Acute Coronary Syndromes (ACS)

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### Introduction to ACS Acute Coronary Syndromes (ACS) represent a spectrum of clinical conditions compatible with acute myocardial ischemia. It is primarily caused by rupture or erosion of an atherosclerotic plaque in a coronary artery, leading to partial or complete occlusion. #### Classification 1. **STEMI (ST-segment Elevation Myocardial Infarction):** Complete or near-complete coronary occlusion, leading to transmural ischemia. 2. **NSTEMI (Non-ST-segment Elevation Myocardial Infarction):** Partial or transient coronary occlusion, leading to subendocardial ischemia. 3. **Unstable Angina (UA):** Partial or transient coronary occlusion, but without myocardial necrosis (no elevation in cardiac biomarkers). ### Pathophysiology The central event is the formation of a thrombus on a disrupted atherosclerotic plaque. - **Plaque Rupture/Erosion:** Exposes thrombogenic material (collagen, tissue factor). - **Platelet Activation & Aggregation:** Forms a platelet plug. - **Coagulation Cascade Activation:** Stabilizes the platelet plug with fibrin mesh, forming a red thrombus. - **Coronary Occlusion:** - **Complete Occlusion:** Leads to STEMI. - **Partial/Transient Occlusion:** Leads to NSTEMI/UA. - **Myocardial Ischemia & Necrosis:** Imbalance between oxygen supply and demand. ### Clinical Presentation #### Symptoms - **Chest Pain:** Most common symptom. - **Location:** Substernal, radiating to left arm, neck, jaw, back, epigastrium. - **Character:** Crushing, squeezing, heavy, pressure-like. - **Duration:** Typically >20 minutes. - **Associated Symptoms:** Dyspnea, diaphoresis, nausea, vomiting, dizziness, syncope, palpitations. - **Atypical Symptoms:** More common in women, elderly, diabetics, and patients with chronic kidney disease (CKD). May present as dyspnea, fatigue, epigastric pain, or weakness without classic chest pain. #### Physical Examination Often normal, but may reveal signs of complications or risk factors: - **Cardiovascular:** Tachycardia, bradycardia, hypotension/hypertension, new murmur (e.g., mitral regurgitation), S3/S4 gallop, JVP elevation, peripheral edema. - **Pulmonary:** Rales (pulmonary edema). - **General:** Diaphoresis. ### Diagnosis #### 1. Electrocardiogram (ECG) - **STEMI:** Persistent ST-segment elevation $\ge 1$ mm in $\ge 2$ contiguous leads (or $\ge 2$ mm in V2-V3) or new LBBB (Left Bundle Branch Block). - **Evolution:** Hyperacute T waves $\rightarrow$ ST elevation $\rightarrow$ Q wave development $\rightarrow$ T wave inversion. - **NSTEMI/UA:** ST-segment depression, T-wave inversion, or non-specific changes. May be normal in UA. - **ST Depression:** Often horizontal or downsloping, $\ge 0.5$ mm in $\ge 2$ contiguous leads. - **T-wave Inversion:** $\ge 1$ mm in $\ge 2$ contiguous leads with prominent R wave or R/S ratio >1. - **Posterior MI:** Large R wave in V1/V2, ST depression in V1-V3. - **Right Ventricular MI:** ST elevation in V4R. #### 2. Cardiac Biomarkers - **Troponins (cTnI, cTnT):** Highly sensitive and specific for myocardial injury. - **Elevation:** Detectable within 3-12 hours of onset, peak at 24-48 hours, remain elevated for 5-14 days. - **NSTEMI:** Elevated troponins. - **UA:** Normal troponins. - **CK-MB (Creatine Kinase-Myocardial Band):** Less specific, peaks earlier than troponins (10-24 hours), normalizes faster (2-3 days). Useful for re-infarction diagnosis. - **Myoglobin:** Early marker (1-4 hours), but very non-specific. #### 3. Imaging (Echocardiography) - **Bedside Echo:** Can assess left ventricular function, wall motion abnormalities, and detect mechanical complications (e.g., VSD, papillary muscle rupture). - **Stress Echo/Nuclear Stress Test:** For risk stratification in low-risk ACS or after initial stabilization. #### 4. Coronary Angiography - **Definitive diagnosis** of coronary artery disease and guide revascularization strategies. ### Risk Stratification (NSTEMI/UA) Used to guide management strategy (early invasive vs. conservative). #### TIMI Risk Score (Thrombolysis In Myocardial Infarction) Points for: - Age $\ge 65$ years - $\ge 3$ CAD risk factors (HTN, DM, Dyslipidemia, Smoking, Family Hx of early CAD) - Known CAD (stenosis $\ge 50\%$) - Aspirin use in past 7 days - Recent severe angina ( $\ge 2$ episodes in 24 hrs) - ST deviation $\ge 0.5$ mm - Elevated cardiac biomarkers **Score 0-2:** Low risk **Score 3-4:** Intermediate risk **Score 5-7:** High risk #### GRACE Score (Global Registry of Acute Coronary Events) More comprehensive, includes age, HR, SBP, Killip class, cardiac arrest at admission, ST deviation, elevated cardiac enzymes, serum creatinine. Estimates in-hospital and 6-month mortality. ### Management: General Principles (MONA BASH) Applies to all ACS patients, as appropriate. - **M**orphine: For pain relief, anxiolysis, venodilatation (reduces preload). Use cautiously in hypotension. - **O**xygen: If SpO2 ### Management: STEMI **Goal:** Rapid and complete reperfusion to restore blood flow. **Time is Myocardium!** #### 1. Reperfusion Therapy (Door-to-balloon time ### Management: NSTEMI / UA **Goal:** Stabilize patient, prevent further ischemia, and risk stratify. #### 1. Anti-ischemic Therapy - Nitroglycerin (IV if persistent pain/HTN, monitor for hypotension). - Beta-blockers (oral preferred, IV only if severe HTN/tachycardia and no HF). - Calcium Channel Blockers (e.g., Diltiazem, Verapamil) IF beta-blockers contraindicated or insufficient, especially for vasospastic angina. #### 2. Antiplatelet Therapy (DAPT) - **Aspirin:** 150-325 mg loading, then 75-100 mg daily indefinitely. - **P2Y12 Inhibitor:** - **Ticagrelor:** 180 mg loading, then 90 mg BID (preferred). - **Clopidogrel:** 600 mg loading, then 75 mg daily (if ticagrelor contraindicated). - **Prasugrel:** Reserved for patients undergoing PCI and not at high bleeding risk. - **Duration:** Typically 12 months for DAPT. #### 3. Anticoagulation - **Fondaparinux:** Preferred due to lower bleeding risk. - **Enoxaparin (LMWH):** If fondaparinux not available. - **UFH:** If high risk of bleeding or planned early PCI. - **Duration:** Until revascularization or discharge (up to 8 days). #### 4. Risk Stratification & Revascularization Strategy - **Early Invasive Strategy (within 24-72 hours):** For high-risk patients (recurrent angina, dynamic ECG changes, elevated troponins, heart failure, hemodynamic instability). - Coronary Angiography $\rightarrow$ PCI or CABG as indicated. - **Conservative Strategy:** For low-risk patients (GRACE score ### Complications of ACS - **Arrhythmias:** Ventricular fibrillation (VF), ventricular tachycardia (VT), bradyarrhythmias, heart blocks. - **Heart Failure:** Acute pulmonary edema, cardiogenic shock. - **Mechanical Complications:** - **Ventricular Septal Rupture (VSR):** New loud holosystolic murmur, thrill, biventricular failure. - **Papillary Muscle Rupture:** Acute severe mitral regurgitation, new loud systolic murmur. - **Free Wall Rupture:** Tamponade, sudden death. - **Pericarditis:** - **Early Pericarditis:** Within days of MI (fibrinous pericarditis). - **Dressler's Syndrome (Post-MI Syndrome):** Autoimmune, weeks to months after MI (pericarditis, pleuritis, fever). - **Recurrent Ischemia/Reinfarction.** - **Left Ventricular Aneurysm:** Chronic complication. ### Secondary Prevention Crucial for long-term prognosis. - **Antiplatelet Therapy:** - Aspirin indefinitely. - P2Y12 inhibitor for 12 months (or longer in select cases). - **Beta-blockers:** Indefinitely, especially with LV dysfunction. - **ACE Inhibitors/ARBs:** Indefinitely, especially with LV dysfunction, diabetes, HTN, or CKD. - **Statins:** High-intensity statin indefinitely (target LDL-C ### Special Situations #### Cardiogenic Shock - Defined as persistent hypotension (SBP