How does aortic stenosis (AS) cause fluid retention and congestive heart failure (CHF)?

Pathophysiology of Fluid Retention and Heart Failure in Aortic Stenosis

Aortic stenosis causes fluid retention and congestive heart failure through progressive left ventricular pressure overload leading to concentric hypertrophy, diastolic dysfunction, elevated filling pressures, and ultimately backward transmission of pressure to the pulmonary circulation and systemic venous system. 1

Primary Hemodynamic Mechanism

The obstruction at the aortic valve creates a chronic pressure overload on the left ventricle that develops gradually over years. 1 This systolic pressure overload triggers several compensatory mechanisms:

• Concentric left ventricular hypertrophy develops as the primary adaptive response, with the ventricle thickening to normalize wall stress according to Laplace's law 1
• Diastolic dysfunction emerges as the hypertrophied, stiffened ventricle becomes less compliant, impairing ventricular filling and elevating left ventricular end-diastolic pressure 1
• Reduced coronary reserve occurs due to increased myocardial oxygen demand from hypertrophy combined with compression of intramyocardial vessels, leading to subendocardial ischemia even without epicardial coronary disease 1

Progression to Heart Failure

As the disease advances, the compensatory mechanisms fail:

• Depressed contractility eventually develops when the ventricle can no longer maintain adequate systolic function against the increased afterload 1
• Elevated left atrial pressure results from backward transmission of elevated LV filling pressures, which then propagates to the pulmonary veins and capillaries 2
• Pulmonary congestion manifests when pulmonary capillary wedge pressure rises significantly (mean 25.5 ± 2.9 mmHg in severe cases with CHF) 2
• Right heart failure can develop from chronic pulmonary hypertension, with mean pulmonary artery pressures reaching 41.9 ± 9 mmHg in patients with severe AS and CHF 2

Fluid Retention Mechanisms

The elevated filling pressures and reduced cardiac output activate neurohormonal systems:

• Reduced cardiac output (as low as 1.9 ± 0.27 L/min/m² in severe cases) triggers compensatory mechanisms including activation of the renin-angiotensin-aldosterone system and sympathetic nervous system 2
• Sodium and water retention occurs through renal hypoperfusion and neurohormonal activation, leading to volume expansion and peripheral edema 1
• Systemic venous congestion develops from elevated right atrial pressures transmitted backward through the venous system 2

Contributing Non-Valvular Factors

Additional factors beyond valve stenosis severity contribute to heart failure symptoms:

• Depressed systemic arterial compliance independently associates with worse heart failure symptoms, with each 0.1 ml/m²/mmHg decrease in compliance increasing odds of more severe symptoms (OR 1.16,95% CI 1.01-1.35) 3
• Global left ventricular afterload (valvulo-arterial impedance) combines valvular obstruction with arterial stiffness to determine total ventricular load 3
• Age-related vascular changes compound the hemodynamic burden, as older patients demonstrate both increased valve calcification and reduced arterial compliance 3

Clinical Manifestations

The hemodynamic derangements produce characteristic clinical findings:

• Dyspnea results from pulmonary venous congestion and elevated pulmonary capillary pressures 1, 4
• Peripheral edema develops from systemic venous congestion and sodium/water retention 1
• Exercise intolerance reflects the inability to augment cardiac output appropriately due to fixed obstruction and impaired ventricular function 3

Prognostic Implications

Once heart failure develops, prognosis deteriorates dramatically:

• Acute heart failure complicating severe AS carries 5-year mortality of 61.8% compared to 37.1% in asymptomatic patients 4
• Survival after symptom onset averages only 2 years with heart failure, 3 years with syncope, and 5 years with angina in medically managed patients 1
• Persistent heart failure after valve replacement occurs in some patients due to irreversible myocardial damage, concomitant conditions, or inadequate reverse remodeling 5

Important Clinical Caveats

• Heart failure can develop even with moderate stenosis when combined with reduced systemic arterial compliance or other cardiac conditions 3
• Left ventricular ejection fraction may remain preserved until late in the disease course due to compensatory hypertrophy, masking significant diastolic dysfunction 1
• Rapid decompensation can occur with triggers such as atrial fibrillation (which eliminates atrial contribution to ventricular filling), anemia, or infection 6