SPC365

Managing Cardiovascular Risk in Cancer Patients: The Impact of Cancer Therapies on New-Onset Heart Failure

Session: SESSÃO DE POSTERS 11 - CARDIONCOLOGIA DE PONTA II
Speaker: Inês Caldeira Araújo

Congress: CPC 2025
Topic: K. Cardiovascular Disease In Special Populations
Theme: 30. Cardiovascular Disease in Special Populations
Subtheme: 30.6 Cardio-Oncology
Session Type: Cartazes
FP Number: ---
Authors: Inês Caldeira Araújo; Andreia Magalhães; Catarina Gregório; Miguel Azaredo Raposo; Ana Abrantes; Marta Vilela; João Cravo; Diogo Ferreira; Daniel Cazeiro; Miguel Nobre Menezes; F. J. Pinto; Manuela Fiúza

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Introduction:</strong></span></span></span></p>

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Advances in oncologic treatments have enabled cancer patients to live longer, however, this has been overshadowed by unintended and often severe cardiac complications that impact overall patient outcomes. Cardiotoxicity, particularly the link between certain cancer therapies and the development of new on-set heart failure (HF), has become an increasingly significant concern.</span></span></span></p>

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<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Purpose:&nbsp;</strong></span></span></span></p>

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">To evaluate the impact of cancer therapies, cardiovascular comorbidities, laboratory and echocardiographic parameters on new-onset HF.&nbsp;</span></span></span></p>

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<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Methods:&nbsp;</strong></span></span></span></p>

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">A retrospective, observational, single-center study was conducted including patients enrolled in a cardio-oncology consultation between 2022 and 2023. New-onset HF was defined by a reduction of left ventricular ejection fraction (LVEF) or signs and symptoms of HF plus an elevation of NT-proBNP. Parametric and non-parametric tests were performed.</span></span></span><span style="font-size:12pt"><span style="font-family:'Times New Roman',serif"><span style="color:#000000">&nbsp;</span></span></span></p>

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<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Results:</strong></span></span></span></p>

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">A total of 185 patients (48% male, mean age 64 &plusmn; 15 years) were included. Of these, 35 patients (19%) developed HF. Cardiovascular comorbidities were similar across both groups. Patients on SGLT2 inhibitors tended to experience a lower incidence of new-onset HF (p=0.089). Regarding cancer therapies, those receiving targeted therapy had a significantly higher incidence of new-onset HF (HR 2.5, p=0.015). Additionally, 20% of patients who developed HF had been treated with anthracyclines (p=0.073) and the combination of target therapy and radiotherapy also potentiated this cardiotoxic effect (p&lt;0.001). Higher baseline troponin levels were associated with an increased likelihood of developing the primary endpoint (p=0.05). Echocardiographic parameters revealed that patients with lower LV strain prior to starting oncological treatment were more likely to develop LV dysfunction or HF (p=0.057). Among patients with new-onset HF, the median LVEF was 43 (36 to 50) (p&lt;0.001), and the median LV strain was -12 (-14.5 to -9.5) (p&lt;0.001). During follow-up, 29% of patients who developed new-onset HF were hospitalized for cardiovascular causes (p&lt;0.001). Elevated NT-proBNP and troponin levels were strongly associated with an increased risk of hospital admissions (p=0.012 and p=0.034, respectively), while lower LVEF and higher LV strain values also correlated with higher rates of cardiovascular admissions. There were no significant differences in mortality between the two groups (p=0.981). Of the patients who developed new-onset HF, 45% suspended treatment, with 6.5% undergoing a temporary interruption and 38.7% permanently discontinuing therapy. Notably, 43% of patients demonstrated full recovery of LVEF.</span></span></span></p>

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<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Conclusion:</strong></span></span></span></p>

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">The results highlight the significant impact of cancer therapies, particularly target therapy, on the development of LV dysfunction and HF. These findings underscore the need for vigilant CV monitoring in cancer patients to manage risks and improve patient outcomes.</span></span></span></p>

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