Cardiac - ACS Flashcards
Differentiate Unstable Angina, NSTEMI and STEMI
□ Unstable angina (UA): severe ischaemia at rest without infarction
□ NSTEMI: partial occlusion of coronary arteries (usually due to critical narrowing) → some myocardial necrosis but not transmural
□ STEMI: complete occlusion of coronary arteries (usually due to acute plaque disruption leading to complete thrombosis) → transmural myocardial necrosis
4 major clinical presentations of ACS
Acute MI Pathophysiology
Phases of myocardial response to AMI
Causes of exertional chest pain vs resting chest pain
Classification of ACS
- Unstable angina
- Plaque rupture with thombus formation > partial occlusion of vessel with No infarction - NSTEMI
- Plaque rupture with thrombus formation > partial occlusion of vessel > subendocardial myocardial injury and infarct - STEMI
- Plaque rupture with thrombus formation > complete occlusion of 1 of 3 major coronary arteries > Transmural myocardial injury and infarct
Outline diagnostic criteria for ACS (4)
- Clinical presentation
- ECG: Acute ischemic changes
- Biochemical: Biomarkers for myocardial injury
+/- 4. Imaging: ECHO or CT coronary angiogram show regional wall motion abnormality
Describe the 4 types of chest pain in ACS
Clinical presentation: can be a new phenomenon or on top of background stable angina
□ Angina at rest: prolonged >20min angina at rest (due to accumulation of toxic metabolites)
□ New-onset angina: transient ectopic beats, pain
□ Increasing angina: previous angina w/ ↑frequency, ↑duration
□ Post-infarct angina: recurrent angina after recent MI
(complete infarct and totally ischemic muscles do not produce toxic metabolites that cause rest pain anymore)
Differentiate ACS and MI
ACS = clinical term referring to patients with suspicion or confirmation of acute myocardial ischaemia or infarction
MI = acute myocardial injury (as evidenced by ↑cTn) in the setting of clinical evidence of acute myocardial ischaemia (as evidenced by chest pain or ECG changes)
MI = all tests done and confirmed
ACS
Clinical presentation
Associated symptoms
Risk factors of ACS
Triggering factors of ACS
Triggers:
□ Unusual heavy exercise
□ Emotional stress
□ Progression from Unstable Angina
□ Surgical procedures
□ Infections, eg. pneumonia
□ Circadian (peak incidence between 6am to 12pm)
Ddx cardiovacular cause of chest pain
Ddx of respiratory cause of acute chest pain
Ddx of gastro-intestinal cause of acute chest pain
Misc. ddx of chest pain
Compare the different acute chest pain due to cardiac causes
AMI
Investigations
Radiological Ix:
- ECG
- Echocardiogram: Regional wall motion abnormality, LVEF, complications such as MR/ VSD/ Pericardial effusion, Stress echo
- Coronary angioraphy: IVCA/ CTCA/ MRCA
AMI ECG
Areas of infarction seen on ECG
ECG features of NSTEMI
Non-ST-elevation ACS (NSTE-ACS):
□ Indicates: partial occlusion of major vessels(or complete occlusion of minor vessels) → unstable angina or subendocardial MI
ECG features:
→ ST depression
→ T wave changes
→ ± some loss of R waves (if infarcted)
Ddx ST elevation on ECG
- Acute STEMI (Convex ST, III>II)
- Acute pericarditis (Concave ST, II>I/III/aVF)
- LVH with strain pattern (Concave ST, V1-2)
- Early repolarization (J point elevation follows S wave, Concave ST, No reciprocal ST depression)
- LBBB
- Ventricular aneurysm
Other ECG features suggestive of acute MI other than ST segment changes
Changes in ECG findings after AMI
□ Hyperacute T wave: occurs within minutes of acute MI
□ Pseudonormalization of T wave: transient normalization of T wave from an inverted form (transient recanalization of coronary artery)
□ Wellens syndrome:** deeply inverted or biphasic T waves in V2-3** (High LAD stenosis)
□ ST elevation in aVR: usually indicates left main stem occlusion
List serum cardiac markers
Function of markers
Biomarkers:
* Myoglobin
* CKMB
* Cardiac Troponin I
* Cardiac Troponin T
* BNP
Compare the time course of each serum cardiac biomarker
1st: Myoglobin
2nd: Creatine kinase MB isoform (CKMB):
Course: rise (4-6h) → peak (12h) → normalize (48-72h)
3rd: Cardiac troponin T or I (cTnT, cTnI):
Course: rise (4-6h) → elevated for up to 2 weeks
Creatinine kinase - muscles, non-specific
Troponin - specific for cardiomyocyte, very sensitive (may have false positive)
Compare the function of Cardiac troponin T or I vs CKMB monitoring
Cardiac Troponin:
□ Advantages: not normally present → ↑sensitivity ↑specificity
□ Use: detection of first infarct event
CKMB:
□ Caveat: not sensitive or specific
(esp consider skeletal muscle damage eg. IM injection)
□ Use: mainly to detect early re-stenosis
5 types of MI
Type 1: MI caused by Atherothrombotic CAD, preciputated by Atherosclerotic plaque disruption (rupture or erosion)
Type 2: MI secondary to ischemia due to imbalance between oxygen demand and supply (no atherothrombosis) eg. coronary spasm, anaemia or hypotension
Type 3: Sudden cardiac death - MI with typical symptoms and new ischemic ECG changes, but died before blood biomarker diagnosis
Type 4: MI related to PCI (procedural complication)
Type 5: MI related to CABG (procedural complication)
Investigations to confirm type 4 and 5 MI
- New ECG changes
- Angiography: evidence of new coronary artery occlusion
- Imaging: evidence of new loss of regional wall movement/ new coronary artery occlusion/ loss of viable myocardium
- Cardiac biomarkers >99 percentile URL
AMI
Diagnostic criteria
Diagnostic criteria of type II MI
Detection of ↑/↓cardiac biomarker values (preferably cTn) with
≥1 value above 99th URL; plus ≥1 of
- Symptoms of ischaemia
- New or presumed new significant ST-T changes or new LBBB
- Development of pathological Q waves
- Imaging evidence of new loss of viable myocardium or new
regional wall motion abnormality
Same as Type 1 criteria but NO EVIDENCE OF CORONARY ATHEROTHROMBOSIS
List some causes of Type II MI
Type 1 = atherosclerosis + thrombus; Type 2 = oxygen supply and demand mismatch, no thrombus
Causes of increased coronary oxygen demand in type 2:
- Coronary spasm
- Coronary microvascular dysfunction
- Coronary embolism
- Coronary artery dissection
- Severe HTN and LVH
- Respiratory failure, severe anaemia, hypotension, shock
Outline the ddx if troponin levels rise/ fall vs stabilize over time
Indication for cardiac imaging
Types of cardiac imaging
Indication: in patients with low-to-intermediate risk for ACS to rule out ACS
Types:
- Echocardiography
- CT coronary angiogram
- Stress imaging: ETT, MPI, stress echo/MRI
Outline the TIMI risk score for NSTE-ACS stratification
Early risk assessment for UA/ NSTEMI
o All patients with UA/ NSTEMI should undergo risk assessment since it can determine prognosis and guide the timing of coronary angiography and possible revascularization
o Early risk stratification tools = TIMI/ GRACE risk score
Outline the GRACE risk score scheme for NSTE-ACS stratification
Early risk assessment for UA/ NSTEMI
o All patients with UA/ NSTEMI should undergo risk assessment since it can determine prognosis and guide the timing of coronary angiography and possible revascularization
o Early risk stratification tools = TIMI/ GRACE risk score
Right coronary artery
Origin
Branches
Supply territory
Areas of corresponding infarct
Left coronary artery
Origin
Branches
Supply territory
Areas of corresponding infarct
Troponin
Sources
Limit for MI
Confounding non-MI causes
Source:
- Myocardial
- Skeletal muscles
cTn reference decision limit for MI
- Any troponin elevation > 99th percentile (URL) = myocardial damage
cTnT and cTnI
- Sensitive and specific
- Cardiac specific but NOT specific for the cause
Creatine kinase
Sources
Isoenzymes
Function
Confounding factors
5 principles of management of ACS
Outline treatment plan
General management:
- ABC, bed rest with continuous ECG monitoring
- Support: Analgesics with morphine, Anxiolytics
- First line investigations
Acute:
- Anti-thrombotic therapy: Anti-platelet + Anti-coagulants
- Anti-ischmeic therapy: BB, CCB, Nitrates
- Support: Analgesics with morphine, Anxiolytics
- Coronary revascularization with fibrinolysis: tPA, rPA, Streptokinase
- Coronary revascularization with PCI
Long-term therapy and secondary prevention:
- Lifelong aspirin +/- warfarin
- ACEi/ARB
- Aldosterone antagonist
- Beta-blockers
- Statin
- Lifestyle modification
Anti-thrombotic therapy for ACS
Drug choices
MoA
Aspirin
- Non-selective COX-1 and COX-2 inhibitors
- ↓ Thromboxane A2 (TXA2) production from COX-1 by platelets
- Inhibits platelet aggregation
Thienopyridine (P2Y12) antagonist
- P2Y12 is a component of ADP receptor
- ADP is stored in platelet dense granules and released upon platelet activation
- Amplifies the initial signal for platelet activation and facilitate platelet aggregation
GP IIb/IIIa antagonist
- bind to the receptor and prevent fibrinogen and von Willebrand factor (vWF) from binding to the receptors
- protection from ischemic events in patients undergoing percutaneous coronary intervention (PCI)
Thienopyridine (P2Y12) antagonist
Choice of P2Y12 antagonist
Use with PCI, fibrinolysis or without fibrinolysis/PCI
GP IIb/IIIa antagonist
Drug choice
Benefit
Contraindications
GP IIb/IIIa antagonist
- bind to the receptor and prevent fibrinogen and von Willebrand factor (vWF) from binding to the receptors
- protection from ischemic events in patients undergoing percutaneous coronary intervention (PCI)
Anti-coagulant for ACS
Drug choice
MoA
S/E
Anti-coagulant for ACS
Advantage of unfractionated heparin vs LMW heparin
Anti-ischemic therapy for ACS
Drug choices
Indications for each drug
Contraindication
MoA
ACS
Supportive medication (apart from anti-thrombotic and anti-ischemic therapy)
Coronary revascularization via fibrinolytic therapy
- Indications
- MoA
- Drug choices
- Major complication
Coronary revascularization via fibrinolytic therapy
Absolute contraindications
Relative contrainfications
Coronary revascularization via PCI
Indications in STEMI
Access
Stent choices
Subsequent therapy
PCI
Complications
ACS
Signs of successful reperfusion
Factors indicating early invasive strategy or ischemia-guided strategy in NSTE-ACS
STEMI treatment flowchart
STEMI PCI choice flowchart
Long-term post-MI management
Structural and conductive complications of AMI
Circulatory complications of AMI
