Why the study?
Do patients with normal LVEF after aortic valve replacement for aortic stenosis have compromised myocardial contractile reserve and exercise capacity compared to matched controls?
Do patients with normal LVEF after aortic valve replacement for aortic stenosis have compromised myocardial contractile reserve and exercise capacity compared to matched controls?
Exercise capacity and myocardial functional reserve remain subnormal after AVR for aortic stenosis despite normal resting LVEF, with peak exercise longitudinal strain rate independently predicting peak oxygen consumption.
Exercise capacity may remain impaired after AVR despite normal LVEF; hypothesis-generating for peak exercise GLSRs in prospective risk stratification.
OBJECTIVE: Despite recovery of left ventricular (LV) function and morphology after aortic valve replacement (AVR) for aortic stenosis (AS), its relationship with exercise capacity remains unknown. Twenty-one AVR patients (age 61 ± 12 years, 14 male) with normal ejection fraction (EF, 64 ± 7%) and 21 age- and sex-matched controls (57 ± 9 years, 10 male, EF 68 ± 8%) were studied. METHODS AND RESULTS: All subjects performed semi-supine bicycle exercise and speckle tracking echocardiography (STE) study. Peak oxygen consumption (pVO(2)) was collected during semi-supine bicycle exercise. Systolic (GLSRs) and early diastolic (GLSRe) longitudinal strain rate using STE and Doppler echocardiographic parameters were measured at rest, submaximal, peak exercise, and 4 min after exercise. The two groups had comparable resting echocardiographic measurements. At peak exercise, pVO(2) was lower in patients than controls (18.5 ± 4.5 vs. 22.1 ± 4.3 L/min/kg, P < 0.05). GLSRs (0.98 ± 0.28 vs. 1.55 ± 0.30 1/s, P < 0.001), septal Sm (7.9 ± 1.4 vs. 11.1 ± 2.3 cm/s, P < 0.001) and their changes between rest and peak exercise (ΔGLSRs: 0.16 ± 0.33 vs. 0.68 ± 0.27 1/s, P < 0.001; ΔSm 2.29 ± 2.23 vs. 4.63 ± 2.29 cm/s, P < 0.01) were significantly lower in patients than controls. There was no correlation between pVO(2) and any echocardiographic measurements in controls. In patients, pVO(2) correlated with peak exercise GLSRs (r = 0.60, P = 0.0007), septal Sm (r = 0.65, P = 0.002), and Em (r = 0.57, P = 0.009). In a multivariate model, peak exercise GLSRs (β = 7.18, P = 0.03) was the only independent predictor of pVO(2) in the patients group. CONCLUSION: Exercise capacity is subnormal after AVR for AS, irrespective of normal LVEF suggesting residual compromised myocardial functional reserve.
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Zhao et al. (2011) studied this question.
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