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Structural and Hemodynamic Bioprosthesis Deterioration
Study Questions:
What are the predictors and impact on outcomes of hemodynamic valve deterioration (HVD) of surgically implanted aortic bioprostheses?
Methods:
This was a prospective longitudinal study. The investigators assessed 137 patients with an aortic bioprosthesis implanted for a median time of 6.7 (interquartile range, 5.1-9.1) years prospectively with (baseline) complete Doppler echocardiography, quantitation of bioprosthesis leaflet calcification by multidetector computed tomography (CT), and a fasting blood sample to assess cardiometabolic risk profile. All patients underwent a second (follow-up) Doppler echocardiography examination at 3 (interquartile range, 2.9-3.3) years post-baseline visit. HVD was defined by an annualized change in mean transprosthetic gradient ≥3 mm Hg/year and/or worsening or transprosthetic regurgitation by ≥1/3 class. The primary endpoint was a nonhierarchical composite of death from any cause or aortic reintervention procedure (redo surgical valve replacement or transcatheter valve-in-valve implantation) for bioprosthesis failure. Time-to-event analyses were performed with the use of Kaplan-Meier estimates and were compared with the use of the log-rank test.
Results:
Thirty-four patients (25.6%) had leaflet calcification on baseline CT, and 18 patients (13.1%) developed an HVD between baseline and follow-up echocardiography. Fifty-two patients (38.0%) met the primary endpoint during subsequent follow-up after the second echo examination. Leaflet calcification (hazard ratio [HR], 2.58; 95% confidence interval [CI], 1.35-4.82; p = 0.005) and HVD (HR, 5.12; 95% CI, 2.57-9.71; p < 0.001) were independent predictors of the primary endpoint. Leaflet calcification, insulin resistance (homeostatic model assessment index ≥2.7), lipoprotein-associated phospholipase A2 activity (Lp-PLA2 per 0.1 nmol/min/ml increase), and high level of proprotein convertase subtilisin/kexin 9 (PCSK9) (≥305 ng/ml) were associated with the development of HVD after adjusting for age, sex, and time interval since aortic valve replacement.
Conclusions:
The authors concluded that HVD identified by Doppler echocardiography is independently associated with a marked increase in the risk of valve reintervention or mortality in patients with a surgical aortic bioprosthesis.
Perspective:
This study reports that dyslipidemic/dysmetabolic profile characterized by elevated plasma Lp-PLA2, PCSK9, and HOMA index are associated with increased risk of HVD at mid-term follow-up in patients with aortic bioprostheses, and that HVD is strongly associated with adverse outcomes. Furthermore, the presence of leaflet calcification on CT is strongly associated with HVD and subsequent adverse clinical outcomes, independently of HVD. It seems that assessing leaflet calcification by CT and HVD by Doppler echocardiography for the surveillance of patients with an aortic bioprosthesis may help identify those who are at risk of bioprosthesis failure and associated cardiac events. Additional prospective studies are indicated to assess whether modification of dysmetabolic profile may improve the durability of bioprosthetic aortic valves.
Keywords: Bioprosthesis, Calcinosis, Cardiac Surgical Procedures, Diagnostic Imaging, Echocardiography, Echocardiography, Doppler, Heart Valve Diseases, Heart Valve Prosthesis, Hemodynamics, Insulin Resistance, Multidetector Computed Tomography, Proprotein Convertases, Secondary Prevention, Subtilisins, Transcatheter Aortic Valve Replacement
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