A 53-year-old woman visits her physician with complaints of shortness of breath and fatigue over the last few weeks. Her past medical history includes hypertension diagnosed 20 years ago. She takes hydrochlorothiazide and losartan daily. Her mother died at the age of 54 from a stroke, and both of her grandparents suffered from cardiovascular disease. She has a 13 pack-year history of smoking and drinks alcohol occasionally. Her blood pressure is 150/120 mm Hg, pulse is 95/min, respiratory rate is 22/min, and temperature is 36.7°C (98.1°F). On physical examination, she has bibasilar rales, distended jugular veins, and pitting edema in both lower extremities. Her pulse is irregularly irregular and her apical pulse is displaced laterally. Fundoscopy reveals ‘copper wiring’ and ‘cotton wool spots’. Which of the following echocardiographic findings will most likely be found in this patient?

Ejection fraction: 40% with increased left ventricular wall thickness

Ejection fraction: 55% with dilated chambers and thin walls

Ejection fraction: 60% with normal left ventricular wall thickness

Ejection fraction: 65% with rapid early diastolic filling and slow late diastolic filling

Ejection fraction: 80% with regurgitant aortic valve

A 70-year-old man presented to a medical clinic for a routine follow-up. He has had hypertension for 20 years and is currently on multiple anti-hypertensive medications. The blood pressure is 150/100 mm Hg. The remainder of the examinations were within normal limits. Echocardiography showed some changes in the left ventricle. What is the most likely reason for the change?

Disordered growth of the cardiac cells

Increase in number of normal cardiac cells

Replacement of cardiac cells into stronger red fiber skeletal cells

An 80-year-old African American male presents complaining of worsening shortness of breath that occurs during his weekly round of golf. He also notes he has been waking up at night "choking and gasping for air", though he has been able to gain some relief by propping his head on a stack of pillows before he goes to bed. Upon auscultation, a low frequency, early diastolic gallop is heard over the apex while the patient rests in the left lateral decubitus position. This finding is most consistent with which of the following?

Left ventricular eccentric hypertrophy

Left ventricular concentric hypertrophy

A 75-year-old woman presents to her physician with a cough and shortness of breath. She says that cough gets worse at night and her shortness of breath occurs with moderate exertion or when lying flat. She says these symptoms have been getting worse over the last 6 months. She mentions that she has to use 3 pillows while sleeping in order to relieve her symptoms. She denies any chest pain, chest tightness, or palpitations. Past medical history is significant for hypertension and diabetes mellitus type 2. Her medications are amiloride, glyburide, and metformin. Family history is significant for her father who also suffered diabetes mellitus type 2 before his death at 90 years old. The patient says she drinks alcohol occasionally but denies any smoking history. Her blood pressure is 130/95 mm Hg, temperature is 36.5°C (97.7°F), and heart rate is 100/min. On physical examination, she has a sustained apical impulse, a normal S1 and S2, and a loud S4 without murmurs. There are bilateral crackles present bilaterally. A chest radiograph shows a mildly enlarged cardiac silhouette. A transesophageal echocardiogram is performed and shows a normal left ventricular ejection fraction. Which of the following myocardial changes is most likely present in this patient?

Ventricular hypertrophy with sarcomeres duplicated in parallel

Asymmetric hypertrophy of the interventricular septum

Ventricular hypertrophy with sarcomeres duplicated in series

Granuloma consisting of lymphocytes, plasma cells and macrophages surrounding necrotic tissue

A 65-year-old man presents to the physician for the evaluation of increasing dyspnea and swelling of the lower extremities over the past year. He has no cough. He also complains of frequent awakenings at night and excessive daytime sleepiness. He has no history of a serious illness. He takes no medications other than zolpidem before sleep. He is a 35-pack-year smoker. His blood pressure is 155/95 mm Hg. His BMI is 37 kg/m2. Oropharyngeal examination shows a small orifice and an enlarged tongue and uvula. The soft palate is low-lying. The examination of the nasal cavity shows no septal deviation or polyps. Symmetric pitting edema is seen below the knee, bilaterally. The lungs are clear to auscultation. Echocardiography shows a mildly dilated right ventricle and an elevated systolic pulmonary artery pressure with no abnormalities of the left heart. A ventilation-perfusion scan shows no abnormalities. Which of the following is the most likely cause of this patient’s symptoms?

Chronic obstructive pulmonary disease

Idiopathic pulmonary artery hypertension

Heart failure with a preserved ejection fraction

Hypertensive heart disease — USMLE Lesson

HHD Pathophysiology - Pressure Overload

Mechanism: Chronic ↑ afterload (e.g., systemic HTN, aortic stenosis) forces the left ventricle (LV) to generate higher pressures.
Cellular Adaptation: Myocytes enlarge (hypertrophy) by adding new sarcomeres in parallel.
- This results in concentric hypertrophy → ↑ LV wall thickness, often with a ↓ in chamber radius.
Physics: Compensatory hypertrophy normalizes wall stress per Laplace’s Law ($Wall Stress = (P \times r) / (2h)$) by increasing wall thickness (h).

Hypertensive Heart Disease: Gross and Microscopic Views

⭐ The earliest manifestation of HHD is typically diastolic dysfunction, leading to Heart Failure with preserved Ejection Fraction (HFpEF). Systolic failure (HFrEF) is a late complication.

Systemic (Left) HHD - The Body's Burden

Pathogenesis: Chronic systemic hypertension imposes a pressure overload (↑ afterload) on the left ventricle (LV), forcing it to work harder.
LV Adaptation & Failure: The ventricle adapts via concentric hypertrophy (thickened wall) to normalize wall stress. This eventually leads to:
- Stiff LV → Impaired diastolic filling (diastolic dysfunction).
- ↑ Myocardial O₂ demand → Susceptibility to ischemia.
- Left atrial enlargement → Risk of atrial fibrillation.

Morphology & Dx:
- Gross: Symmetrically thickened LV wall (>1.2 cm), ↑ heart weight.
- Micro: Enlarged myocytes with "boxcar" nuclei; interstitial fibrosis.
- ECG: May show LVH criteria (e.g., Sokolow-Lyon: S in V1 + R in V5/V6 > 35 mm).

LVH vs. Normal Heart: Gross Specimen Comparison

⭐ The earliest manifestation is often diastolic dysfunction with preserved ejection fraction (HFpEF), as the stiff, hypertrophied ventricle cannot relax and fill properly.

Pulmonary (Right) HHD - Cor Pulmonale

Definition: Right ventricular (RV) hypertrophy and/or dilation resulting from pulmonary hypertension (PH) caused by diseases of the lung parenchyma or vasculature.
Pathophysiology Flow:

Common Causes:
- COPD (most frequent)
- Interstitial lung disease
- Chronic thromboembolic disease (CTEPH)
- Obstructive sleep apnea
Clinical Findings:
- Symptoms of underlying lung disease + signs of right heart failure (JVD, peripheral edema, hepatomegaly).
- Loud P2, tricuspid regurgitation murmur.
Diagnosis:
- Echo: Shows RVH, estimates pulmonary artery pressure.
- Right Heart Cath: Gold standard to confirm PH.

⭐ The most common cause of right-sided heart failure is left-sided heart failure. Cor pulmonale is specifically right-sided failure due to lung pathology.

Cor Pulmonale: Healthy Heart vs. Right-Sided Heart Failure

HHD Morphology - Sizing Up Damage

Systemic (Left) HHD:
- Gross: Symmetrical, concentric left ventricular hypertrophy (LVH) without dilation initially. ↑ heart weight.
- Wall thickness can exceed 2.0 cm.
- Micro: Enlarged cardiomyocytes with prominent, hyperchromatic "boxcar" nuclei.
- Interstitial fibrosis develops over time.
Pulmonary (Right) HHD / Cor Pulmonale:
- Gross: Right ventricular hypertrophy and dilation, often with wall thickness >1.0 cm.

Hypertensive Heart Disease: Gross and Microscopic Pathology

⭐ A stiff, non-compliant LV from chronic hypertrophy leads to impaired diastolic filling, often manifesting as a prominent S4 heart sound.

High‑Yield Points - ⚡ Biggest Takeaways

Systemic hypertension is the fundamental cause, creating pressure overload on the left ventricle.

The heart adapts via concentric left ventricular hypertrophy (LVH).

Histology classically shows enlarged myocytes with prominent "boxcar" nuclei.

Clinically, it first manifests as diastolic dysfunction (HFpEF).

An S4 gallop is a common auscultatory finding.

Uncontrolled, it can progress to systolic dysfunction and overt heart failure.

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