Acute Coronary Syndrome (ACS) is an umbrella term for conditions caused by sudden, reduced blood flow to the heart due to myocardial ischemia. It includes:
- Unstable angina (UA)
- Non–ST-segment elevation myocardial infarction (NSTEMI)
- ST-segment elevation myocardial infarction (STEMI)
ACS is a medical emergency requiring prompt diagnosis and management to prevent myocardial necrosis, heart failure, or death.
Classification of ACS
| Type | ECG Changes | Cardiac Biomarkers | Pathology |
|---|---|---|---|
| STEMI | ST elevation | ↑ Troponins | Transmural infarction due to complete coronary occlusion |
| NSTEMI | ST depression/Normal | ↑ Troponins | Subendocardial infarction due to partial occlusion |
| Unstable Angina | ST depression/Normal | Normal | Myocardial ischemia without necrosis |
Etiology & Risk Factors
- Atherosclerotic plaque rupture (most common)
- Coronary artery spasm (e.g., Prinzmetal angina)
- Thromboembolism
- Cocaine use
- Severe hypertension
- Aortic dissection (can occlude coronary ostia)
Risk Factors : Hypertension, hyperlipidemia, diabetes mellitus, smoking, sedentary lifestyle, family history of CAD.
Pathophysiology
- Plaque rupture or erosion → exposure of subendothelial matrix
- Platelet adhesion & aggregation
- Thrombus formation :
- White clot (platelet-rich): partial occlusion (NSTEMI/UA)
- Red clot (fibrin-rich): complete occlusion (STEMI)
- ↓ Coronary perfusion → myocardial ischemia → infarction
Types of Myocardial Infarction (MI)
(Fourth Universal Definition of MI)
| Type | Description |
|---|---|
| Type 1 | Spontaneous MI due to atherosclerotic plaque rupture (classic MI) |
| Type 2 | MI secondary to ↑ demand or ↓ supply (e.g., anemia, hypotension) |
| Type 3 | Sudden cardiac death with ECG/angiographic evidence of ischemia |
| Type 4a | MI related to percutaneous coronary intervention (PCI) |
| Type 4b | MI due to stent thrombosis |
| Type 5 | MI related to coronary artery bypass grafting (CABG) |
Clinical Features
Typical Presentation (SOCRATES)
- S ite: Central chest
- O nset: Sudden
- C haracter: Crushing, tight
- R adiation: Left arm, jaw, neck
- A ssociated: Dyspnea, diaphoresis, nausea
- T iming: Lasts >15–20 minutes
- E xacerbating: Exertion, emotion
- S everity: Severe
Atypical Presentations
- Common in elderly, women, diabetics
- Dyspnea, fatigue, syncope
- Silent MI: no pain, seen in 20–30% of diabetics
Physical Findings
- Pallor, diaphoresis
- Bradycardia or tachycardia
- Hypotension or hypertension
- S3 or S4 gallop
- Crackles (if heart failure)
- Pericardial rub (if pericarditis)
Diagnostic Workup
Electrocardiogram (ECG)
- First-line test : within 10 minutes of presentation
- Repeat at 15–30 min intervals if initial ECG is nondiagnostic but suspicion is high
Cardiac Biomarkers
- Troponin I/T : Most sensitive and specific
- Elevated within 3–6 hrs, peak at 12–24 hrs
- Persist elevated for 7–10 days
- CK-MB: Useful for reinfarction (rises and falls quicker)
Other Lab Tests
- CBC : Anemia, baseline before anticoagulation
- Urea & Electrolytes : Renal function
- Blood Glucose : Stress hyperglycemia
- Lipid Profile : Check within 24 hours
- BNP : Elevated if heart failure
Imaging
- Chest X-ray : Rule out pneumonia, aortic dissection
- Echocardiography : Assess wall motion, EF, complications
- Coronary angiography : Definitive test for diagnosis and intervention
Management
Immediate (MONA-BASH)
| Treatment | Purpose |
|---|---|
| M orphine | Pain and anxiety relief |
| O xygen | If O2 sat < 90% |
| N itrates | Vasodilation to reduce preload/afterload |
| A spirin | Antiplatelet (chewable, 300 mg) |
| B eta-blockers | Reduce oxygen demand (e.g., metoprolol) |
| A ntiplatelets (P2Y12 inhibitor) | Clopidogrel, ticagrelor |
| S tatins | High-intensity (e.g., atorvastatin 80 mg) |
| H eparin | Anticoagulation (UFH, LMWH, or fondaparinux) |
Definitive Treatment
STEMI
- Primary PCI within 120 minutes of first medical contact
- If PCI unavailable: Fibrinolysis (alteplase, tenecteplase) within 30 min
NSTEMI / Unstable Angina
- Risk stratify (TIMI or GRACE)
- Early invasive strategy (angiography within 24–72 hrs)
- Continue dual antiplatelets + anticoagulants
Complications of ACS
| Type | Examples |
|---|---|
| Cardiac | Heart failure, cardiogenic shock, arrhythmias, reinfarction |
| Mechanical | Ventricular septal rupture, papillary muscle rupture, free wall rupture |
| Pericardial | Pericarditis (early or Dressler syndrome) |
| Embolic | Stroke, systemic embolism |
| Others | Acute mitral regurgitation, ventricular aneurysm |
Prognosis & Long-Term Management
- Risk stratification and secondary prevention are critical
- Lifestyle modification: Smoking cessation, diet, exercise
- Long-term medications:
- Aspirin + P2Y12 inhibitor for 12 months
- Beta-blocker
- ACE inhibitors / ARBs
- Statins
Mnemonic for ACS Management: "BAANS"
- B eta-blockers
- A CE inhibitors/ARBs
- A spirin + P2Y12 inhibitor
- N itrates
- S tatins
High-Yield
- STEMI diagnosis is based on ECG to prevent treatment delay.
- NSTEMI is defined by positive troponin without ST elevation.
- Troponin elevation ≠ MI always; consider other causes (HEART DIES mnemonic).
- Fibrinolytics contraindicated in active bleeding, recent stroke, or aortic dissection.
- Monitor for mechanical complications post-MI in the first 3–5 days.
