Baseline cardiovascular toxicity risk stratification is critical in cardio-oncology. The Heart Failure Association (HFA) and International Cardio-Oncology Society (ICOS) score aims to assess this risk but lacks real-life validation. This study validates the HFA-ICOS score for anthracycline-induced cardiovascular toxicity. Anthracycline-treated patients in the CARDIOTOX registry (NCT02039622) were stratified by the HFA-ICOS score. The primary endpoint was symptomatic or moderate to severe asymptomatic cancer therapy-related cardiac dysfunction (CTRCD), with all-cause mortality and cardiovascular mortality as secondary endpoints. The analysis included 1066 patients (mean age 54 ± 14 years; 81.9% women; 24.5% ≥65 years). According to the HFA-ICOS criteria, 571 patients (53.6%) were classified as low risk, 333 (31.2%) as moderate risk, 152 (14.3%) as high risk, and 10 (0.9%) as very high risk. Median follow-up was 54.8 months (interquartile range 24.6–81.8). A total of 197 patients (18.4%) died, and 718 (67.3%) developed CTRCD (symptomatic: n = 45; moderate to severe asymptomatic: n = 24; and mild asymptomatic: n = 649). Incidence rates of symptomatic or moderate to severe symptomatic CTRCD and all-cause mortality significantly increased with HFA-ICOS score [hazard ratio 28.74, 95% confidence interval (CI) 9.33–88.5; P < .001, and hazard ratio 7.43, 95% CI 3.21–17.2; P < .001) for very high-risk patients. The predictive model demonstrated good calibration (Brier score 0.04, 95% CI 0.03–0.05) and discrimination (area under the curve 0.78, 95% CI 0.70–0.82; Uno’s C-statistic 0.78, 95% CI 0.71–0.84) for predicting symptomatic or severe/moderate asymptomatic CTRCD at 12 months. The HFA-ICOS score effectively categorizes patients by cardiovascular toxicity risk and demonstrates strong predictive ability for high-risk anthracycline-related cardiovascular toxicity and all-cause mortality. This study aimed to validate the Heart Failure Association and International Cardio-Oncology Society score for anthracycline-induced cardiovascular toxicity in a real-world cohort, the CARDIOTOX registry (NCT02039622). The Heart Failure Association and International Cardio-Oncology Society score effectively categorized patients based on their cardiovascular toxicity risk, demonstrating strong predictive capabilities for high-risk anthracycline-related cardiovascular toxicity and all-cause mortality.

Cardiovascular disease remains the world’s leading cause of death, and even when patients reach guideline low-density lipoprotein cholesterol targets, a substantial “residual risk” persists, underscoring the need for more nuanced assessment and intervention. At the same time, rapid advances in high-resolution lipidomics, connected point-of-care diagnostics, and RNA- or gene-based lipid-modifying therapies are transforming what clinicians can measure, monitor, and treat. Integrating multimodal data through machine learning algorithms capable of handling high-dimensional datasets has the potential to improve cardiovascular risk prediction and re-stratification compared to traditional models. This narrative review therefore sets out to (i) trace how these emerging technologies expand our understanding of dyslipidemia beyond the traditional lipid panel, (ii) examine their potential to enable earlier, more personalized and durable cardiovascular risk reduction, and (iii) highlight the scientific, regulatory and ethical hurdles that must be cleared before such innovations can deliver widespread, equitable benefit.

The role of cardiac myosin inhibitors in patients with obstructive hypertrophic cardiomyopathy (oHCM) and active malignancy remains unexplored. A 68-year-old woman with colon cancer presented with worsening dyspnea. Echocardiography showed severe asymmetric septal hypertrophy, systolic anterior motion of the mitral valve, and a peak left ventricular outflow tract gradient of 115 mm Hg. Beta-blocker therapy failed to control symptoms. After multidisciplinary cardio-oncology evaluation, mavacamten therapy was initiated. Within 4 weeks, the patient's left ventricular outflow tract gradient decreased to 10 mm Hg, her NYHA functional class improved to I, and her NT-proBNP levels dropped markedly. Chemotherapy continued without interruption. Nine months later, her oncologic disease progressed, and palliative care was adopted. This case highlights mavacamten as a safe and effective therapy for oHCM in a patient actively receiving chemotherapy. It underscores the potential value of cardiac myosin inhibition in complex comorbid scenarios. Mavacamten can substantially improve quality of life in oHCM, even in patients with active malignancy.

Maintaining continuous access to the right heart chambers during lead extraction is essential, especially when venous stenosis is present. The Cowboy Bridge technique is a novel and reproducible approach that implies retrograde snaring from a femoral access. We report our results applying this technique in two patients with venous stenosis who required a device upgrade with lead extraction. This procedure facilitates the implantation of new leads by maintaining thorough-and-through access and lowering the risk of perforation compared to anterograde or retrograde attempts to traverse the stenotic site with additional wires or catheters.

To determine the effects of the comprehensive disease-modifying pharmacological approach among patients with heart failure with reduced ejection fraction, a cross-trial, aggregate-data analysis was performed to estimate the expected combined effect of quintuple therapy by multiplying trial-level HRs, assuming independent and multiplicative treatment effects from Phase III randomised clinical trials: EMPHASIS-HF, PARADIGM-HF, pooled DAPA-HF and EMPEROR-Reduced, and pooled VICTORIA and VICTOR. The imputed aggregate treatment effects on the primary endpoint of cardiovascular death or first heart failure hospitalisation were favourable to the quintuple compared with conventional therapy (HR 0.34; 95% CI [0.27–0.42]). This also occurred for cardiovascular death alone (HR 0.47; 95% CI [0.35–0.63]), first heart failure hospitalisation (HR 0.31; 95% CI [0.23–0.40]) and all-cause mortality (HR 0.51; 95% CI [0.39–0.67]). The numbers needed to treat per year for the primary outcome, cardiovascular death and first heart failure hospitalisation were 10, 23 and 15, respectively. Our findings support the potential benefit of comprehensive therapy, with the incremental role of vericiguat likely greatest in higher-risk patients or those with recent worsening heart failure.