can commonly be mistaken for non-ST-segment elevation myocardial infarction (NSTEMI).

67
Q

What are some common investigations for hypertrophic cardiomyopathy (HCM)?

A

Investigations include ECG, echocardiography or MRI (to assess asymmetric left ventricular hypertrophy, left ventricular outflow tract gradient, and systolic anterior motion of the mitral valve), and genetic testing (which may reveal multiple abnormalities, with around 35% involving the β myosin heavy chain and 15% involving troponin T).

68
Q

What is arrhythmogenic right ventricular cardiomyopathy (ARVC)?

A

ARVC is characterized by fatty infiltration of the right ventricular free wall, right ventricular hypertrophy or dilatation, and is often familial (30-50% of cases). It can present with exertional dizziness or loss of consciousness.

69
Q

How is arrhythmogenic right ventricular cardiomyopathy (ARVC) diagnosed?

A

ARVC can be difficult to diagnose and may require a combination of clinical evaluation, ECG findings (such as epsilon waves), echocardiography (which may be challenging), and cardiac magnetic resonance (MR) imaging (which is considered the best investigation).

70
Q

What is the annual risk of sudden cardiac death (SCD) in arrhythmogenic right ventricular cardiomyopathy (ARVC)?

A

The annual risk of SCD in ARVC is approximately 2%.

71
Q

What are some examples of channelopathies related to cardiac action potentials?

A

Long QT syndrome (and variants) caused by Na+ or K+ channel abnormalities, Brugada syndrome caused by Na+ channel abnormalities, and catecholaminergic polymorphic ventricular tachycardia caused by abnormal intracellular Ca2+ handling.

72
Q

What are some characteristics of long QT syndrome (LQTS) on an ECG?

A

Long QT interval on the ECG is a characteristic finding in LQTS. Triggers such as swimming and alarm clocks can lead to arrhythmias.

73
Q

What are some characteristics of Brugada syndrome on an ECG?

A

Brugada syndrome is characterized by high ST take-off on V1-V2 on the ECG. It is often unmasked during sleep.

74
Q

What are some characteristics of catecholaminergic polymorphic ventricular tachycardia (CPVT)?

A

CPVT is associated with abnormal intracellular Ca2+ handling and often presents with a normal resting ECG. Exercise can trigger arrhythmias. It may be associated with deafness.

75
Q

What are some screening methods for inherited cardiac conditions?

A

Screening methods may include ECG and echocardiogram, genetic testing, and screening of first-degree relatives of index cases. Adults may undergo 5-yearly screening, while children may undergo annual screening.

76
Q

How often should first-degree relatives of individuals with inherited cardiac conditions undergo screening?

A

First-degree relatives should undergo screening every 5 years.

77
Q

How often should children with inherited cardiac conditions undergo screening?

A

Children with inherited cardiac conditions should undergo annual screening.

78
Q

How many first-degree relatives and second-degree relatives do you have?

A

I have 9 first-degree relatives and 32 second-degree relatives.

79
Q

What are some common causes of ventricular tachycardia (VT)?

A

Ventricular tachycardia is usually due to re-entry around left ventricular (LV) scarring, typically seen in established myocardial infarction (MI) or other structural heart diseases such as hypertrophic cardiomyopathy, dilated cardiomyopathies, and RV cardiomyopathy. It presents with regular, broad complexes and may degenerate into ventricular fibrillation (VF).

80
Q

What are some characteristics of supraventricular tachycardia (SVT)?

A

SVT is most commonly seen in younger patients with normal hearts. It presents with regular, narrow complexes. Generally, SVT is considered benign, but it can have adverse effects in certain situations.

81
Q

What is Wolff-Parkinson-White (WPW) syndrome?

A

WPW syndrome is characterized by the presence of an accessory pathway (bundle of Kent) that bypasses the normal conduction system, connecting the atria and ventricles. This pathway can conduct electrical signals rapidly, leading to various arrhythmias.

82
Q

What does the ECG of Wolff-Parkinson-White (WPW) syndrome show?

A

The ECG in WPW syndrome shows a characteristic delta wave, which represents early ventricular depolarization due to the presence of the accessory pathway.

83
Q

What are some examples of anti-arrhythmic drugs classified according to the Vaughan Williams classification?

A

Class Ia drugs prolong the action potential duration (e.g., disopyramide), Class Ib drugs block sodium channels and shorten the action potential duration (e.g., lignocaine), Class Ic drugs have no effect on the action potential duration (e.g., flecainide), Class II drugs are beta-blockers that block beta receptors (e.g., bisoprolol), Class III drugs are potassium channel blockers (e.g., amiodarone), and Class IV drugs are calcium channel blockers that block calcium channels (e.g., verapamil).

84
Q

Which drugs target the sinus node in the Vaughan Williams classification?

A

Drugs targeting the sinus node include Class II drugs (e.g., bisoprolol) and other drugs like ivabradine.

85
Q

Which drugs act on atrial muscle in the Vaughan Williams classification?

A

Atrial muscle can be affected by Class Ia (e.g., disopyramide), Class Ic (e.g., flecainide), Class II (e.g., bisoprolol), and Class III (e.g., amiodarone) drugs, among others.

86
Q

Which drugs target the AV node in the Vaughan Williams classification?

A

Drugs targeting the AV node include Class II (e.g., bisoprolol), Class III (e.g., amiodarone), and Class IV (e.g., verapamil) drugs, as well as others like digoxin and adenosine.

87
Q

Which drugs act on the left ventricular muscle in the Vaughan Williams classification?

A

Left ventricular muscle can be affected by Class Ia-c (e.g., disopyramide, flecainide), Class II (e.g., bisoprolol), and Class IV (e.g., verapamil) drugs, as well as others like lignocaine, magnesium (Mg2+), and amiodarone.

88
Q

What is the prognosis of anti-arrhythmic drugs in general?

A

In general, anti-arrhythmic drugs can reduce the frequency of arrhythmias and alleviate symptoms but do not improve prognosis. However, beta-blockers have shown benefit in long QT syndrome.

89
Q

What is Torsade de Pointes?

A

Torsade de Pointes is a specific type of ventricular tachycardia characterized by a twisting pattern on the ECG. It is often associated with prolonged QT intervals and can lead to syncope or sudden cardiac death.

90
Q

What is syncope?

A

Syncope is a transient loss of consciousness due to cerebral hypo-perfusion. It has a rapid onset, short duration, and spontaneous complete recovery. It is most commonly attributed to vaso-vagal syncope but can also be caused by arrhythmias, mechanical problems, or other factors.

91
Q

What are some red flags associated with syncope?

A

Red flags associated with syncope include sudden onset (less than 10 seconds), exertional or supine syncope, associated chest pain or breathlessness, known cardiac disease, loud murmur, significant injury, and abnormal ECG.

92
Q

Who are suitable candidates for implantable cardioverter-defibrillator (ICD) placement?

A

Suitable candidates for ICD placement include survivors of sudden cardiac death (excluding acute myocardial infarction), patients with poorly tolerated ventricular tachycardia, those with high-risk features such as poor left ventricular (LV) function (especially if there is a large scar), coronary disease, broad QRS complexes on ECG, and certain conditions like hypertrophic cardiomyopathy (HCM), long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (CPMVT), and arrhythmogenic right ventricular cardiomyopathy (ARVC).

93
Q

What are some risk factors used to assess sudden cardiac death (SCD) risk in hypertrophic cardiomyopathy (HCM)?

A

Risk factors for SCD in HCM include increased left ventricular (LV) thickness, family history of SCD, unexplained syncope, non-sustained ventricular tachycardia (VT) on ECGs, LV outflow tract (LVOT) gradient, age, and left atrial (LA) size. ICD placement is recommended for SCD survivors and for those with a 5-year SCD risk greater than 6%.

94
Q

What is the concept of “number needed to treat” in the context of implantable cardioverter-defibrillators (ICDs)?

A

The “number needed to treat” represents the number of patients who need to receive an ICD to save one life. This value varies depending on the patient population and their risk profiles.