Key result
Paradoxical low-flow severe AS is linked to ~33% greater valvuloarterial impedance and impaired longitudinal strain.
Why the study?
Are increased ventricular hydraulic load and reduced longitudinal strain associated with paradoxical low-flow severe aortic stenosis compared to normal-flow aortic stenosis?
Observational (n=120)
Are increased ventricular hydraulic load and reduced longitudinal strain associated with paradoxical low-flow severe aortic stenosis compared to normal-flow aortic stenosis?
Paradoxical low-flow severe aortic stenosis is characterized by increased hydraulic load (from more severe valvular stenosis and increased vascular resistance) and impaired longitudinal strain.
Does not support practice changes in aortic stenosis; leaves open whether targeting impedance or strain improves outcomes in paradoxical low-flow disease.
AIMS: Patients with paradoxical low-flow severe aortic stenosis (PLF-AS) reportedly have higher left ventricular hydraulic load and more systolic strain dysfunction than patients with normal-flow aortic stenosis. This study investigates the relationship of systolic loading and strain to PLF-AS to further define its pathophysiology. METHODS: One hundred and twenty patients (age 79 ± 12 years, 37% men) with an indexed aortic valve area (AVAi) of 0.6 cm/m or less and an ejection fraction of 50% or higher were divided into two groups based on indexed stroke volume (SVi): PLF-AS, SVi ≤ 35 ml/m, N = 46; normal-flow aortic stenosis, SVi > 35 ml/m, N = 74). Valvular and arterial load were assessed using multiple measurements, and strain was assessed using speckle-tracking echocardiography. RESULTS: Patients with PLF-AS were found to have more valvular load (lower AVAi, P = 0.028; lower energy loss coefficient, P = 0.001), more arterial load [decreased arterial compliance and increased systemic vascular resistance (SVR), both P < 0.001] and more total hydraulic load [increased valvuloarterial impedance (Zva), P < 0.001]. Transvalvular gradients and arterial pressures were similar. Longitudinal strain was lower in PLF-AS (P < 0.001), but circumferential and rotation strains were similar. On adjusted regression, AVAi, SVR and longitudinal strain were associated with PLF-AS [odds ratio (OR) = 1.34, P = 0.043; OR = 1.31, P = 0.004; OR = 1.34, P = 0.011, respectively]. When SVR and AVAi were replaced with Zva, longitudinal strain and Zva (OR = 1.38, P = 0.015; OR = 1.33, P < 0.001 for both, respectively) were associated with PLF-AS. CONCLUSION: Increased hydraulic load, from more severe valvular stenosis and increased vascular resistance, and longitudinal strain impairment are associated with PLF-AS and their interplay is likely fundamental to its pathophysiology.
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Holmes et al. (2015) conducted an observational in Severe aortic stenosis (n=120). Paradoxical low-flow severe aortic stenosis (SVi ≤ 35 ml/m) vs. Normal-flow aortic stenosis (SVi > 35 ml/m) was evaluated on Association with paradoxical low-flow severe aortic stenosis (OR 1.33, p=<0.001). Paradoxical low-flow severe aortic stenosis was significantly associated with increased valvuloarterial impedance (OR 1.33, P<0.001) and impaired longitudinal strain (OR 1.38, P=0.015).
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