• Inflammatory Markers Add to TAVR Risk Stratification

    What is the role of inflammation in aortic valve stenosis and TAVR valve degeneration?

    PARIS -- Certain inflammatory leukocyte and marker levels may aid in risk prediction for transcatheter aortic valve replacement (TAVR) candidates, new research suggests.

    An analysis of 129 TAVR patients showed that lower levels of the circulating helper T-cell Th2 as well as higher levels of interleukin-6 (IL-6), helper T-cell Th17, and non-classic monocytes were independently associated with increased all-cause mortality at 12 months, Jedrzej Hoffmann, MD, of Frankfurt am Main in Germany, and colleagues reported during a poster session here at the European Society of Cardiology annual congress.

    The research also showed these biomarkers helped better predict 12-month mortality when incorporated into the Society of Thoracic Surgeons (STS) risk score, as shown by improvements in the area under the receiver operating characteristic curve (AUC).

    Adding IL-6 levels increased AUC from 0.737 to 0.750 and led to a category-free net reclassification improvement of 0.48. When non-classical monocyte levels were added on top of IL-6, the AUC increased to 0.753, while the net reclassification improved to 0.74. And when Th2 was added to IL-6, AUC increased to 0.765, with a net reclassification improvement of 0.39.

    "Our findings demonstrate for the first time an association of inflammatory leukocyte phenotypes with increased mortality after [TAVR]. Specific monocytic and T-cell signatures might provide novel additive biomarkers to improve individual risk stratification in patients with severe aortic stenosis," the authors concluded.

    Systemic inflammatory response syndrome, identified by an increase in total leukocyte counts among other criteria, had been previously shown to be a predictor of mortality after TAVR.

    "Since the pathology of atherosclerosis and aortic valve stenosis is similar, it is reasonable that inflammation plays a role even in aortic valve stenosis," commented Peter Stachon, MD, of University Heart Center Freiburg in Germany. But although a thrombotic-derived type of aortic valve stenosis probably exists, there's no treatment to improve such stenosis -- the only option is aortic valve replacement, he said.

    The study hints at the potential for anti-inflammatory therapies' -- such as statins, PCSK9 inhibitors, and even canakinumab (Ilaris) -- to help prevent TAVR valve deterioration, according to Stachon, who was not involved with the study.

    The single-center study included 129 consecutive patients undergoing TAVR for severe symptomatic aortic stenosis. All had peripheral whole-blood samples taken (before TAVR, immediately after the procedure, at 24 hours, and at 3 days) and assayed for high-sensitivity CRP, IL-6, high-sensitivity troponin T, and NT-proBNP.

    Patients in the study had a mean age of 82.3, and 58.9% were men. The cohort tended to be at high operative risk, with mean EuroSCORE II and STS scores of 5.9% and 4.1%, respectively. Median aortic valve mean gradient was 45 mm Hg, and median aortic valve area was 0.7 cm2.

    "Further cross-sectional studies in different populations of octogenarians should possibly define assay-specific and gender- or age-adjusted cut-off values for distinct cell subsets to facilitate their implementation into routine laboratory diagnostic or immunological assessment of the future [TAVR] candidates," Hoffmann's group wrote.

    The lack of data on cause of death, however, makes it unclear whether patients died from TAVR deterioration related to inflammation or from another inflammatory disease such as coronary heart disease, pneumonia, or cancer, Stachon told MedPage Today.

    Ultimately, the data could have been strongly influenced by confounders and should be replicated in larger multicenter studies, commented Francesco Maisano, MD, of University Hospital Zurich, Switzerland.

    "It is, however, important to remind that we need to improve our risk stratification standards since in current era up to 25% of patients undergoing [TAVR] do not survive at 1 year. To avoid futility, risk stratification models incorporating clinical features and biomarkers are welcome," he maintained.

     

    Hoffmann and co-authors had no disclosures.

    Source:

    European Society of Cardiology

    Source Reference: Hoffmann J, et al "Inflammatory leukocyte phenotypes are associated with increased mortality after transfemoral transcatheter aortic valve implantation" ESC 2019; Abstract P930.

    Read the original article on Medpage Today: Inflammatory Markers Add to TAVR Risk Stratification

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