Cardiology

Diagnostic Testing 

Initial Tests 

I) 12-lead ECG (immediately): 

        It is the best initial test to evaluate ACS. 

• • • STEMI: ST elevations ≥1 mm in 2 or more contiguous leads 

• • • NSTEMI/UA: ST depressions, T-wave inversions, or nonspecific changes 

MI Location, Artery Involved, and ECG Leads 

II) Cardiac Biomarkers/Enzymes: 

• CK-MB, Troponins (I/T) : Elevation = myocardial injury; used to distinguish NSTEMI from UA 

• Elevated in STEMI and NSTEMI 

• Unstable Angina: Normal cardiac enzymes 

• Recheck every 3–6 hours 

Cardiac Enzymes in MI: Onset, Peak, and Duration 

Additional Lab Tests 

• CBC, CMP, lipid panel, glucose, coagulation panel 

• BNP if heart failure is suspected 

• ABG if hypoxia present 

• Urine drug screen in young patients with unclear etiology 

Imaging 

I) Coronary angiography:

It is the most accurate test to diagnose CAD. Gold standard for evaluating coronary anatomy.  

It is used to detect the anatomic location of coronary artery disease. Surgically correctable disease generally begins with 70% or greater stenosis. 

II) Chest X-ray: Rule out pneumonia, aortic dissection, pneumothorax 

III) Echocardiography: Evaluate wall motion abnormalities and ejection fraction. Decreased wall motion is seen in CAD. Ischemia causes reversible wall motion. Infarction is irreversible/fixed. 

Types of ACS 

Differential Diagnosis of Chest Pain

Cardiac 

• • Pericarditis: Pleuritic pain, pericardial friction rub, diffuse ST elevation 

• • Aortic dissection: Tearing pain radiating to back, pulse deficits 

• • Heart failure exacerbation: Dyspnea, orthopnea, edema 

Pulmonary 

• • Pulmonary embolism: Sudden dyspnea, pleuritic chest pain, tachycardia 

• • Pneumothorax: Unilateral decreased breath sounds, hyperresonance 

• • Pneumonia: Fever, cough, focal consolidation 

Gastrointestinal (GI) 

• • GERD: Burning sensation, worsens when lying flat 

• • Esophageal spasm: Mimics angina, unresponsive to nitroglycerin 

• • Peptic ulcer disease: Epigastric pain, relief with antacids 

Musculoskeletal (MSK) 

• • Costochondritis: Reproducible chest wall tenderness 

Muscle strain: Focal pain, history of exertion

Treatment

Current ACC/AHA and ESC guidelines (2021–2024 updates) have refined the initial management of Acute Coronary Syndrome (ACS). The emphasis now is on evidence-based pharmacotherapy, rapid reperfusion, and risk stratification.

Note: In inferior wall MI (ie, RV infarction), avoid nitrates and diuretics due to risk of severe hypotension (preload dependent). IV fluids are best administered to improve hemodynamics by increasing preload.  

Reperfusion Therapy (Door-to-balloon time for STEMI) 

• • Primary Percutaneous Coronary Intervention (PCI) within 90 minutes of first medical contact (gold standard) 

• • Thrombolytics (e.g., alteplase) if PCI is unavailable within 120 minutes 

• • Contraindications include active bleeding, recent stroke, or severe hypertension 

Adjuncts

• • Glycoprotein IIb/IIIa inhibitors (e.g., abciximab) in selected high-risk PCI patients.

  • Aldosterone antagonists (eplerenone, spironolactone) if EF ≤40% + diabetes or HF, post-MI.

  • Proton pump inhibitors if high bleeding risk on DAPT.

Types of Stents in PCI 

Indications for Coronary Artery Bypass Graft (CABG) 

• • Left main coronary artery disease 

• • Multi-vessel disease (especially in diabetics or reduced EF) 

• • Failed PCI 

• • Severe proximal LAD stenosis with complex anatomy 

Long-Term Treatment and Mortality-Reducing Therapies 

Post-MI Complications 

I) Immediate (0–24 hours) Arrhythmias

• • • Types: Ventricular fibrillation (VF), ventricular tachycardia (VT), atrial fibrillation, AV block 

• • • Pathophysiology: Electrical instability due to ischemic myocardium 

• • • Clues: Sudden cardiac arrest, palpitations, syncope, bradycardia 

• • • High risk: Anterior MI and inferior MI (AV nodal ischemia) 

II) Early (1–3 Days)

Pericarditis (early)

• • Pathophysiology: Inflammatory response of pericardium over infarcted myocardium 

• • Presentation: Sharp, pleuritic chest pain relieved by leaning forward; pericardial friction rub; diffuse ST elevation without reciprocal changes 
  • Treatment: Aspirin

III) Subacute (3–7 Days)

1. Papillary Muscle Rupture

• • Pathophysiology: Infarction → necrosis → rupture, especially of posteromedial muscle (RCA-dependent) 

• • Clues: Acute severe mitral regurgitation, flash pulmonary edema, hypotension, new loud holosystolic murmur at apex 

• • Seen in: Inferior MI

2. Interventricular Septal Rupture

• • Pathophysiology: Full-thickness necrosis of septum leads to left-to-right shunt 

• • Clues: Sudden heart failure, cardiogenic shock, harsh holosystolic murmur at LSB, oxygen step-up in RV

3. Free Wall Rupture

• • Pathophysiology: Full-thickness LV rupture leads to hemopericardium → tamponade → PEA 

• • Clues: Sudden death, pulseless electrical activity, hypotension, distended neck veins, muffled heart sounds (Beck’s triad) 

• • Seen in: Elderly, female, first MI, no prior infarct/scar 

IV) Late (1–2 Weeks)

Mural Thrombus

• • Pathophysiology: Akinesis + endocardial damage → thrombus formation in LV 

• • Clues: Asymptomatic or systemic embolism (stroke, limb ischemia) 

• • Dx: Echocardiogram 

• • Tx: Anticoagulation (e.g., warfarin) 

V) Chronic (2 Weeks to Months)

1. Left Ventricular Aneurysm

• • Pathophysiology: Scarred, thinned myocardium balloons outward during systole 

• • Clues: Persistent ST elevations on ECG, HF symptoms, embolic strokes, ventricular arrhythmias

2. Dressler Syndrome (Post-MI Syndrome)

• • Pathophysiology: Autoimmune pericarditis triggered by myocardial antigens 

• • Clues: Fever, pleuritic chest pain, pericardial effusion, elevated ESR 

• • Tx: NSAIDs (ibuprofen) ± colchicine; avoid anticoagulation due to bleeding risk with effusion