Coronary Artery Anatomy and Atherosclerosis
📌 The four main coronary vessels discussed are the Posterior Descending Artery (PDA), Right Coronary Artery (RCA), Left Anterior Descending Artery (LAD), and Left Circumflex Artery (LCX).
🩸 The most common cause of Coronary Artery Disease (CAD) is atherosclerosis, involving fatty plaque buildup within the vessel walls.
⚠️ Key risk factors for atherosclerosis, summarized by the mnemonic SAD CHF, include Smoking, Advanced age (>45 for males, >55 for females), Diabetes, Cholesterol issues (high LDL, low HDL), Hypertension, and Family history.

Stable vs. Acute Coronary Syndromes (ACS)
🔹 Stable CAD involves a stable plaque causing luminal stenosis, leading to reduced oxygen supply ($\text{O}_2$ Supply). Angina occurs when $\text{O}_2$ Demand increases (e.g., during exertion, increasing heart rate or blood pressure) and resolves with rest.
💔 ACS (Unstable Angina, NSTEMI, STEMI) involves plaque rupture, leading to thrombus formation and a massive reduction in $\text{O}_2$ Supply.
🔪 NSTEMI involves subendocardial infarction (tissue death) indicated by positive troponins and ST segment depression/T wave inversion, whereas Unstable Angina involves subendocardial ischemia with negative troponins.

STEMI and Post-Infarction Complications
🧱 STEMI results from a total occlusion, causing transmural infarction (death of the entire wall), characterized by ST segment elevation on EKG and typically high troponin levels.
🚑 Major complications arising within the first 24 hours post-MI include arrhythmias (especially with RCA occlusion causing AV block or LAD/LCX occlusion causing VT/VF), acute heart failure (leading to hypotension, cardiogenic shock, and pulmonary edema due to reduced Ejection Fraction), and pericarditis.
💥 Severe, often catastrophic complications include Ventricular Septal Defect (VSD) (usually due to LAD occlusion rupturing the septum), acute mitral regurgitation (often due to papillary muscle rupture from RCA occlusion), and free wall rupture leading to cardiac tamponade (often from large LAD occlusion).

Diagnosis and Treatment Approach
🔎 Initial workup for chest pain starts with EKG followed by cardiac biomarkers (Troponin) to differentiate ACS from stable angina.
🏃 Stable Angina workup involves stress testing (treadmill, Myocardial Perfusion Imaging (MPI), or Echo) to induce ischemia; if the patient cannot exercise, pharmacological stress agents like Adenosine/Dipyridamole (causing coronary steal) or Dobutamine are used.
📈 STEMI diagnosis mandates immediate localization via EKG leads (e.g., V1-V4 for anterior/LAD; II, III, aVF for inferior/RCA) and prompt cardiac catheterization for PCI (stenting).
💊 Standard therapy for stable CAD includes Aspirin, Beta-blockers, and Nitroglycerin (sublingual PRN); revascularization (PCI or CABG) is needed for high-risk/refractory cases.
🛑 For Unstable Angina/NSTEMI, patients receive Dual Antiplatelet Therapy (Aspirin + Clopidogrel) plus Heparin loading prior to revascularization if indicated by high TIMI scores, shock, or refractory angina.

Key Points & Insights
➡️ Plaque rupture exposes highly thrombogenic material, initiating clot formation, which distinguishes Acute Coronary Syndromes (ACS) from stable plaque narrowing.
➡️ Angina in Stable CAD is predictably worse with exertion and better with rest/Nitro, while ACS angina can occur at rest, is more intense, and more frequent.
➡️ Post-MI complications like arrhythmias and cardiogenic shock are most profound in the first 24 hours; monitoring for profound bradycardia after RCA occlusion (due to AV node involvement) is crucial.
➡️ Patients receiving stents must be placed on Dual Antiplatelet Therapy (DAPT), typically for one year, to prevent fatal stent thrombosis.

📸 Video summarized with SummaryTube.com on Nov 17, 2025, 10:46 UTC