Myocardial Infarction Flashcards
5 subtypes of MI
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
type 1 myocardial infarction
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
type 2 myocardial infarction
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)
type 3 myocardial infarction
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
type 4 myocardial infarction
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
pathophysiology of NSTEMI
partial coronary artery occlusion causes decreased myocardial blood flow
supply demand mismatch -> myocardial ischaemia
usually affects the inner layer of the myocardium (subendocardial infarction)
why is the inner layer of the heart muscle affected first in coronary artery occlusion
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
pathophysiology of STEMI
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)
stable atherosclerotic plaque
manifests as stable angina (symptomatic during exertion)
unstable atherosclerotic plaque
lipid rich and covered in thin fibrous caps
high risk of rupture and acute coronary syndrome
pathogenesis of type 1 coronary artery occlusion
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
non ischaemic myocardial injury
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
infarction of the anterior wall
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
infarction of the inferior wall
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
how to remember ECG leads with maximal elevation in anterior MI
SAL
Septal V1,V2
Apical V3, V4
Lateral V5, V6
ECG changes in severe posterior wall infarction
there may not be ST elevation in standard 12 lead ECG in severe transmural posterior wall infarction
troponin levels
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
laboratory studies
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
coronary angiography
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
transthoracic echocardiography
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
reperfusion injury
can occur spontaneously or after PCI
typically occurs when reperfusion occurs >3 hours after the acute coronary occlusion
why does reperfusion injury occurs
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
critical management
?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
adjunctive therapy
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
