Biomarker and Invasive Hemodynamic Assessment of Cardiac Damage Class in Aortic Stenosis

ABSTRACT

Background: Aortic valve stenosis (AS) results in significant cardiovascular morbidity and mortality. To guide patient stratification and treatment in AS, echocardiographically defined cardiac damage classes have been proposed. This prospective cross-sectional study hypothesized that these classes would correlate with biomarkers and invasive hemodynamic measures of cardiovascular dysfunction.

Methods: 44 patients with symptomatic severe AS referred for transcatheter aortic valve replacement (TAVR) were assigned damage classes (0–4) echocardiographically. 14 patients were assigned classes 0–1; 24 class 2; and 6 classes 3–4. Immediately before TAVR, serum biomarker levels were measured, and invasive right and left heart catheterization performed.

Results: Preprocedural biomarkers were progressively more abnormal with increasing damage class, including overall number abnormal (r_s = 0.34, p = 0.02); high-sensitivity cardiac troponin T (r_s = 0.25, p = 0.10); NT-proBNP (r_s = 0.33, p = 0.03); and soluble ST2 (r_s = 0.35, p = 0.02). Further, damage classes correlated with preprocedural invasive hemodynamic measures, including pulmonary artery compliance (r_s = −0.29, p = 0.05), pulmonary vascular resistance (r_s = 0.32, p = 0.04), and stroke volume index (r_s = −0.31, p = 0.04). Increasing damage class was associated with greater likelihood of low-flow states.

Conclusions: Noninvasive classification of cardiac damage in AS correlates with several biomarkers and invasive hemodynamic measures of AS severity and cardiovascular dysfunction. These data provide physiologic and biochemical support to this classification, suggest that higher classes of cardiac damage reflect grades of accumulating cardiovascular dysfunction, and may enable more refined periprocedural patient selection and stratification.

KEYWORDS:

• Echocardiography
• biomarker
• hemodynamic
• cardiac damage
• aortic stenosis

Disclosure statement

None.

Additional information

Funding

This work was supported by institutional funding from Mayo Clinic (Rochester, MN).