Does improving severe aortic stenosis (AS) improve systolic heart failure (HF)?

Yes, treating severe aortic stenosis (AS) significantly improves systolic heart failure outcomes, with aortic valve replacement (AVR) being the definitive treatment that relieves symptoms, improves left ventricular ejection fraction (LVEF), and prolongs survival.

Mechanism of Improvement in Systolic Heart Failure

The depressed LVEF in patients with severe AS is frequently caused by excessive afterload (afterload mismatch), and left ventricular function improves after AVR in these patients. 1 The pressure overload from stenotic lesions causes ventricular hypertrophy, myocardial ischemia, and progressive dysfunction leading to heart failure. 2 When the primary reason for poor LV performance is excessive afterload, the prognosis following AVR is usually good. 1

Expected Functional Recovery

• LVEF typically increases by 10 ejection fraction units after AVR and may return to normal if afterload mismatch was the cause of LV systolic dysfunction. 1
• Even when LV dysfunction is not solely caused by afterload mismatch, survival is still improved after AVR, likely because of the reduced afterload, though improvement in LV function and resolution of symptoms might not be complete. 1
• Myocardial damage in severe AS progresses through four identifiable stages, from no myocardial damage (Stage 0,1-year mortality 4.4%) to Stage 4 with significant right ventricular dysfunction (25% 1-year mortality). 1

Guideline-Based Indications for Intervention

Symptomatic Severe AS with Reduced LVEF

Both ACC/AHA and ESC/EACTS guidelines provide Class I recommendations (highest level) for AVR in symptomatic patients with severe AS and reduced LVEF. 1

• AVR is recommended in symptomatic patients with severe AS (stage D1) with decreased systolic opening of a calcified or congenitally stenotic aortic valve, aortic velocity ≥4.0 m/s or mean pressure gradient ≥40 mm Hg, and symptoms of heart failure. 1
• In symptomatic patients with severe AS, ample evidence demonstrates the beneficial effects of AVR on survival, symptoms, and LV systolic function. 1

Low-Flow Low-Gradient Severe AS with Reduced LVEF

AVR is recommended in symptomatic patients with low-flow low-gradient (LFLG) severe AS with reduced LVEF, particularly when contractile reserve is present on dobutamine stress echocardiography. 1

• The document "Echocardiographic Assessment of Valve Stenosis" defines severe AS on dobutamine stress testing as maximum velocity >4.0 m/s with valve area ≤1.0 cm² at any point during the test protocol. 1
• Patients with low gradient, low EF who have the best prognosis are those with inotropic reserve (shown by an increase in stroke volume with dobutamine infusion), who have limited coronary disease and a mean gradient that exceeds 20 mm Hg. 1
• Even patients without contractile reserve may benefit from AVR, but decisions in these high-risk patients must be individualized because outcomes are poor with either surgical or medical therapy. 1

Evidence for Survival Benefit

Historical observation studies and randomized controlled trials comparing transcatheter aortic valve intervention (TAVI) with palliative care in patients with prohibitive surgical risk confirm improved survival with AVR. 1

• In patients who present with severe AS and NYHA class IV heart failure, survival is better in those who undergo AVR than in those treated medically. 1
• Although operative mortality can be as high as 20% in low-flow/low-gradient AS patients with reduced contractility, 5-year survival is still reported to be better in patients treated surgically compared to medical management. 1

The Emerging Role of Moderate AS

Current guidelines do not recommend AVR for moderate AS with systolic dysfunction, but emerging evidence suggests this population may benefit from intervention. 1

• In patients with heart failure with reduced ejection fraction (HFrEF), moderate AS is associated with increased rates of heart failure hospitalization and mortality, with outcomes similar to severe AS. 3
• Over a median follow-up of 3.1 years, the primary outcome (composite of all-cause mortality and HF hospitalization) occurred in 62.7% of patients with moderate AS versus 45.9% with no AS (P < 0.0001). 3
• The TAVI UNLOAD trial (NCT02661451) is randomizing 600 patients with moderate AS and HFrEF to guideline-directed HF therapy alone versus guideline-directed HF therapy plus TAVI to evaluate whether early intervention improves outcomes. 1, 4

Critical Clinical Pitfalls

Underestimating the severity of valve disease before irreversible ventricular dysfunction develops is a critical pitfall—early intervention is crucial to address valvular pathology before ejection fraction decline becomes irreversible. 2

• There is a decline in LVEF before the onset of severe AS, with accelerated deterioration once the aortic valve area falls below 1.2 cm². 1
• Exposure to persistent afterload elevation has a detrimental effect on LV function, and volume overload from regurgitant lesions leads to ventricular dilation, reduced ejection fraction, and eventual heart failure. 2
• Clinical vigilance is needed to recognize early symptoms and proceed promptly to AVR, as more severe "classical" symptoms of AS, including heart failure, syncope, or angina, can be avoided by appropriate treatment at the onset of even mild symptoms. 1

Medical Management Considerations

While awaiting AVR, hypertension should be treated according to standard guideline-directed medical therapy (GDMT), started at a low dose and gradually titrated upward with frequent clinical monitoring. 1

• ACE inhibitors may be advantageous due to potential beneficial effects on LV fibrosis in addition to control of hypertension. 1
• In patients who present with severe AS and NYHA class IV heart failure, vasodilator therapy may be reasonable if used with invasive hemodynamic monitoring in the acute management before urgent AVR. 1
• Invasive monitoring of LV filling pressures, cardiac output, and systemic vascular resistance is essential because a sudden decline in systemic vascular resistance might result in an acute decline in cardiac output across the obstructed aortic valve. 1