Available prediction models are inaccurate in elderly who underwent transcatheter
aortic valve implantation (TAVI). The aim of present study was to analyze the separate
and combined prognostic values of baseline HDL-C and C-reactive protein (CRP) levels
in patients treated successfully with TAVI who had complete 2-year follow-up. We analyzed
334 patients treated with TAVI from 01/2010 to 07/2017 who had measurements of HDL-C
and CRP on admission or during qualification for the procedure. Baseline HDL-C ≤46
mg/dl (areas under the curve [AUC] = 0.657) and CRP ≥0.20 mg/dl (AUC = 0.634) were
predictive of 2-year mortality. After stratification with both cutoffs, patients with
low HDL-C and concomitant high CRP most often had LVEF ≤50% and were high risk as
per EuroSCORE II. Those with isolated CRP elevation had the lowest frequency of LVEF
≤50%, but more sarcopenia (based on psoas muscle area). After adjustment in the multivariate
analysis for other identified predictors including EuroSCORE II and statin therapy,
isolated HDL-C ≤46 mg/dl (identified in 40 patients) and isolated CRP ≥0.20 mg/dl
(n = 109) were both independent predictors of 2-year mortality (hazard ratio [HR] = 2.92
and HR = 2.42, respectively) compared with patients with both markers within established
cutoffs (n = 105) who had the lowest 2-year mortality (9.5%). Patients with both markers
exceeding cutoffs (n = 80) had the highest risk (HR = 4.53) with 2-year mortality
of 42.5%. High CRP was associated with increased mortality within the first year of
follow-up, whereas low HDL-C increased mortality in the second year. The combination
of both markers with EuroSCORE II enhanced mortality prediction (AUC = 0.697). In
conclusion, low baseline HDL-C and high CRP jointly contribute to the prediction of
increased all-cause mortality after TAVI.
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Article Info
Publication History
Published online: April 08, 2020
Received in revised form:
March 27,
2020
Received:
January 13,
2020
Footnotes
Where the work was performed: Institute of Cardiology ul. Alpejska 42, 04–628 Warszawa, Poland
Funding: none.
Identification
Copyright
© 2020 Elsevier Inc. All rights reserved.
