Serum Biomarkers to Dynamically Predict the Risk of Cardiovascular Events in Patients under Oncologic Therapy. A Multicenter Observational Study.

STEPP analysis anticancer therapies cardio-oncology cardiovascular toxicity oxidative stress biomarkers

Journal

Reviews in cardiovascular medicine
ISSN: 2153-8174
Titre abrégé: Rev Cardiovasc Med
Pays: Singapore
ID NLM: 100960007

Informations de publication

Date de publication:
Jul 2024
Historique:
received: 08 12 2023
revised: 10 01 2024
accepted: 23 01 2024
medline: 14 8 2024
pubmed: 14 8 2024
entrez: 14 8 2024
Statut: epublish

Résumé

Serum biomarkers have been investigated as predictive risk factors for cancer-related cardiovascular (CV) risk, but their analysis is limited to their baseline level rather than their overtime change. Besides historically validated causal factors, inflammatory and oxidative stress (OS) related markers seem to be correlated to CV events but this association needs to be further explored. We conducted an observational study to determine the predictive role of the longitudinal changes of commonly used and OS-related biomarkers during the cancer treatment period. Patients undergoing anticancer therapies, either aged 75+ years old or younger with an increased CV risk according to European Society of Cardiology guidelines, were enrolled. We assessed the predictive value of biomarkers for the onset of CV events at baseline and during therapy using Cox model, Subpopulation Treatment-Effect Pattern Plot (STEPP) method and repeated measures analysis of longitudinal data. From April 2018 to August 2021, 182 subjects were enrolled, of whom 168 were evaluable. Twenty-eight CV events were recorded after a median follow up of 9.2 months (Interquartile range, IQR: 5.1-14.7). Fibrinogen and troponin levels were independent risk factors for CV events. Specifically, patients with higher than the median levels of fibrinogen and troponin at baseline had higher risk compared with patients with values below the medians, hazard ratio (HR) = 3.95, 95% CI, 1.25-12.45 and HR = 2.48, 0.67-9.25, respectively. STEPP analysis applied to Cox model showed that cumulative event-free survival at 18 and 24 months worsened almost linearly as median values of fibrinogen increased. Repeated measure analysis showed an increase over time of D-Dimer ( Higher levels of fibrinogen and troponin at baseline and an increase over time of D-Dimer and blood pressure are associated to a higher risk of CV events in patients undergoing anticancer therapies. The role of OS in fibrinogen increase and the longitudinal monitoring of D-dimer and blood pressure levels should be further assessed.

Sections du résumé

Background UNASSIGNED
Serum biomarkers have been investigated as predictive risk factors for cancer-related cardiovascular (CV) risk, but their analysis is limited to their baseline level rather than their overtime change. Besides historically validated causal factors, inflammatory and oxidative stress (OS) related markers seem to be correlated to CV events but this association needs to be further explored. We conducted an observational study to determine the predictive role of the longitudinal changes of commonly used and OS-related biomarkers during the cancer treatment period.
Methods UNASSIGNED
Patients undergoing anticancer therapies, either aged 75+ years old or younger with an increased CV risk according to European Society of Cardiology guidelines, were enrolled. We assessed the predictive value of biomarkers for the onset of CV events at baseline and during therapy using Cox model, Subpopulation Treatment-Effect Pattern Plot (STEPP) method and repeated measures analysis of longitudinal data.
Results UNASSIGNED
From April 2018 to August 2021, 182 subjects were enrolled, of whom 168 were evaluable. Twenty-eight CV events were recorded after a median follow up of 9.2 months (Interquartile range, IQR: 5.1-14.7). Fibrinogen and troponin levels were independent risk factors for CV events. Specifically, patients with higher than the median levels of fibrinogen and troponin at baseline had higher risk compared with patients with values below the medians, hazard ratio (HR) = 3.95, 95% CI, 1.25-12.45 and HR = 2.48, 0.67-9.25, respectively. STEPP analysis applied to Cox model showed that cumulative event-free survival at 18 and 24 months worsened almost linearly as median values of fibrinogen increased. Repeated measure analysis showed an increase over time of D-Dimer (
Conclusions UNASSIGNED
Higher levels of fibrinogen and troponin at baseline and an increase over time of D-Dimer and blood pressure are associated to a higher risk of CV events in patients undergoing anticancer therapies. The role of OS in fibrinogen increase and the longitudinal monitoring of D-dimer and blood pressure levels should be further assessed.

Identifiants

pubmed: 39139415
doi: 10.31083/j.rcm2507256
pii: S1530-6550(24)01320-6
pmc: PMC11317344
doi:

Types de publication

Journal Article

Langues

eng

Pagination

256

Informations de copyright

Copyright: © 2024 The Author(s). Published by IMR Press.

Déclaration de conflit d'intérêts

The authors declare no conflict of interest.

Auteurs

Nicoletta Provinciali (N)

Division of Medical Oncology, Ente Ospedaliero Ospedali Galliera, 16128 Genoa, Italy.
Department of Experimental Medicine, University of Genoa, 16126 Genoa, Italy.

Marco Piccininno (M)

Cardiology Unit, Ente Ospedaliero Ospedali Galliera, 16128 Genoa, Italy.

Giacomo Siri (G)

Clinical Trial Unit, Office of the Scientific Director, Ente Ospedaliero Ospedali Galliera, 16128 Genoa, Italy.

Alessandra Gennari (A)

Division of Oncology, Maggiore della Carità University Hospital, 28100 Novara, Italy.
Department of Traslational Medicine, University of Piemonte Orientale, 28100 Novara, Italy.

Giancarlo Antonucci (G)

Internal Medicine Unit, Ente Ospedaliero Ospedali Galliera, 16128 Genoa, Italy.

Damiano Ricci (D)

Cardiology Unit, Ente Ospedaliero Ospedali Galliera, 16128 Genoa, Italy.

Emmanuela Devoto (E)

Cardiology Unit, Ente Ospedaliero Ospedali Galliera, 16128 Genoa, Italy.

Roberta Miceli (R)

Cardiology Unit, Ente Ospedaliero Ospedali Galliera, 16128 Genoa, Italy.

Pietro Cortesi (P)

Oncology Unit, Istituto Romagnolo Per Lo Studio Dei Tumori "Dino Amadori" (IRST) IRCCS, 47014 Meldola, Italy.

Chiara Pazzi (C)

Oncology Unit, Istituto Romagnolo Per Lo Studio Dei Tumori "Dino Amadori" (IRST) IRCCS, 47014 Meldola, Italy.

Oriana Nanni (O)

Biostatistics and Clinical Trial Unit, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST), IRCCS, 47014 Meldola, Italy.

Francesca Mannozzi (F)

Biostatistics and Clinical Trial Unit, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST), IRCCS, 47014 Meldola, Italy.

Ilaria Pastina (I)

Oncology Unit, Ospedale Misericordia, 52100 Grosseto, Italy.

Luciana Messuti (L)

Oncology Unit, Ospedale Misericordia, 52100 Grosseto, Italy.

Carmelo Bengala (C)

Oncology Unit, Ospedale Misericordia, 52100 Grosseto, Italy.

Giovanni Luca Frassineti (GL)

Oncology Unit, Istituto Romagnolo Per Lo Studio Dei Tumori "Dino Amadori" (IRST) IRCCS, 47014 Meldola, Italy.

Carlo Cattrini (C)

Division of Oncology, Maggiore della Carità University Hospital, 28100 Novara, Italy.

Marianna Fava (M)

Division of Medical Oncology, Ente Ospedaliero Ospedali Galliera, 16128 Genoa, Italy.

Tania Buttiron Webber (T)

Division of Medical Oncology, Ente Ospedaliero Ospedali Galliera, 16128 Genoa, Italy.

Irene Maria Briata (IM)

Division of Medical Oncology, Ente Ospedaliero Ospedali Galliera, 16128 Genoa, Italy.

Davide Corradengo (D)

Division of Medical Oncology, Ente Ospedaliero Ospedali Galliera, 16128 Genoa, Italy.

Andrea DeCensi (A)

Division of Medical Oncology, Ente Ospedaliero Ospedali Galliera, 16128 Genoa, Italy.
Wolfson Institute of Population Health, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, E1 2AD London, UK.

Matteo Puntoni (M)

Clinical and Epidemiological Research Unit, University Hospital of Parma, 43126 Parma, Italy.

Classifications MeSH