How valvular disease is tested on Step 1
Expect a patient with a murmur and a cause (rheumatic fever history, Marfan habitus, IV drug use, age-related calcification) and a question about the lesion, its remodeling pattern, or a complication.
A chamber pushing against a closed door (stenosis) thickens its wall — concentric hypertrophy. A chamber receiving extra blood back (regurgitation) stretches — eccentric hypertrophy and dilation.
Four left-sided lesions
The aortic and mitral valves are affected far more often than the right-sided valves because they face higher pressures.
| Lesion | Common causes | Remodeling | Key findings |
|---|---|---|---|
| Aortic stenosis | Age-related calcification; bicuspid valve (< 70 years) | Concentric LVH | Angina, syncope, HF; slow-rising pulse; ejection murmur to carotids |
| Aortic regurgitation | Root dilation (Marfan, hypertension, syphilis), bicuspid valve, endocarditis | LV dilation, eccentric LVH | Wide pulse pressure, bounding pulses, head bobbing, early diastolic murmur |
| Mitral stenosis | Rheumatic heart disease | LA dilation; LV normal or small | Atrial fibrillation, LA thrombus, hemoptysis, dysphagia, hoarseness (Ortner) |
| Mitral regurgitation | MVP, ischemic papillary muscle, LV dilation, endocarditis, rheumatic | LA and LV dilation | Holosystolic murmur to axilla; acute MR → flash pulmonary edema |
Acute severe regurgitation (papillary muscle rupture, endocarditis) causes sudden pulmonary edema because the chambers have not had time to dilate.
Rheumatic heart disease
Rheumatic fever follows untreated group A streptococcal pharyngitis. Antibodies against M protein cross-react with cardiac tissue (molecular mimicry, type II hypersensitivity).
| Jones major criteria | Feature |
|---|---|
| Carditis | Pancarditis — endocardium, myocardium, pericardium |
| Polyarthritis | Migratory, large joints |
| Sydenham chorea | Involuntary movements, often late |
| Erythema marginatum | Annular rash with clear center |
| Subcutaneous nodules | Over extensor surfaces |
Diagnosis requires evidence of prior strep infection plus 2 major, or 1 major and 2 minor, criteria. Penicillin prevents recurrences.
Endocarditis and prosthetic valves
Damaged or prosthetic valves are prone to infection and thrombosis.
| Valve type | Advantage | Drawback |
|---|---|---|
| Mechanical | Lasts decades | Lifelong warfarin (DOACs contraindicated); hemolysis (schistocytes) |
| Bioprosthetic (tissue) | No long-term anticoagulation | Degenerates in 10–20 years |
Prosthetic valves raise endocarditis risk (Staphylococcus epidermidis early after surgery) and warrant antibiotic prophylaxis before some dental procedures.
Clinical application
Physical findings plus a systemic clue usually identify the lesion and its cause.
A tall 30-year-old man with long fingers and lens dislocation has blood pressure 150/40 mm Hg, bounding pulses, and an early diastolic decrescendo murmur at the left sternal border. What is the lesion and its mechanism?
- Tall stature, arachnodactyly, and lens dislocation suggest Marfan syndrome (fibrillin-1 defect).
- Weak connective tissue leads to aortic root dilation, which pulls the aortic leaflets apart.
- Blood leaks back into the LV in diastole: diastolic pressure falls and stroke volume rises, widening pulse pressure.
Answer. Aortic regurgitation from aortic root dilation in Marfan syndrome. The LV remodels with eccentric hypertrophy; risk of aortic dissection is high.