Valvular Heart Disease

Stenosis Versus Regurgitation

A stenotic valve does not open adequately, forcing the upstream chamber to generate more pressure. A regurgitant valve does not close adequately, allowing blood to return backward and increasing chamber volume. Pressure overload tends to cause hypertrophy; volume overload tends to cause dilation (Kusumoto, 2019).

Lesion	Primary load	Typical chamber response
Aortic stenosis	LV pressure overload	Concentric LV hypertrophy
Aortic regurgitation	LV volume overload	LV dilation/eccentric hypertrophy
Mitral stenosis	LA pressure overload; impaired LV filling	LA dilation, pulmonary congestion
Mitral regurgitation	LA and LV volume overload	LA/LV dilation

Etiology and Risk Factors

Valve disease may be degenerative, congenital, rheumatic, ischemic, infectious, or related to disease of the supporting apparatus or great vessels. Calcific degeneration and congenital bicuspid anatomy are important mechanisms of aortic stenosis. Aortic regurgitation may result from leaflet disease or dilation of the aortic root. Mitral stenosis is classically associated with rheumatic valve injury, whereas mitral regurgitation may arise from primary leaflet/chordal disease or secondary ventricular remodeling, ischemia, or papillary-muscle dysfunction. Identifying the mechanism matters because two patients with the same regurgitant jet may have very different ventricular geometry, tempo, and treatment implications (Kusumoto, 2019; Norris, 2020; Otto et al., 2021).

Aortic Stenosis

Aortic valve narrowing increases LV outflow resistance. The ventricle generates higher systolic pressure and develops concentric hypertrophy. Hypertrophy initially reduces wall stress but raises oxygen demand and reduces compliance. Exertional angina can occur from supply-demand mismatch, exertional syncope from fixed outflow limitation, and HF when filling pressures or systolic dysfunction progress (Kusumoto, 2019; Otto et al., 2021).

Aortic Regurgitation

Aortic valve incompetence allows diastolic backflow from the aorta into the LV. Chronic volume overload increases end-diastolic volume and leads to LV dilation and eccentric hypertrophy. Chronic compensation can preserve forward output for years. Acute severe AR is poorly tolerated because a noncompliant LV cannot accommodate the sudden regurgitant volume, causing abrupt pressure rise and pulmonary edema (Kusumoto, 2019; Otto et al., 2021).

Mitral Stenosis

Mitral narrowing obstructs diastolic flow from the LA to the LV. Left atrial pressure rises and is transmitted backward into the pulmonary veins and capillaries. LA dilation predisposes to AF; loss of atrial contraction can further impair LV filling. Dilated atria and AF also promote thrombus formation and systemic embolization (Kusumoto, 2019; Otto et al., 2021).

Mitral Regurgitation

During systole, blood regurgitates from the LV into the LA, increasing LA pressure and volume. During the next diastole, that regurgitant volume returns to the LV in addition to normal pulmonary venous return, producing LV volume overload. Chronic MR permits adaptive dilation; acute MR can produce sudden pulmonary edema and shock because the LA has not had time to enlarge (Kusumoto, 2019; Otto et al., 2021).

Murmur Timing

Lesion	Timing	Why
Aortic stenosis	Systolic	Turbulent ejection through narrowed aortic valve
Mitral regurgitation	Systolic	Backflow through incompetent mitral valve
Mitral stenosis	Diastolic	Turbulent filling through narrowed mitral valve
Aortic regurgitation	Diastolic	Backflow through incompetent aortic valve

Physical Examination Clues Linked to Flow

Lesion	Typical auscultatory clue	Physiologic link
Aortic stenosis	Crescendo-decrescendo systolic ejection murmur; often radiates toward carotids	Turbulent forward ejection through a narrowed valve
Aortic regurgitation	Early diastolic decrescendo murmur	Diastolic backflow from aorta to LV
Mitral stenosis	Low-pitched diastolic rumble	Turbulent diastolic filling across narrowed mitral valve
Mitral regurgitation	Holosystolic murmur, classically toward axilla	Systolic backflow from LV to LA

Diagnostic Approach

Transthoracic echocardiography is the primary noninvasive test for defining valve anatomy, severity, chamber response, and hemodynamic consequences. History and physical findings should be correlated with noninvasive testing; when findings are discordant, additional imaging or invasive assessment may be needed (Otto et al., 2021).

Clinical Manifestations

Manifestations depend on the valve and severity. Aortic stenosis classically progresses to exertional dyspnea, angina, syncope, or heart failure. Mitral stenosis commonly produces exertional dyspnea and may lead to AF and pulmonary congestion. Chronic aortic or mitral regurgitation may remain compensated for years before dyspnea, fatigue, palpitations, or heart failure develops (Kusumoto, 2019).

Findings That Refine the Diagnosis

The murmur identifies abnormal flow timing but does not by itself determine lesion severity. Chamber enlargement, ventricular hypertrophy or dilation, pulmonary pressures, rhythm changes, and symptom burden help determine the physiologic consequence. Acute pulmonary edema or shock in a patient with new regurgitation suggests an abrupt lesion that has not had time to remodel (Kusumoto, 2019; Otto et al., 2021).

Differential Diagnosis

Dyspnea, chest discomfort, syncope, and murmurs may also occur with coronary disease, cardiomyopathy, heart failure without primary valvular disease, arrhythmias, congenital lesions, or pericardial disease. Echocardiography is used to establish the valve lesion and its hemodynamic consequences (Otto et al., 2021).

Treatment Principles

Medical therapy may reduce congestion, blood pressure burden, or rhythm-related complications, but it does not remove a fixed mechanical obstruction or permanently correct severe structural regurgitation. Definitive management therefore depends on lesion severity, symptoms, ventricular response, procedural risk, and whether repair, surgical replacement, or transcatheter intervention is indicated (Otto et al., 2021).

Red Flags

• Exertional syncope or new heart-failure symptoms with suspected severe aortic stenosis (Kusumoto, 2019; Otto et al., 2021).
• Acute pulmonary edema, hypotension, or shock with new severe mitral or aortic regurgitation (Kusumoto, 2019; Otto et al., 2021).
• New murmur and hemodynamic deterioration after myocardial infarction, raising concern for a mechanical complication (Kusumoto, 2019; Otto et al., 2021).
• Rapidly progressive dyspnea or evidence of severe pulmonary hypertension (Kusumoto, 2019; Otto et al., 2021).

High-Yield Distinctions

• Stenosis = obstruction to forward flow; regurgitation = backward flow.
• Aortic stenosis is a pressure-overload lesion; aortic regurgitation is a volume-overload lesion.
• Mitral stenosis primarily raises LA and pulmonary venous pressures.
• Acute regurgitation is generally less well tolerated than chronic regurgitation because compensatory chamber dilation has not occurred.

Related YourDNP Resources

• Cardiac Pathophysiology Foundations
• Heart Failure
• Arrhythmias

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References

Kusumoto, F. M. (2019). Cardiovascular disorders: Heart disease. In G. D. Hammer & S. J. McPhee (Eds.), Pathophysiology of disease: An introduction to clinical medicine (8th ed., pp. 289–328). McGraw-Hill Education.

Norris, T. L. (2020). Porth’s essentials of pathophysiology (5th ed.). Wolters Kluwer.

Otto, C. M., Nishimura, R. A., Bonow, R. O., Carabello, B. A., Erwin, J. P., III, Gentile, F., Jneid, H., Krieger, E. V., Mack, M., McLeod, C., O’Gara, P. T., Rigolin, V. H., Sundt, T. M., III, Thompson, A., & Toly, C. (2021). 2020 ACC/AHA guideline for the management of patients with valvular heart disease. Circulation, 143, e72–e227. https://doi.org/10.1161/CIR.0000000000000923