Valvular heart disease (VHD) is a major contributor to cardiovascular morbidity and mortality worldwide. It encompasses structural or functional abnormalities of one or more of the cardiac valves—aortic, mitral, tricuspid, or pulmonary—that impair the heart’s ability to maintain unidirectional blood flow. Although congenital defects exist, most clinically relevant VHD in adults arises from degenerative changes, rheumatic fever, infective endocarditis, or calcific processes.
The pathophysiology of valvular disease revolves around two fundamental processes:
- Stenosis – failure of a valve to open completely, creating obstruction to forward flow.
- Regurgitation (or insufficiency) – failure of a valve to close completely, allowing backward flow.
Both conditions alter hemodynamics, chamber pressures, and cardiac remodeling, ultimately leading to symptoms of heart failure, arrhythmias, or sudden cardiac death if untreated.
This article explores the mechanisms behind valvular heart disease, with emphasis on anatomical changes, hemodynamic consequences, and compensatory mechanisms.
1. Normal Valve Function: A Brief Review
The human heart has four valves:
- Atrioventricular valves: Mitral (left AV) and tricuspid (right AV).
- Semilunar valves: Aortic and pulmonary.
Structure and Function
- Valves are thin, fibrous leaflets anchored by fibrous rings (annuli).
- Atrioventricular valves are supported by chordae tendineae and papillary muscles, preventing prolapse into the atria.
- Semilunar valves have cusps without chordal support, relying on their geometric structure for competence.
Physiological Role
- Valves function passively in response to pressure gradients between chambers.
- They ensure unidirectional blood flow, preventing regurgitation.
- In normal physiology, valves open widely with negligible resistance and close tightly with no leakage.
2. Pathophysiological Principles of Valvular Dysfunction
When valve anatomy is compromised, hemodynamic derangements follow.
A. Stenosis
- Defined as narrowing of the valve orifice.
- Causes pressure overload in the proximal chamber.
- Leads to concentric hypertrophy as the myocardium adapts to increased afterload.
- Common examples: aortic stenosis (calcific), mitral stenosis (rheumatic).
B. Regurgitation
- Defined as incomplete closure, allowing backflow.
- Causes volume overload in both upstream and downstream chambers.
- Leads to eccentric hypertrophy as the myocardium dilates to accommodate increased volume.
- Common examples: mitral regurgitation (prolapse, rheumatic, ischemic), aortic regurgitation (endocarditis, root dilation).
C. Mixed Lesions
- Many patients develop both stenosis and regurgitation, especially in rheumatic disease.
- The hemodynamic picture depends on which lesion predominates.
3. Pathophysiology of Specific Valve Diseases
A. Aortic Stenosis (AS)
Etiology:
- Calcific degeneration (elderly, most common in developed nations).
- Congenital bicuspid aortic valve (earlier onset).
- Rheumatic heart disease (developing regions).
Hemodynamics:
- Narrowed orifice increases resistance to LV outflow.
- LV pressure rises significantly compared to aortic pressure (large transvalvular gradient).
- Chronic pressure overload → concentric LV hypertrophy.
- Initially preserves cardiac output but reduces compliance, raising filling pressures.
- Advanced disease leads to reduced ejection fraction and HF.
Clinical Triad: Angina, syncope, dyspnea (classic for severe AS).
B. Aortic Regurgitation (AR)
Etiology:
- Valve cusp pathology (endocarditis, rheumatic disease, congenital abnormalities).
- Aortic root dilation (Marfan, aortitis, hypertension).
Hemodynamics:
- During diastole, blood leaks from the aorta back into LV.
- LV experiences combined volume and pressure overload.
- Compensatory eccentric hypertrophy and dilatation.
- High stroke volume → widened pulse pressure (“water-hammer pulse”).
- Eventually, LV fails → systolic dysfunction and HF.
C. Mitral Stenosis (MS)
Etiology:
- Almost always rheumatic fever in endemic regions.
- Rarely calcific degeneration.
Hemodynamics:
- Narrow mitral orifice impedes LV filling during diastole.
- Left atrial pressure rises significantly.
- Consequences: left atrial enlargement, atrial fibrillation, pulmonary hypertension.
- Right-sided failure may ensue in advanced cases.
Key Point: Unlike other lesions, MS is a low-output disease without hypertrophy of LV (since LV filling is limited).
D. Mitral Regurgitation (MR)
Etiology:
- Primary: Mitral valve prolapse, rheumatic disease, endocarditis.
- Secondary (functional): Ischemic cardiomyopathy, LV dilatation.
Hemodynamics:
- During systole, blood regurgitates into LA.
- LV stroke volume is split: forward stroke volume (into aorta) + regurgitant volume (into LA).
- LA dilates and LV undergoes eccentric hypertrophy.
- Acute MR (e.g., papillary muscle rupture) → sudden pulmonary edema.
- Chronic MR allows gradual adaptation but eventually leads to HF.
E. Tricuspid Valve Disease
- Tricuspid stenosis: Usually rheumatic, rare, leads to systemic venous congestion.
- Tricuspid regurgitation: Often secondary to pulmonary hypertension or RV dilatation.
- Causes systemic venous hypertension → hepatomegaly, ascites, peripheral edema.
F. Pulmonic Valve Disease
- Rare in adults.
- Stenosis: congenital most common.
- Regurgitation: usually secondary to pulmonary hypertension or surgical repair.
4. Hemodynamics: Systole and Diastole
Valvular lesions alter the normal cardiac cycle.
- Stenosis:
- In systole: obstructed outflow (AS, PS) → high proximal pressure.
- In diastole: impaired inflow (MS, TS) → high atrial pressure.
- Regurgitation:
- In systole: MR, TR → retrograde flow into atria.
- In diastole: AR, PR → leakage back into ventricles.
These changes are reflected in pressure-volume loops:
- Stenosis: increased afterload, reduced stroke volume.
- Regurgitation: enlarged loops, reflecting volume overload.
5. Compensatory Mechanisms
The heart adapts to valvular lesions through:
- Hypertrophy:
- Concentric (pressure overload, stenosis).
- Eccentric (volume overload, regurgitation).
- Neurohormonal activation:
- RAAS and sympathetic system activation maintain output but accelerate remodeling.
- Chamber dilatation:
- Atria enlarge in MR/MS; ventricles in AR/MR.
- Predisposes to arrhythmias (atrial fibrillation).
Ultimately, compensation fails, leading to heart failure.
6. Pressure Gradients and Valve Area
The severity of stenotic lesions is quantified by:
- Pressure gradient across valve (measured by Doppler echocardiography or catheterization).
- Valve area: e.g., normal mitral area 4–6 cm², severe MS < 1.0 cm².
In regurgitant lesions, severity is assessed by:
- Regurgitant volume/fraction.
- Effective regurgitant orifice area (EROA).
These measurements are crucial for timing interventions.
7. Clinical Consequences of Valvular Pathophysiology
- Heart failure: Dyspnea, edema, fatigue.
- Arrhythmias: Atrial fibrillation common in MS/MR due to atrial dilatation.
- Thromboembolism: Especially in MS with AF.
- Sudden death: Severe AS or AR can cause arrhythmia-induced death.
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