Invasive Measures of Afterload in Low Gradient Severe Aortic Stenosis With Preserved Ejection Fraction

Background The pathophysiology of low flow, low gradient severe aortic stenosis (LGSAS) with preserved ejection fraction is poorly understood. It has been proposed that abnormalities of arterial circulation are a major contributor to this syndrome. Methods and Results We invasively examined systemic arterial afterload (effective arterial elastance, Ea; total arterial compliance, Ca; and systemic vascular resistance index) in patients with LGSAS (mean gradient, <40 mmHg; aortic valve area, <1.0 cm(2)) and preserved ejection fraction (50%), and compared these findings with patients with high gradient (40 mmHg) severe aortic stenosis (HGSAS) and moderate AS (mean gradient, <40 mmHg; aortic valve area, >1.0 cm(2)). Patients with LGSAS (n=36), HGSAS (n=31), and moderate AS (n=19) were similar with respect to age, sex, body size, symptoms, comorbidities, and ejection fraction. Aortic valve area was similar between groups with LGSAS and HGSAS, but the patients with LGSAS had reduced stroke volume index and cardiac index (P=0.003 for both). In comparison with patients with HGSAS and moderate AS, measures of afterload, including Ea (4.020.98 versus 3.13 +/- 0.81 and 3.06 +/- 0.79 mmHgm(2)/mL; P<0.0001) and systemic vascular resistance index (3116 +/- 799 versus 2515 +/- 645 and 2380 +/- 546 dynsm(2)/cm(5); P=0.001), were significantly higher in LGSAS, whereas Ca was lower (0.46 +/- 0.16 versus 0.57 +/- 0.13 and 0.59 +/- 0.19 mL/m(2) per mmHg; P=0.002). All invasive measures of arterial afterload were related to stroke volume index. Conclusions Patients with LGSAS and preserved ejection fraction display elevated arterial afterload compared with patients with HGSAS and moderate AS. These findings identify systemic arterial effects that contribute to the hemodynamic presentation in patients with LGSAS and help to further define this entity.