CardiologyTier 1Disease (DEADMAN)

Acute coronary syndromes - non-ST elevation myocardial infarction (NSTEMI)

Description

ACS without persistent ST elevation, with a troponin rise and/or fall
- Same presentation, no troponin rise = unstable angina
Type 1 - plaque rupture or erosion, non-occlusive or transiently occlusive thrombus
Type 2 - supply-demand mismatch with no acute plaque event
- Sepsis, tachyarrhythmia, anaemia, hypoxia, hypotension, severe HTN
- *Treating type 2 with DAPT and angiography causes harm - treat the precipitant*
MINOCA - MI with non-obstructive coronaries; always needs a cause found
- SCAD, spasm, embolism, microvascular disease, or a myocarditis mimic

Now more common than STEMI, and rising with high-sensitivity troponin
Cohort is older, more comorbid, more often female, more often CKD than STEMI
Lower in-hospital mortality than STEMI but equal or higher mortality at 6-12 months

Plaque rupture or erosion -> platelet-rich thrombus
- -> subtotal occlusion, or total occlusion with collateral supply
- -> subendocardial ischaemia (the subendocardium is the watershed)
- -> subendocardial infarction
Distal embolisation of platelet aggregates -> microvascular obstruction
Type 2 mechanism: inc myocardial O2 demand or dec supply against a fixed or absent stenosis
Risk factors as for all atherosclerotic disease

Clinical

Ischaemic chest pain - at rest, prolonged, or crescendo
Atypical presentation commoner in women, diabetes, the elderly and CKD - dyspnoea, fatigue, epigastric pain

ECG

ST depression, T-wave inversion, transient ST elevation, or normal
A normal ECG does not exclude NSTEMI - repeat it serially
De Winter T waves and Wellens' pattern = critical LAD - treat as very high risk
ST depression maximal V1-V3 with tall R = posterior STEMI. Do posterior leads

Troponin

Risk stratification

GRACE score - age, HR, SBP, creatinine, cardiac arrest, ST deviation, troponin, Killip class
TIMI score - simpler, 7 equally weighted items
High-risk clinical features:
- Ongoing or recurrent pain despite therapy
- Dynamic ST/T change, especially ST depression >2 mm
- Haemodynamic instability, new MR, Killip >I
- VT or syncope
- EF <40%
- Prior MI, PCI or CABG

Immediate - all patients

Aspirin 300 mg, continuous monitoring, IV access, serial ECG and troponin
O2 only if SpO2 <93%
Anti-ischaemic: nitrate, beta blocker
- Avoid beta blocker if bradycardic, hypotensive, cocaine-related, or acutely decompensated HF

Antithrombotic

DAPT - aspirin + ticagrelor (clopidogrel if high bleeding risk or on an anticoagulant)
- Routine P2Y12 pre-treatment before the anatomy is known is no longer recommended when early angiography is planned
Anticoagulate - enoxaparin or fondaparinux
- Fondaparinux has the best efficacy-bleeding balance (OASIS-5) but needs additional UFH at PCI
GPIIb/IIIa inhibitors - bail-out use at PCI only

Timing of angiography - driven by risk

Risk category	Timing
Very high - instability, refractory pain, malignant arrhythmia, mechanical complication	Immediate, <2 h
High - troponin rise consistent with MI, dynamic ST/T change, GRACE >140	Early invasive, <24 h
Intermediate	Invasive within 72 h
Low	Non-invasive testing first

*Fibrinolysis has no role in NSTEMI and is harmful*
Revascularisation by anatomy - PCI, or CABG for left main and complex multivessel disease

Secondary prevention - start before discharge

In-hospital mortality lower than STEMI; 6-12 month mortality equals or exceeds it
Driven by age, comorbidity, extent of CAD, renal function and EF

Complications

Recurrent ischaemia and reinfarction
Arrhythmia
Heart failure and adverse remodelling
Bleeding on antithrombotic therapy - a mortality-relevant complication, not a nuisance

Monitor

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