# Clinical Cases: Coronary Circulation

## Case 1: Stable Angina Pectoris - Supply-Demand Mismatch

### Patient Presentation
**Demographics:** 62-year-old male

**Chief Complaint:** Chest discomfort with exertion for 3 months

**History of Present Illness:**
A 62-year-old male with history of hypertension, hyperlipidemia, and type 2 diabetes presents with 3 months of substernal chest pressure that occurs when climbing 2 flights of stairs or walking briskly. The discomfort is described as "tightness" radiating to his left shoulder. Symptoms resolve within 5 minutes of rest. He has been using sublingual nitroglycerin (prescribed by his PCP) with good relief. He denies symptoms at rest.

**Physical Examination:**
- Vital Signs: BP 142/88 mmHg, HR 72 bpm, RR 14/min, SpO2 99% on room air
- General: Overweight, no acute distress at rest
- Cardiovascular: Regular rhythm, S4 gallop, no murmurs
- Lungs: Clear
- Extremities: No edema, pulses 2+ throughout

### Workup
- **ECG at rest:** Normal sinus rhythm, nonspecific ST-T changes
- **Labs:**
  - Fasting glucose: 145 mg/dL
  - HbA1c: 7.8%
  - LDL: 142 mg/dL
  - Total cholesterol: 228 mg/dL
- **Exercise stress ECG:**
  - Achieved 7 METs (adequate)
  - Horizontal ST depression 2 mm in V4-V6 at peak exercise
  - Chest discomfort reproduced
  - ST changes resolved with rest
- **Coronary CT angiography:** 75% stenosis of mid-LAD, 50% stenosis of proximal RCA

### Diagnosis
**Chronic stable angina pectoris (Canadian Cardiovascular Society Class II) due to coronary artery disease**

*Coronary Circulation Correlation:*

**Myocardial oxygen supply-demand balance:**

**Oxygen Supply determined by:**
1. Coronary blood flow
   - Occurs primarily in diastole (LV relaxation)
   - Autoregulation maintains flow over perfusion pressures 60-180 mmHg
2. Oxygen content of blood (hemoglobin, SaO2)

**Oxygen Demand (MVO2) determined by:**
1. Heart rate (major determinant)
2. Wall tension (preload, afterload) - Laplace's law
3. Contractility
4. Basal metabolism

**Rate-pressure product (RPP):** HR × SBP (correlates with MVO2)

**Pathophysiology of exertional angina:**
1. Fixed coronary stenosis (75% LAD)
2. At rest: Adequate flow despite stenosis (autoregulation compensates)
3. With exertion: ↑ HR, ↑ BP → ↑ MVO2
4. Stenosis limits flow augmentation → supply cannot meet demand
5. Ischemia → anaerobic metabolism → lactate → chest pain

**Why diastolic perfusion matters:**
- Coronary flow is predominantly diastolic
- Tachycardia shortens diastole → ↓ perfusion time
- Elevated LVEDP (from ischemia) → ↓ perfusion gradient

**Coronary flow reserve:**
- Normal: Can increase flow 4-5× with demand
- With 75% stenosis: Flow reserve significantly reduced

### Treatment
1. **Anti-anginal medications:**
   - Beta-blocker (metoprolol): ↓ HR, ↓ contractility → ↓ MVO2
   - Long-acting nitrate (isosorbide mononitrate): Venodilation (↓ preload), coronary vasodilation
   - Calcium channel blocker if needed (amlodipine)
2. **Aspirin 81 mg daily** (antithrombotic)
3. **High-intensity statin** (atorvastatin 80 mg)
4. **Risk factor modification:**
   - Blood pressure goal <130/80
   - LDL goal <70 mg/dL
   - HbA1c optimization
   - Smoking cessation
5. **Consider invasive evaluation:** Coronary angiography ± PCI for refractory symptoms

### Clinical Image
![Coronary Angiogram Stenosis](case_01_image.jpg)

**Image Description:** Coronary angiogram showing significant stenosis (narrowing) of the left anterior descending artery. The stenosis appears as a focal area of reduced contrast filling, indicating reduced blood flow through the affected segment.

**Source:** Wikimedia Commons - Coronary artery stenosis
**License:** CC BY-SA 3.0
**URL:** https://commons.wikimedia.org/wiki/File:Coronary_angiography.jpg

---

## Case 2: Acute STEMI - Complete Coronary Occlusion

### Patient Presentation
**Demographics:** 55-year-old male

**Chief Complaint:** Crushing chest pain for 90 minutes

**History of Present Illness:**
A 55-year-old male with history of smoking (30 pack-years) and untreated hypertension presents via EMS with crushing substernal chest pain that began 90 minutes ago while watching TV. Pain radiates to his left arm and jaw. He describes it as the worst pain of his life. Associated symptoms include diaphoresis, nausea, and a "sense of doom." He took 3 aspirin at home without relief. EMS activated catheterization lab en route.

**Physical Examination:**
- Vital Signs: BP 155/95 mmHg, HR 105 bpm, RR 22/min, SpO2 94% on room air
- General: Diaphoretic, pale, severe distress, clutching chest
- Cardiovascular: Tachycardic, S4 gallop, no murmurs
- Lungs: Clear
- Extremities: Cool, no edema

### Workup
- **ECG:** ST elevation 4-5 mm in V1-V4, reciprocal ST depression II, III, aVF, hyperacute T waves
- **Troponin I:** 2.8 ng/mL (elevated, rising)
- **Coronary Angiography (emergent):**
  - 100% thrombotic occlusion of proximal LAD
  - TIMI 0 flow (no distal perfusion)
  - Moderate disease in RCA
- **Post-PCI:** Successful stent placement, TIMI 3 flow restored
- **Echocardiogram (post-procedure):** Anterior and apical hypokinesis, EF 40%

### Diagnosis
**Acute anterior ST-elevation myocardial infarction due to complete LAD occlusion - "Widow maker"**

*Coronary Circulation Correlation:*

**Complete coronary occlusion cascade:**
1. Atherosclerotic plaque rupture exposes thrombogenic core
2. Platelet adhesion, activation, aggregation
3. Coagulation cascade → thrombus formation
4. Complete vessel occlusion → zero flow to downstream territory

**Time is myocardium:**
- After occlusion, ischemia progresses from endocardium → epicardium (wavefront phenomenon)
- Irreversible myocyte death begins within 20-30 minutes
- By 6 hours, most at-risk myocardium is infarcted

**Coronary flow and collaterals:**
- Collateral vessels may provide some flow but usually insufficient
- TIMI flow grades:
  - TIMI 0: No perfusion
  - TIMI 1: Minimal perfusion
  - TIMI 2: Partial perfusion
  - TIMI 3: Normal perfusion

**LAD territory consequences:**
- Supplies anterior wall, septum, apex
- Large territory → significant myocardial loss
- High risk of: LV dysfunction, heart failure, cardiogenic shock, arrhythmias

**Coronary blood flow during ischemia:**
- Loss of autoregulation in ischemic zone
- Stunning: Prolonged dysfunction after reperfusion despite viable tissue
- No-reflow: Microvascular obstruction despite epicardial vessel patency

### Treatment
1. **Primary PCI** (door-to-balloon <90 minutes):
   - Aspiration thrombectomy
   - Drug-eluting stent placement
   - Goal: Restore TIMI 3 flow
2. **Antiplatelet therapy:**
   - Aspirin 325 mg (given pre-hospital)
   - P2Y12 inhibitor (prasugrel or ticagrelor loading dose)
3. **Anticoagulation:** Heparin during procedure
4. **Post-MI management:**
   - Beta-blocker, ACE inhibitor, statin
   - Dual antiplatelet therapy (DAPT) for 12 months
   - Cardiac rehabilitation
5. **Monitor for complications:**
   - Arrhythmias, heart failure, mechanical complications

### Clinical Image
![STEMI Coronary Occlusion](case_02_image.jpg)

**Image Description:** Coronary angiogram showing complete thrombotic occlusion of the left anterior descending artery with abrupt cutoff of contrast flow (TIMI 0 flow). No distal filling is visible beyond the point of occlusion.

**Source:** Wikimedia Commons - LAD occlusion angiography
**License:** CC BY-SA 4.0
**URL:** https://commons.wikimedia.org/wiki/File:AMI_LAD_angiogram.jpg

---

## Case 3: Prinzmetal's (Variant) Angina - Coronary Vasospasm

### Patient Presentation
**Demographics:** 42-year-old female

**Chief Complaint:** Severe chest pain awakening her from sleep

**History of Present Illness:**
A 42-year-old female with history of migraines presents with recurrent episodes of severe chest pain occurring at rest, typically between 2-5 AM, awakening her from sleep. Episodes last 5-15 minutes and resolve spontaneously or with sublingual nitroglycerin. She denies exertional chest pain. She smokes 1 pack per day. Episodes have increased in frequency over the past month. She was evaluated 6 months ago with a normal stress test.

**Physical Examination (during episode):**
- Vital Signs: BP 145/90 mmHg, HR 88 bpm, RR 18/min, SpO2 98% on room air
- General: Anxious, diaphoretic, in moderate distress
- Cardiovascular: Regular rhythm, no murmurs
- Lungs: Clear

### Workup
- **ECG during episode:**
  - Marked ST elevation in inferior leads (II, III, aVF)
  - ST changes resolved completely within 15 minutes after nitroglycerin
- **ECG at baseline:** Normal, no ST changes
- **Troponin:** Negative (multiple checks)
- **Echocardiogram:** Normal LV function, no wall motion abnormalities
- **Coronary Angiography:**
  - No obstructive coronary artery disease
  - Provocation testing with acetylcholine: 90% focal spasm of RCA with chest pain and ST elevation (reproduced symptoms)
  - Spasm relieved with intracoronary nitroglycerin

### Diagnosis
**Prinzmetal's variant angina (coronary vasospasm) - right coronary artery**

*Coronary Circulation Correlation:*

**Normal coronary vascular tone regulation:**
- **Vasodilators:** Nitric oxide (NO), prostacyclin, adenosine
- **Vasoconstrictors:** Endothelin-1, thromboxane A2, serotonin, α-adrenergic
- Balance maintained by healthy endothelium

**Pathophysiology of coronary vasospasm:**
1. **Endothelial dysfunction:**
   - ↓ NO production or bioavailability
   - ↑ Sensitivity to vasoconstrictors
2. **Smooth muscle hyperreactivity:**
   - Enhanced contraction to normal stimuli
   - May involve Rho-kinase pathway
3. **Triggers:**
   - Smoking (endothelial damage)
   - Cocaine, amphetamines
   - Circadian variation (early morning surge)
   - Cold exposure
   - Hyperventilation (alkalosis)
   - Acetylcholine (normally causes NO release → vasodilation)

**Why rest/nocturnal episodes?**
- Parasympathetic (vagal) tone predominates at rest/sleep
- Acetylcholine → vasodilation in normal vessels
- With endothelial dysfunction → direct smooth muscle constriction
- Early morning: Peak cortisol, catecholamines, platelet aggregability

**Coronary blood flow during spasm:**
- Complete spasm → zero flow → transmural ischemia → ST elevation
- Partial spasm → reduced flow → subendocardial ischemia
- Transient nature differentiates from thrombotic occlusion

### Treatment
1. **Calcium channel blockers (first-line):**
   - Diltiazem or verapamil (non-dihydropyridine)
   - Or nifedipine (dihydropyridine)
   - Prevents smooth muscle contraction
2. **Long-acting nitrates:**
   - Isosorbide mononitrate nightly
   - Direct coronary vasodilation
3. **Sublingual nitroglycerin PRN** for acute episodes
4. **Smoking cessation (essential)** - smoking is major trigger
5. **Avoid:**
   - Beta-blockers (unopposed α-mediated vasoconstriction)
   - Triptans
   - Cocaine/stimulants
6. **Statins:** Improve endothelial function

### Clinical Image
![Coronary Vasospasm Angiography](case_03_image.jpg)

**Image Description:** Coronary angiogram demonstrating focal coronary artery spasm with severe narrowing during provocation testing. The vessel appears nearly completely occluded at the site of spasm, with restoration of normal caliber after administration of nitroglycerin.

**Source:** Radiopaedia - Coronary vasospasm
**License:** CC BY-NC-SA 3.0
**URL:** https://radiopaedia.org/cases/prinzmetal-angina