Author + information
- Rafael de la Espriella-Juan, MD,
- Eduardo Núñez, MD, MPH,
- Juan Sanchis, MD, PhD,
- Antoni Bayés-Genis, MD, PhD and
- Julio Núñez, MD, PhD∗ ()
- ↵∗Address for correspondence:
Cardiology Department, Hospital Clínico Universitario de Valencia, INCLIVA, Departamento de Medicina, Universitat de València Avenida Blasco Ibáñez 17, Valencia 46010, Spain
The recent State-of-the-Art paper published by Girerd et al. (1) summarized the array of tools available for identifying, quantifying, and monitoring congestion in heart failure (HF) in clinical practice. Due to the limited diagnostic accuracy of traditional tools in this setting, the authors propose using a multimodal, integrative approach at key stages of patient management.
We concur that there is an unmet need for instruments that accurately identify different congestion phenotypes, especially tools that help physicians to tailor the intensity of depletive treatment. In this context, the authors discuss the strengths and limitations of using circulating biomarkers, imaging techniques, and pressure–impedance tools.
Given the comprehensive nature of this review (1), it was surprising that the authors do not mention the clinical usefulness of plasma levels of carbohydrate antigen-125 (CA125) as a bona fide biomarker of congestion in HF (2–5). CA125, a high-molecular-weight glycoprotein, has been used for years to monitor ovarian cancer (2). CA125 has value in HF because it is synthesized by epithelial serous cells (the pericardium, pleura, and/or peritoneum) in response to mechanical (hydrostatic pressures) and/or cytokine stimuli (2). Elevated CA125 values are found in two-thirds of patients with acute decompensated HF (ADHF). In this setting, CA125 positively correlates with symptoms/signs of fluid overload, high atrial and pulmonary pressures, right ventricular dysfunction, and a greater risk of adverse events; notably, these findings are independent of well-known prognostic markers, such as natriuretic peptides (2).
One of the most attractive properties of CA125 is its potential for monitoring and guiding depletive therapy after an episode of ADHF (3–5). In a recent study of 946 consecutive patients discharged for ADHF, the long-term trajectory delineated by repeated measures of CA125 (3,402 observations) independently predicted the risk of long-term mortality (3). Indeed, within the first month after discharge, CA125 decreased toward normal values in the subset of lower risk patients. Conversely, there was a higher risk of events in patients in whom CA125 levels remained high or increased (3,4). In this context, a randomized, multicenter clinical trial was conducted to evaluate the prognostic role of CA125-guided therapy versus standard of care after hospitalization for ADHF (5). The CA125-guided strategy significantly reduced the primary endpoint (a composite of 1-year all-cause mortality or HF readmission), the cumulative readmission rate (HF-related and all-cause readmission), and the number of emergency room visits. Interestingly, the furosemide-equivalent dose titration (up and down) in patients allocated to CA125-guided treatment was approximately 50% more frequent, and up to 21% of patients in this group received ambulatory administration of intravenous furosemide based on their CA125 status (5).
As opposed to natriuretic peptides, CA125 levels are not influenced by age, renal function, or patient weight. In addition, CA125 testing is widely available and low-cost, making it attractive for use in routine clinical practice (2).
In summary, we think that there is substantial evidence that CA125 has clinical usefulness as a surrogate of congestion in HF and suggest that it should be included in the schematic multimodal pathway proposed by Girerd et al. (1).
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2018 American College of Cardiology Foundation
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