Myocardial Infarction

Question 1

5 subtypes of MI

Answer 1

type 1: caused by atherosclerotic plaque
type 2: secondary to oxygen supply/demand mismatch
type 3: MI resulting in death when biomarkers are not available
type 4: MI related to PCI
type 5: MI related to CABG

Question 2

type 1 myocardial infarction

Answer 2

MI caused by atherosclerotic plaque disruption or acute coronary thrombosis
most common form
caused by acute thrombosis due to erosion, ulceration, fissuring, dissection, or rupture of an atherosclerotic plaque
decreased myocardial blood flow causes sudden death of myocardial cells
usually manifests as STEMI

Question 3

type 2 myocardial infarction

Answer 3

MI secondary to an oxygen supply/demand mismatch
less common form (14%)
occurs predominantly in women and in individuals with comorbidities eg. diabetes, previous NSTEMI)
not due to plaque rupture and caused by a condition other than coronary artery disease
ischaemia is caused by increased oxygen demand eg. anaemia or decreased coronary blood supply (eg. coronary artery spasm)

Question 4

type 3 myocardial infarction

Answer 4

MI resulting in death when biomarker values are unavailable
this is not synonymous with sudden cardiac death
MI is caused by ischaemic damage to the myocardium, whereas sudden cardiac death can also be caused by acute arrythmia that may be unrelated to ischaemia

Question 5

type 4 myocardial infarction

Answer 5

MI related to PCI
type 4a: MI < 48 hours after PCI
type 4b: MI related to stent thrombosis
tybe 4c: MI associated with restenosis after PCI

Question 6

pathophysiology of NSTEMI

Answer 6

partial coronary artery occlusion causes decreased myocardial blood flow
supply demand mismatch -> myocardial ischaemia
usually affects the inner layer of the myocardium (subendocardial infarction)

Question 7

why is the inner layer of the heart muscle affected first in coronary artery occlusion

Answer 7

because the blood flow is directed from the outer to the inner heart
as a result, the inner layer is the least perfused and most affected

Question 8

pathophysiology of STEMI

Answer 8

complete coronary artery occlusion
impaired myocardial blood flow
sudden death of myocardial cells (if no reperfusion occurs)
usually affects the full thickness of the myocardium (transmural infarction)

Question 9

stable atherosclerotic plaque

Answer 9

manifests as stable angina (symptomatic during exertion)

Question 10

unstable atherosclerotic plaque

Answer 10

lipid rich and covered in thin fibrous caps
high risk of rupture and acute coronary syndrome

Question 11

pathogenesis of type 1 coronary artery occlusion

Answer 11

inflammatory cells in the plaque eg. macrophages secrete matrix metalloproteinases causing breakdown of extracellular matrix and weakening of fibrous cap
minor stress ruptures the fibrous cap and exposes the highly thrombogenic lipid core
this causes thrombus formation and coronary artery occluion

Question 12

non ischaemic myocardial injury

Answer 12

necrosis of myocardial tissue without ischaemia eg. in sepsis
the pathophysiology of myocardial damage is not completely understood, but potential explanations include
- inflammatory cytokines
- toxicity of high catecholamine levels

Question 13

infarction of the anterior wall

Answer 13

caused by obstruction of the LAD or its branches
results in ECG changes in the anterior wall leads which are V1-6 and/or I and aVL

Question 14

infarction of the inferior wall

Answer 14

infarction of the inferior wall is caused by obstruction of the Left circumflex artery LCX or right coronary artery RCA or their branches, and ECG changes are seen in lead II, III, and aVF

Question 15

how to remember ECG leads with maximal elevation in anterior MI

Answer 15

SAL
Septal V1,V2
Apical V3, V4
Lateral V5, V6

Question 16

ECG changes in severe posterior wall infarction

Answer 16

there may not be ST elevation in standard 12 lead ECG in severe transmural posterior wall infarction

Question 17

troponin levels

Answer 17

degree of elevation correlates with the size of the infarct and risk of mortality
troponin levels on day 3-4 after myocardial infarction can help to estimate the extent of myocardial necrosis
normalises after 7-10 days

Question 18

laboratory studies

Answer 18

hemoglobin: anaemia can exacerbate myocardial ischaemia
platelets to evaluate for thrombocytopaenia (may affect management options and use of anticoagulants)
elevated inflammatory markers: associated with increased risk of ischeameia and cardiac death
BNP and NT-proBNP: may be elevated, especially in concurrent heart failure

Question 19

coronary angiography

Answer 19

best test for definitive diagnosis of acute coronary occlusion to identify site and degree of vessel occlusion
can be used for concurrent intervention eg. PCI with stent placement

Question 20

transthoracic echocardiography

Answer 20

identification of any wall motion abnormalities and assessment of LV function
evaluation for complications: aneurysms, mitral valve regurgitation, pericardial effusion, free wall rupture
risk assessment: in STEMI, the best predictor of survival is LVEF

Question 21

reperfusion injury

Answer 21

can occur spontaneously or after PCI
typically occurs when reperfusion occurs >3 hours after the acute coronary occlusion

Question 22

why does reperfusion injury occurs

Answer 22

when blood flow is restored
damaged myocytes release reactive oxygen species
mitochondrial permeability transition pores are formed
there is cell swelling and cell death
Ca2+ entry into the cytosol, hypercontraction of myocytes
contraction band necrosis and increase in infarct size

Question 23

critical management

Answer 23

?revascularisation
monitoring with 12 lead ECG, continuous cardiac monitoring, serial serum troponins
DAPT: aspirin loading dose 162-325mg plus ADP receptor inhibitor
anticoagulation: unfractioned heparin or LMWH

Question 24

adjunctive therapy

Answer 24

oxygen: for severe dyspnoea, cyanosis or SpO2 <90%
sublingual or IV nitrate for symptomatic relief of chest pain
morphine IV or SQ
beta blockers
statins
ACE inhiibitor/ARBs
aldosterone antagonists

Question 25

contraindcations of nitrate and nitroglycerin

Answer 25

inferior wall infarct due to risk for hypotension
hypotension
PDE5 inhibitor taken within the last 24 hours

Question 26

prevention of recurrent MI

Answer 26

lifestyle modifications
lipid lowering therapy: all patients should start on a high intensity statin eg. atorvastatin
life long low dose aspirin
DAPT: duration is an individual decision based on bleeding risk and risk of stent thrombosis
management of comorbidities
beta blocker
ACE inhibitor/ARB

Question 27

sudden cardiac death

Answer 27

Sudden cardiac death presumably caused by cardiac arrythmia or hemodynamic catastrophe

Question 28

how to prevent sudden cardiac death

Answer 28

installation of implantable cardioverter-defribrillator device

Question 29

complications in first 24 hours following MI

Answer 29

sudden cardiac death
arrythmias
acute left heart failure
cardiogenic shock

Question 30

cause of acute left heart failure following MI

Answer 30

death of affected myocardium
absence of myocardial contraction
pulmonary oedema

Question 31

complications 1-3 days post MI

Answer 31

early infarct-associated pericarditis

Question 32

ealry infarct associated pericarditis

Answer 32

typically occurs within the first week of a large infarct close to the pericardium
myocardial necrosis triggers localized inflammation with clinical features of acute pericarditis
treat with supportive care, usually self limiting

Question 33

clinical features of early infarct associated pericarditis

Answer 33

friction rub
pleuritic chest pain, dry cough
diffuse ST elevations on ECG
pericardial effusion

Question 34

how to prevent early infarct associated pericarditis

Answer 34

early coronary reperfusion therapy to reduce the extent of necrotic myocardial tissue