From the Guidelines
Aortic valve atherosclerosis causes significant hemodynamic changes, primarily increased resistance to blood flow, leading to left ventricular hypertrophy, elevated left ventricular end-diastolic pressure, and potentially pulmonary congestion and heart failure symptoms. The primary hemodynamic effect is increased resistance to blood flow from the left ventricle into the aorta, creating a pressure gradient across the valve. This obstruction forces the left ventricle to generate higher pressures to maintain adequate cardiac output, leading to concentric left ventricular hypertrophy as a compensatory mechanism 1. As the disease progresses, the increased workload on the heart results in elevated left ventricular end-diastolic pressure, which can back up into the pulmonary circulation, potentially causing pulmonary congestion and symptoms of heart failure.
Key Hemodynamic Effects
- Increased resistance to blood flow from the left ventricle into the aorta
- Elevated left ventricular end-diastolic pressure
- Concentric left ventricular hypertrophy
- Potential pulmonary congestion and heart failure symptoms
- Cardiac output becomes fixed and eventually diminishes, especially during exercise when the heart cannot increase output to meet metabolic demands 1
Clinical Implications
The hemodynamic changes associated with aortic valve atherosclerosis can lead to significant morbidity and mortality if left untreated. Symptomatic patients with severe aortic stenosis should be considered for aortic valve replacement (AVR) to improve survival, symptoms, and left ventricular systolic function 1. The choice between surgical AVR (SAVR) and transcatheter AVR (TAVI) depends on the patient's surgical risk, with TAVI being a viable option for patients at increased surgical risk.
Diagnostic Considerations
Severe aortic stenosis is typically defined by valve hemodynamics, including AV Vmax ≥4 m/s, mean DP ≥40 mm Hg, or AVA typically ≤1.0 cm² (or AVAi ≤0.6 cm/m²) 1. However, in patients with low left ventricular ejection fraction (LVEF) (<50%), these hemodynamic thresholds may not be achieved, and adjunctive diagnostic modalities such as dobutamine stress echocardiography may be needed to confirm the diagnosis.
From the Research
Hemodynamic Effects of Aortic Valve Atherosclerosis
The hemodynamic effects of aortic valve atherosclerosis, also known as aortic stenosis (AS), can be significant and have been studied in various research papers 2, 3, 4, 5, 6.
- Changes in Aortic Valve Area: In patients with severe AS, small changes in aortic valve area can lead to large changes in hemodynamics 4.
- Pressure Recovery Phenomenon: The pressure recovery phenomenon is an important factor in the evaluation of patients with aortic stenosis, as it can affect the assessment of the severity of the condition 4.
- Valvular Arterial Impedance: Valvular arterial impedance is another novel tool used in the evaluation of patients with aortic stenosis, providing valuable information on the hemodynamic effects of the condition 4.
- Effects of Transcatheter Aortic Valve Implantation (TAVI): TAVI has been shown to have a significant impact on hemodynamics in patients with severe AS, with improvements in aortic and left ventricular pressures, as well as left ventricular ejection fraction 3.
- Hemodynamic Subtypes of Severe Aortic Valve Stenosis: Research has identified different hemodynamic subtypes of severe AS, including paradoxical low flow low gradient (pLFLG), classic LFLG, and high gradient AS (HGAS), each with distinct hemodynamic characteristics and outcomes after TAVR 5.
Hemodynamic Changes During Aortic Valve Surgery
Hemodynamic changes during aortic valve surgery have also been studied, with findings including:
- Decrease in Cardiac Index (CI) and Stroke Volume Index (SVi): General anesthesia can lead to a decrease in CI and SVi in patients with severe AS 6.
- Effects of Dobutamine Infusion: Dobutamine infusion can increase CI, but its effect on SVi is highly variable and associated with baseline left ventricular ejection fraction (LVEF) 6.
- Effects of Fluid Bolus: Fluid bolus can increase CI, SVi, and pulmonary capillary wedge pressure (PCWP), with the increase in PCWP being more pronounced in patients with a larger left atrial volume index 6.