# Clinical Cases: Heart Failure

## Case 1: Heart Failure with Reduced Ejection Fraction (HFrEF) - Post-MI Cardiomyopathy

### Patient Presentation
**Demographics:** 67-year-old male

**Chief Complaint:** Progressive shortness of breath and leg swelling for 6 weeks

**History of Present Illness:**
A 67-year-old male with history of anterior STEMI 18 months ago (treated with primary PCI to LAD) presents with progressive dyspnea on exertion over the past 6 weeks. He previously could walk 2 blocks without difficulty but now becomes short of breath after walking 50 feet. He reports orthopnea, requiring 3 pillows to sleep, and describes episodes of waking up gasping for air at night (PND). He has noticed bilateral leg swelling and a 10-pound weight gain over the past month. He admits to dietary indiscretion with high salt intake and occasionally forgetting his medications.

**Physical Examination:**
- Vital Signs: BP 102/68 mmHg, HR 92 bpm, RR 22/min, SpO2 92% on room air
- General: Fatigued appearance, mild respiratory distress
- Cardiovascular:
  - JVP elevated to 12 cm H2O
  - PMI displaced laterally and inferiorly to 6th intercostal space, anterior axillary line
  - S3 gallop present
  - Soft holosystolic murmur at apex (functional MR)
- Lungs: Bilateral basilar crackles to mid-lung fields
- Abdomen: Hepatomegaly, positive hepatojugular reflux
- Extremities: 2+ pitting edema to knees bilaterally

### Workup
- **BNP:** 1,840 pg/mL (elevated, normal <100)
- **Labs:**
  - Na 132, K 4.8, Cr 1.6, BUN 38
  - Troponin negative
- **ECG:** Sinus rhythm, Q waves V1-V4 (prior anterior MI), low voltage
- **Chest X-ray:**
  - Cardiomegaly (CTR >0.5)
  - Bilateral pleural effusions
  - Cephalization of pulmonary vessels
  - Kerley B lines
- **Echocardiogram:**
  - LV ejection fraction 25%
  - Anterior and apical akinesis (scar from prior MI)
  - LV end-diastolic dimension 6.8 cm (dilated)
  - Moderate functional mitral regurgitation
  - Elevated E/e' ratio suggesting elevated filling pressures

### Diagnosis
**Acute decompensated heart failure with reduced ejection fraction (HFrEF) - NYHA Class III**
**Etiology: Ischemic cardiomyopathy (post-anterior MI)**

*Heart Failure Correlation:*

**Pathophysiology of Systolic Dysfunction:**

1. **Primary Insult - Myocardial Infarction:**
   - LAD occlusion caused anterior wall and apical infarction
   - Irreversible myocyte death and scar formation
   - Loss of contractile tissue

2. **Ventricular Remodeling:**
   - Eccentric hypertrophy: sarcomeres added in series
   - Chamber dilation to maintain stroke volume (Frank-Starling)
   - Spherical shape change from normal ellipse
   - Increased wall stress (Law of LaPlace: T = P x r / 2h)

3. **Neurohormonal Activation:**
   - Reduced cardiac output triggers compensatory mechanisms:
     - **Sympathetic activation:** Increases HR and contractility acutely
     - **RAAS activation:** Causes vasoconstriction and fluid retention
     - **ADH release:** Water retention, hyponatremia
   - Initially compensatory, becomes maladaptive chronically:
     - Myocyte toxicity from catecholamines
     - Fibrosis from angiotensin II and aldosterone
     - Progressive remodeling and dysfunction

4. **Functional Mitral Regurgitation:**
   - LV dilation stretches mitral annulus
   - Papillary muscle displacement prevents leaflet coaptation
   - MR creates additional volume overload - vicious cycle

**Why Symptoms Develop:**

**Elevated Filling Pressures (Congestion):**
- Dilated, non-compliant LV requires higher filling pressures
- Transmitted backward to LA, pulmonary veins
- Pulmonary congestion causes dyspnea, orthopnea, PND
- Systemic congestion causes JVD, edema, hepatomegaly

**Reduced Cardiac Output:**
- Damaged ventricle cannot meet metabolic demands
- Fatigue, exercise intolerance
- Prerenal azotemia (elevated Cr/BUN)
- Hyponatremia from water retention exceeding sodium

### Treatment
**Acute Management:**
1. **Diuresis:**
   - IV furosemide 40-80 mg bolus
   - Goal: 1-2 L negative fluid balance daily
   - Monitor electrolytes, creatinine
2. **Oxygen supplementation**
3. **Sodium and fluid restriction**

**Guideline-Directed Medical Therapy (GDMT):**

1. **ACE Inhibitor/ARNI:**
   - Sacubitril/valsartan (ARNI) preferred over ACE-I
   - Blocks RAAS, prevents remodeling
   - Mortality reduction proven

2. **Beta-Blocker:**
   - Carvedilol, metoprolol succinate, or bisoprolol
   - Start low, titrate slowly after euvolemia achieved
   - Blocks maladaptive sympathetic activation
   - Mortality reduction and reverse remodeling

3. **Mineralocorticoid Receptor Antagonist:**
   - Spironolactone or eplerenone
   - Blocks aldosterone-mediated fibrosis and sodium retention
   - Mortality reduction in HFrEF

4. **SGLT2 Inhibitor:**
   - Dapagliflozin or empagliflozin
   - Cardiovascular benefit regardless of diabetes status
   - Reduces HF hospitalizations and mortality

**Device Therapy:**
- **ICD:** Primary prevention (EF 35% despite 3 months GDMT)
- **CRT:** If LBBB with QRS >150 ms and persistent symptoms

### Clinical Image
![Cardiomegaly Chest X-ray](case_01_image.jpg)

**Image Description:** Chest radiograph demonstrating cardiomegaly with an enlarged cardiac silhouette. The cardiothoracic ratio exceeds 50%, indicating significant cardiac enlargement consistent with heart failure. Additional findings may include pulmonary vascular congestion.

**Source:** Wikimedia Commons - Cardiomegaly
**License:** Public Domain
**URL:** https://commons.wikimedia.org/wiki/File:Cardiomegally.PNG

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## Case 2: Heart Failure with Preserved Ejection Fraction (HFpEF)

### Patient Presentation
**Demographics:** 72-year-old female

**Chief Complaint:** Shortness of breath with exertion and leg swelling

**History of Present Illness:**
A 72-year-old female with long-standing hypertension, type 2 diabetes, obesity (BMI 34), and atrial fibrillation presents with 2 months of worsening dyspnea on exertion. She becomes short of breath climbing one flight of stairs. She reports leg swelling that worsens throughout the day and occasional difficulty lying flat. She denies chest pain. She has been compliant with her medications but notes her blood pressure has been difficult to control.

**Physical Examination:**
- Vital Signs: BP 158/92 mmHg, HR 88 bpm (irregular), RR 18/min, SpO2 96% on room air, BMI 34
- General: Obese, mild respiratory effort
- Cardiovascular:
  - JVP 10 cm H2O
  - Irregularly irregular rhythm
  - S4 gallop, no S3
  - PMI not displaced
  - No murmurs
- Lungs: Fine bibasilar crackles
- Abdomen: Obese, mild hepatomegaly
- Extremities: 2+ pitting edema to mid-shins

### Workup
- **NT-proBNP:** 890 pg/mL (elevated for age/sex, but less marked than HFrEF)
- **Labs:**
  - HbA1c 7.6%
  - Cr 1.2, eGFR 52
  - Na 138, K 4.2
- **ECG:** Atrial fibrillation, rate 88, LVH by voltage criteria
- **Echocardiogram:**
  - LV ejection fraction 58% (preserved)
  - Concentric LVH (wall thickness 1.4 cm)
  - Grade II diastolic dysfunction
  - E/e' ratio 16 (elevated filling pressures)
  - LA enlargement (48 mL/m2)
  - Normal LV cavity size

### Diagnosis
**Heart Failure with Preserved Ejection Fraction (HFpEF) - NYHA Class II-III**

*Heart Failure Correlation:*

**Pathophysiology of Diastolic Dysfunction:**

1. **Concentric Hypertrophy:**
   - Chronic hypertension increases afterload
   - LV adds sarcomeres in parallel (wall thickening)
   - Maintains normal wall stress (Law of LaPlace)
   - But reduces chamber compliance

2. **Impaired Relaxation:**
   - Hypertrophied myocytes have abnormal calcium handling
   - Reduced SERCA activity slows calcium reuptake
   - Prolonged relaxation time
   - Especially problematic with tachycardia (shortened diastole)

3. **Increased Passive Stiffness:**
   - Myocardial fibrosis from chronic pressure overload
   - Altered titin isoforms increase stiffness
   - Reduced compliance: small volume changes cause large pressure changes

4. **Elevated Filling Pressures Despite Normal EF:**
   - Stiff ventricle requires high pressure to fill adequately
   - E/e' ratio reflects elevated LVEDP
   - Transmitted to LA (enlargement, AF)
   - Transmitted to pulmonary veins (congestion)

**Contributing Comorbidities:**
- **Hypertension:** Primary driver of LVH and diastolic dysfunction
- **Diabetes:** Myocardial stiffening, microvascular disease
- **Obesity:** Increased blood volume, systemic inflammation
- **Atrial fibrillation:** Loss of atrial kick, rapid rates worsen filling
- **CKD:** Volume overload, neurohormonal activation

**Why EF Is "Preserved" but Heart Still Fails:**
- EF measures systolic function (emptying)
- HFpEF has normal emptying but abnormal filling
- Reduced stroke volume from inadequate diastolic filling
- Inability to augment cardiac output with exercise

**Pressure-Volume Loop:**
- Steepened EDPVR (end-diastolic pressure-volume relationship)
- Higher pressures for same filling volume
- Normal ESPVR (contractility preserved)

### Treatment
**Congestion Management:**
1. **Diuretics:**
   - Loop diuretics for volume control
   - Careful titration - HFpEF patients are preload-dependent
   - Avoid over-diuresis (hypotension, renal dysfunction)

**SGLT2 Inhibitor:**
- Empagliflozin or dapagliflozin
- EMPEROR-Preserved and DELIVER trials showed benefit in HFpEF
- First medication class proven to improve outcomes in HFpEF

**Comorbidity Management (Essential):**
1. **Blood Pressure Control:**
   - Target <130/80 mmHg
   - Reduces ongoing LV remodeling
2. **Rate Control for AF:**
   - Beta-blocker or diltiazem
   - Avoid tachycardia (reduces filling time)
3. **Diabetes Management:**
   - Optimize glycemic control
   - SGLT2 inhibitors have dual benefit
4. **Weight Loss:**
   - Significant symptomatic benefit with weight reduction
5. **Treat Sleep Apnea:**
   - High prevalence in HFpEF
   - CPAP may improve symptoms

**Lifestyle:**
- Sodium restriction (<2g/day)
- Daily weights to detect fluid accumulation
- Exercise training improves functional capacity

### Clinical Pearl
**HFrEF vs HFpEF - Key Distinctions:**

| Feature | HFrEF | HFpEF |
|---------|-------|-------|
| EF | <40% | >50% |
| LV Size | Dilated | Normal/small |
| Wall Thickness | Normal/thin | Often thickened |
| Remodeling | Eccentric | Concentric |
| Primary Defect | Contractility | Relaxation/Compliance |
| BNP Elevation | Marked | Moderate |
| Proven GDMT | 4 drug classes | SGLT2 inhibitors |

**Neurohormonal Activation in Both:**
Both HFrEF and HFpEF involve sympathetic and RAAS activation, but the myocardial response differs. Understanding that HFpEF is not simply "mild" heart failure but a distinct pathophysiologic entity explains why therapies proven in HFrEF (ACE-I, beta-blockers, MRA) have not shown clear mortality benefit in HFpEF.