Elderly patients with non-Hodgkin lymphoma, or patients with pre-existing cardiovascular comorbidities, are frequently treated with chemotherapy regimens containing non-PEGylated liposomal anthracycline, in order to reduce cardiotoxicity incidence. For patients candidate to anthracycline, the 2022 European Society of Cardiology (ESC) cardio-oncology guidelines recommend risk stratification through established proformas, but their real-world validation for patients candidate to liposomal anthracycline remains limited.
We retrospectively collected data on patients with newly diagnosed non-Hodgkin lymphoma treated with rituximab, cyclophosphamide, non-PEGylated doxorubicin, vincristine, and prednisone (R-COMP) between 2014 and 2025. Baseline demographics, cardiovascular history, echocardiographic and laboratory parameters, and baseline therapy were recorded. Patients were stratified into risk categories according to the Heart Failure Association International Cardio-Oncology Society (HFA-ICOS) score. Outcomes included overall survival (OS), cardiovascular events occurrence (including asymptomatic left ventricular dysfunction, new-onset or worsening heart failure and acute coronary syndrome) and progression-free survival (PFS).
The cohort consisted of 265 patients [median age 73 years (69 – 77); 51% males]; 41% were classified as moderate risk, 55% as high risk, and 4% as very high risk. During a median follow-up of 29 months, 38 patients (14%) died. OS and cardiovascular events occurrence significantly differed across HFA-ICOS risk categories (p=0.005 and p<0.0001, respectively). Very high-risk patients exhibited substantially higher hazards of mortality (HR 5.8) and cardiovascular events (HR 40.4). Cardioprotective therapy at baseline did not influence cardiovascular outcomes.
The HFA-ICOS score effectively stratifies mortality and cardiotoxicity risk among R-COMP–treated patients. These findings support its application in routine treatment of lymphomas requiring anthracycline-based therapy.
M. Camilli, I. Torre, L. Leo et al.· European Heart Journal, Supp...· 0 citations
Lipoprotein(a) (Lp(a)) is increasingly recognized as a genetically determined and clinically relevant contributor to residual cardiovascular risk. Through pro-atherogenic, pro-inflammatory, pro-thrombotic, and pro-calcific mechanisms, Lp(a) appears to play a significant role in both coronary artery disease and aortic valve disease. In patients undergoing percutaneous coronary intervention, elevated Lp(a) has been associated with worse long-term outcomes, including recurrent ischemic events, repeat revascularization, and in-stent restenosis, even in the setting of controlled low-density lipoprotein cholesterol. In parallel, experimental, genetic, and clinical data support a role for Lp(a) in the initiation and progression of calcific aortic stenosis, while its prognostic significance after transcatheter aortic valve interventions remains less clearly defined. Current guidelines now recognize Lp(a) as a relevant risk-enhancing factor, and emerging targeted therapies are achieving substantial reductions in circulating levels. Overall, Lp(a) should be regarded as both a meaningful biomarker and a promising therapeutic target, although ongoing outcome trials are needed to determine whether selective Lp(a) lowering translates into clinical benefit across interventional cardiovascular settings. The aim of this narrative review is to provide a single, comprehensive account of lipoprotein(a) [Lp(a)] in interventional cardiology, following this lipoprotein from its biology and pathophysiology through to its clinical impact and to the therapies that are now reaching the clinic, with a specific focus on the two most frequent catheter-based procedures in which it may carry prognostic weight: percutaneous coronary intervention (PCI) and transcatheter aortic valve implantation (TAVI). PCI and TAVI are deliberately addressed within the same review since they share a common upstream biology: Lp(a) contributes both to the atherosclerotic process that underlies coronary disease and to the calcific process that underlies aortic valve disease, and the corresponding patient populations overlap considerably in everyday interventional practice. Covering them together offers the interventional cardiologist a single, practical reference on how a patient with elevated Lp(a) may be approached in both scenarios.
F. M. Animati, Simone Proietti, Francesco Auletta et al.· Journal of Clinical Medicine· 0 citations
BACKGROUND
Cancer and heart failure (HF) frequently coexist due to population ageing and improved survival for both conditions. HF is a well-recognised complication of oncologic therapies and a potential association between HF and subsequent cancer incidence has been recently noticed. We therefore conducted a meta-analysis to quantify cancer incidence and mortality in patients with and without HF.
METHODS
Databases were searched from inception to 15 February 2026. Data from observational studies and randomised trials on individuals with and without HF and reporting cancer incidence and/or mortality during follow-up were included. The main outcome of interest was the incidence of any cancer; secondary outcomes included site-specific cancer incidence (lung, colorectal, breast, and prostate) and all-cause, cardiovascular, and cancer-related mortality.
RESULTS
Twelve studies comprising 8,979,195 individuals were included. HF was associated with a higher incidence of cancer (hazard ratio [HR] 1.33, 95% confidence interval [CI] 1.14-1.54), with substantial heterogeneity (I2 = 99.7%). Cancer site-specific analyses showed increased incidences of lung (HR 1.70, 95% CI 1.26-2.29), colorectal (HR 1.28, 95% CI 1.11-1.48), and breast (HR 1.19, 95% CI 1.04-1.37), but not prostate, cancer. Effect estimates varied according to analytical strategy: matched HF and non-HF cohorts reported higher risk estimates than those using covariate adjustment without matching. Mortality data were sparse and heterogeneous.
CONCLUSIONS
HF is associated with a higher incidence of cancer, although with marked heterogeneity among studies and cancer types. Mortality and cause of death were rarely reported. The observed HF-cancer association is influenced by statistical methodology, shared risk factors, differences in surveillance intensity and cancer type, that confound analyses investigating possible causal biological links. More granular and harmonised studies are required.
L. Sanasi, A. Iaconelli, Danila Azzolina et al.· European Journal of Heart Fa...· 0 citations
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