Coronary Artery Disease and Acute Coronary Syndrome

Coronary Artery Disease (CAD)

Commonly caused by atherosclerosis: Lipid-rich plaque in coronary artery walls

Endothelial injury → lipid buildup + inflammation → plaque growth

Causes narrowing and plaque rupture/erosion (leads to platelet activation + thrombus)

Risk Factors: Smoking, HTN, ↑LDL, diabetes, obesity, inactivity, age, family history

Ischemia

Myocardial O2 demand > supply → insufficient O2 to myocardium (heart)

Brief ischemia may reverse, prolonged severe ischemia → necrosis → MI

Angina, dyspnea, diaphoresis, nausea, fatigue, lightheadedness

Can impair pumping + arrhythmias; early reperfusion may prevent MI

↓Supply in Myocardial Ischemia

Atherosclerosis → narrowing

Plaque rupture → thrombus → ↓coronary flow

Vasospasm/Small vessel dysfunction → ↓flow (even w/o major blockage)

↑Demand in Myocardial Ischemia

Exercise/Stress → ↑HR, BP, contractility → ↑cardiac work

Collateral Flow

Small coronary connections may enlarge with gradual narrowing, providing alternate blood flow around a blockage

May reduce ischemia but often insufficient, especially with sudden occlusion

Ischemic Cell Injury

↓O2 = ↓ATP + anaerobic metabolism

↓Energy = impaired relaxation/contraction + disturbed ion balance → arrhythmias

Angina

Chest pressure/tightness/discomfort from ischemia ± radiation to one/both arms, jaw, neck or back

Chest pain

Stable Angina

Narrowed coronary artery + ↑demand → predictable exertion/stress symptoms

Relieved by rest or sublingual nitroglycerin

Management: Beta blocker (↓demand) or calcium channel blocker (↑supply, vasodilator) = symptom control; NTG (relief)

Lipid lowering + risk reduction = event prevention

Acute Coronary Syndrome

New, worsening, or rest symptoms. Often due to plaque rupture/erosion → thrombus

1. Unstable angina

2. NSTEMI/STEMI = non ST/ST elevation MI

ECG + troponin test

Suspect ACS if change in usual angina

Myocardial Infarction

Plaque rupture → platelets + fibrin thrombus

Requires injury + ischemic evidence (symptoms, ECG changes or image findings)

If troponin rise/fall = acute injury

Primary, secondary, or procedure-related MI

STEMI/NSTEMI describes presentation, type of MI describes cause and guides treatment

Primary MI

Acute coronary problem, commonly atherothrombosis

Secondary MI

Acute illness → O2 supply/demand imbalance (anemia, hypoxemia, hypotension, tachyarrhythmia)

Procedure-Related MI

Cardiac procedure complication → ischemic injury

Troponin

Myocardial injury marker

MI = rise/fall above sex-specific 99th percentile + ischemic evidence

Unstable Angina (UA)

Ischemic symptoms w/o acute ischemic troponin rise/fall

ST depression/T inversion or normal ECG

Risk-based NSTE-ACS care; NO fibrinolysis

NSTEMI (non-ST elevation MI)

Troponin will likely be elevated; acute injury + ischemic evidence

No persistent ST elevation; ECG may be normal

Risk-based invasive strategy; NO fibrinolysis

STEMI (ST elevation MI)

EMERGENCY

Acute ischemic presentation; troponin may be normal initially and then rise

Diagnostic ST elevation

Immediate reperfusion, do NOT wait for troponin

CAD/ACS Diagnostic Testing

1. ECG (12-lead ECG ≤10min)

2. High-Sensitivity Troponin

3. Echocardiogram (assess wall motion, pumping fx, complications)

4. Stress Test (↑cardiac workload to check for ischemia in stable pts)

5. Coronary Imaging (CT angiography, cardiac catherization)

ST-Depression

Downward ST segment ≥1mm

Suggests subendocardial ischemia; can also be reciprocal change or posterior MI

T-Wave Inversion

Inverted/Negative T wave

May indicate ischemia, especially when new, deep or dynamic

ST Elevation

Upward ST segment ≥1mm

Suggests acute injury/occlusion (STEMI)

EMERGENCY

Q Waves

Wide and deep (≥0.04sec and/or ≥25% of R wave)

May indicate prior MI or evolving myocardial necrosis

STEMI

Restore blood flow immediately

PCI preferred (balloon/stent opens the artery)

Fibrinolytics if PCI will take >120min or symptoms <12h and no contraindications

Antiplatelets, anticoagulation, anti-ischemic therapy, high-intensity statin

NSTEMI/Unstable Angina (UA)

Persistent pain despite treatment or unstable BP/rhythm → immediate angiography

Stable but high-risk → angiography <24h

Antiplatelets, anticoagulation, anti-ischemic therapy, high-intensity statin

Percutaneous Coronary Intervention (PCI)

Balloon opens the narrowed artery and stent supports the artery

Rapidly restores blood flow

Preferred for STEMI pts, single-vessel disease, or suitable anatomy

Coronary Artery Bypass Grafting (CABG)

Creates a new pathway around blocked arteries using grafts

Improves blood flow to large areas of the heart

Preferred for left main disease, multivessel disease (diabetics), or complex anatomy

Use if PCI is not possible or failed

Aspirin

Antiplatelet

Cox-1 inhibition → ↓thromboxane A2 → vasoconstriction

Clopidogrel

P2Y2 Inhibitors

P2Y12 blockade → ↓ADP signaling → ↓platelet aggregation

ACS + stent thrombosis prevention, usually use w/ aspirin (DAPT)

ADRs: Bleeding/bruising, GI upset, rare TTP (thrombotic thrombocytopenic purpura)

Contraindications: Active bleeding/allergy

Avoid omeprazole/esomeprazole (↓drug activation)

DAPT (Dual Antiplatelet Therapy)

Aspirin + P2Y12 inhibitor = inhibit platelet aggregation

ACS PCI: Ticagrelol/prasugrel preferred if suitable

Fibrinolysis: Clopidogrel

Anticoagulants

Inhibit clotting factors → ↓fibrin formation → limit clot extension

Unfractionated Heparin (UFH)

↑Antithrombotic activity → inhibits thrombin + Xa → limits fibrin/clot extensionn

STEMI/NSTEMI, PCI anticoagulation

ADRs: Bleeding, HIT (heparin-induced thrombocytopenia, thrombosis despite ↓platelets)

Contraindications: Prior HIT, uncontrolled bleeding, drug/pork allergy, inability to monitor coagulation

Monitor aPTT/anti-Xa, blood count, protamine reverses UFH

Enoxaparin (Low Molecular Weight Heparin)

↑Antithrombotic activity → inhibits Xa > IIa → limits clot formation

UA/NSTEMI + selected STEMI (based on reperfusion strat)

ADRs: Bleeding, thrombocytopenia/HIT, injection reactions. Neuraxial hematoma = neurologic injury

Contraindications: Major active bleeding, immune HIT ≤100 days/HIT antibodies, allergy

↓Renal clearance → ↑exposure/bleeding. Protamine = partial reversal

Eptifibatide (GP IIb/IIIa inhibitors)

GP IIb/IIIa blockade → prevents fibrinogen linking platelets → ↓aggregation

Selected PCI (large thrombus or inadequate restored flow)

ADRs: Bleeding, acute thrombocytopenia ± hypotension/bradycardia

Contraindications: Bleeding ≤30 days, major surgery ≤6wks, stroke ≤30 days or any hemorrhagic stroke

Potent IV antiplatelet → close bleeding surveillance; select situations only

Fibrinolytics

Plasminogen → plasmin → fibrin breakdown

Not for everyone — major bleeding risk

Tenecteplase (TNKase)

Fibrinolytic

Plasminogen → plasmin → fibrin breakdown → clot dissolution

STEMI only when PCI unavailable

ADR: Major bleeding/intracranial hemorrhage (ICH), reperfusion arrhythmias

Contraindications: Active internal bleeding, bleeding diathesis, severe uncontrolled HTN, hi-risk brain lesions; brain/spinal surgery/trauma ≤2mo, prior ICH, ischemic stroke ≤3mo

Give within 12h of symptoms (PCI not possible in 120min); door-to-needle goal ≤30min

Nitrates

Venodilation → ↓preload (venous return) → ↓wall stress/O2 demand → angina relief

Nitroglycerin (NTG)

Convert to nitric oxide → venodilation → ↓preload (ventricular filling) → ↓O2 demand

Angina/ACS pain. IV: Persistent ischemica, HF, or HTN

ADRs: Headache, ↓BP, dizziness, reflex tachycardia

Contraindications: PDE-5 drugs/riociguat, shock, severe anemia, ↑intracranial pressure

Sublingual. NO PDE-5 (severe hypotension)

Statin

Atorvastatin OR rosuvastatin

HMG-CoA reductase inhibition → ↓hepatic cholesterol/LDL → ↓recurrent events

Assess muscle symptoms/interactions

Metoprolol

B1 blockade → ↓HR/contractility → ↓O2 demand

Oral start within 24h if appropriate

Avoid acute HF/shock risk, severe bradycardia/block, active bronchospasm

ACE Inhibitor/ARM

↓Afterload (ejection resistance) + ↓harmful remodeling (ventricular size/shape change)

Monitor BP, K, renal function

Pump Failure

Damaged myocardium → ↓contraction/output → HF or shock

Assess lungs, BP, urine output, peripheral perfusion

Escalate if worsening perfusion

Arrhythmias

Ischemia/Reperfusion → Ventricular tachycardia/fibrillation, bradycardia, or AV block

Assess continuous ECG + pt perfusion

Report/Treat unstable rhythms immediately

Mechanical Rupture

Papillary muscle → acute mitral regurgitation

Septum → shunt

Free wall → tamponade

New murmur + sudden deterioration → emergency escalation

Recurrent Ischemia

New pain → reassess + obtain ECG

Pain relief ≠ proof of reperfusion

Escalate recurrent ischemic findings