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.

Antibodies directed against donor-specific human leukocyte antigens (HLAs) can be detected de novo after heart transplantation and play a key role in long-term survival. De novo donor-specific antibodies (dnDSAs) have been associated with cardiac allograft vasculopathy, antibody-mediated rejection, and mortality. Advances in detection methods and international guideline recommendations have encouraged the adoption of screening protocols among heart transplant units. However, there is still a lack of consensus about the correct course of action after dnDSA detection. Treatment is usually started when antibody-mediated rejection is present; however, some dnDSAs appear years before graft failure is detected, and at this point, damage may be irreversible. In particular, class II, anti-HLA-DQ, complement binding, and persistent dnDSAs have been associated with worse outcomes. Growing evidence points towards a more aggressive management of dnDSA. For that purpose, better diagnostic tools are needed in order to identify subclinical graft injury. Cardiac magnetic resonance, strain techniques, or coronary physiology parameters could provide valuable information to identify patients at risk. Treatment of dnDSA usually involves plasmapheresis, intravenous immunoglobulin, immunoadsorption, and ritxumab, but the benefit of these therapies is still controversial. Future efforts should focus on establishing effective treatment protocols in order to improve long-term survival of heart transplant recipients.

Background Current evidence supports the role of circulating carbohydrate antigen 125 (CA125) in risk assessment, disease monitoring and therapeutic guidance in heart failure (HF). However, there is limited data on its diagnostic applicability. This study aimed to assess the diagnostic performance of CA125 in identifying HF with preserved ejection fraction (HFpEF) in an outpatient population. Methods This was a prospective, multicentre study involving 246 consecutive patients with clinically suspected HF. Patients with a left ventricular ejection fraction 23 U/mL, 12.4% of the sample) exhibited high specificity (0.97), a positive predictive value of 80.8% and correctly classified 77.1% of cases as HFpEF. Conversely, CA125 levels<9 U/mL were associated with a high negative predictive value (85.7%). Conclusion In an ambulatory setting, CA125 exhibits acceptable diagnostic performance for identifying HFpEF and may complement NT-proBNP in clinical practice.

An 84-year-old male presented with refractory angina despite optimal medical treatment and multiple coronary revascularization procedures. Coronary sinus (CS) reducer implantation was programmed. Clinical Images from Journal of Invasive Cardiology. device migration pulmonary artery

Background/Objectives: Current guidelines recommend 24–48 h Holter for risk stratification and atrial fibrillation (AF) screening in hypertrophic cardiomyopathy (HCM). However, the limited duration of this approach may not provide optimal sensitivity. In addition, extended ECG monitoring has been demonstrated to be more effective in detecting arrhythmias in other clinical entities. We aimed to assess the utility of extended ECG monitoring for 30 days in a non-high-risk cohort of HCM patients. Methods: We conducted a prospective multicentre study with 113 non-high-risk HCM patients who underwent 30-day ECG monitoring with a dedicated device. We compared the detection of relevant arrhythmias (AF, atrial flutter, and non-sustained ventricular tachycardia) during 30-day monitoring with the findings observed during the first 24 h. Results: Extended ECG monitoring detected relevant arrhythmias in 63.7% of patients, compared with 12.4% during the first 24 h (p < 0.001). This difference was mainly driven by non-sustained ventricular tachycardia (NSVT) (61.1% vs. 8.9%, p < 0.001). Atrial fibrillation episodes were detected in 10.6% of patients after completing prolonged monitoring vs. 6.2% during the first 24 h (p = 0.066). Extended monitoring resulted in a reclassification of 21.2% of patients to a higher sudden cardiac death (SCD) risk category using the HCM-SCD calculator. Conclusions: Extended ECG monitoring significantly enhances the detection of arrhythmias in HCM. Using this technique, NSVT were detected in most patients of a non-high-risk HCM cohort. Further investigation is warranted to determine the role of extended monitoring in SCD risk stratification and AF screening.