A 52-year-old man from Delhi with a 10-year history of hypertension presents to the emergency department with acute-onset severe headache, chest pain, and sweating. His blood pressure is 210/130 mmHg, heart rate 115 bpm, and ECG shows ST-segment depression in leads V2–V4. Serum troponin I is 0.8 ng/mL (elevated). Plasma free metanephrines are markedly elevated (norepinephrine 4.2 nmol/L, normal <0.9). Abdominal CT reveals a 4 cm right adrenal mass. What is the most likely explanation for his acute coronary syndrome presentation?

Explanation

## Pheochromocytoma Presenting as Acute Coronary Syndrome **Key Point:** Pheochromocytoma can mimic acute MI through **catecholamine-induced coronary vasospasm** and **demand ischemia**. This is a classic high-yield trap in NEET PG. ### Clinical Context: Why This Is Pheochromocytoma, Not Simple CAD | Feature | This Patient | Typical CAD | |---------|--------------|------------| | **Presentation** | Acute episodic with severe headache, diaphoresis | Gradual or stable angina | | **BP pattern** | Markedly elevated acutely (210/130) | Chronically elevated | | **Plasma metanephrines** | Markedly elevated (4.2 nmol/L) | Normal | | **Imaging** | 4 cm adrenal mass on CT | No adrenal pathology | | **Troponin elevation** | Present (0.8 ng/mL) | Present in MI | | **ECG** | ST depression (subendocardial ischemia) | Variable (STEMI, NSTEMI, or normal) | ### Mechanism: How Pheochromocytoma Causes ACS 1. **Massive catecholamine surge** (norepinephrine 4.2 nmol/L, normal <0.9) - Triggers coronary vasoconstriction and vasospasm - Increases myocardial oxygen demand - Results in demand ischemia or Takotsubo cardiomyopathy 2. **Coronary vasospasm** (Prinzmetal-like mechanism) - Alpha-adrenergic stimulation of coronary smooth muscle - Can occur even in angiographically normal coronaries 3. **Myocardial injury patterns** - Subendocardial ischemia (ST depression in precordial leads) - Troponin elevation from catecholamine-induced myocardial necrosis - ~~Transmural MI~~ (STEMI) is less typical unless coronary occlusion occurs **Clinical Pearl:** Pheochromocytoma-induced ACS often has **angiographically normal or minimally diseased coronaries** on cardiac catheterization. The ischemia is functional (vasospasm + demand), not structural (plaque rupture). ### Stress Cardiomyopathy (Takotsubo) Association **High-Yield:** Pheochromocytoma is a known trigger for **stress-induced cardiomyopathy (Takotsubo syndrome)**: - Acute LV apical ballooning - Elevated troponin and BNP - Reversible systolic dysfunction - Can coexist with coronary vasospasm ### Diagnostic Clue: The Adrenal Mass + Elevated Metanephrines The combination of: - 4 cm right adrenal mass on CT - Markedly elevated plasma free metanephrines (4.2 nmol/L) - Acute hypertensive crisis with ACS ...is pathognomonic for **pheochromocytoma-induced acute coronary syndrome**, not atherosclerotic CAD. ### Management Priorities 1. **Alpha-blockade** (phentolamine IV 5 mg bolus, then infusion) for acute hypertensive crisis 2. **Beta-blockade** (propranolol IV) after alpha-blockade established 3. **Avoid coronary angiography initially** unless ongoing ischemia despite blockade (risk of catecholamine surge during instrumentation) 4. **Definitive treatment:** Surgical resection of pheochromocytoma after stabilization [cite:Harrison 21e Ch 405; Robbins 10e Ch 24]