Search Results (343)

Background: Pulmonary embolism (PE) is a leading cause of morbidity and mortality worldwide, ranking third among cardiovascular-related deaths after myocardial infarction and stroke. Despite extensive research, data on PE incidence and characteristics within the Israeli population remain limited. This study aimed to investigate the demographic, clinical, and prognostic factors associated with provoked (PPE) and unprovoked PE (UPE) cases in Israel. Methods: We conducted a retrospective observational study analyzing medical records of patients diagnosed with PE at Ziv Medical Center, Safed, Israel, from 2017 to 2022. Patients were classified into PPE or UPE groups based on identifiable risk factors. Demographic data, clinical characteristics, and mortality outcomes were compared using descriptive and inferential statistical methods, including the Mann–Whitney U test, chi-square test, logistic regression, Kaplan–Meier survival analysis, and Cox proportional hazards modeling. Results: A total of 348 patients (mean age: 68.6 ± 17.6 years; 54.3% female) were included, with 189 (54.3%) classified as PPE and 159 (45.7%) as UPE. Female patients were significantly older than males (p < 0.001), and Jewish patients were slightly older than Arab patients (p = 0.060). The average hospital stay was 10.7 ± 16.2 days. Although no group differences emerged in unadjusted analyses, male sex was associated with longer hospitalization and UPE with shorter hospitalization than PPE in the adjusted model. Ethnicity emerged as a significant predictor of PE type, with Jewish patients less likely to have UPE (OR = 0.457, 95% CI 0.256–0.817, p = 0.008). Among PPE cases, 67.2% were of Jewish origin and 32.8% were Arab, compared to 56.0% and 44.0%, respectively, in the UPE group. In-hospital mortality was 16.1% (n = 56). Age was a significant predictor of mortality (HR = 1.03, 95% CI 1.00–1.06, p = 0.020), while ethnicity, gender, and PE type showed no significant associations in multivariable models. Conclusions: Our findings highlight key demographic and clinical factors influencing PE outcomes in Israel. The significant association between ethnicity and PE type warrants further investigation to refine diagnostic and therapeutic strategies for high-risk populations. Full article

Background: Obesity has evolved from a morphometric descriptor to a chronic, relapsing, multisystem disease in which low-grade adipose-tissue inflammation, insulin resistance, endothelial dysfunction, and a prothrombotic, pro-tumorigenic milieu coexist. Venous thromboembolism (VTE) and malignancy share this substrate through a well-established bidirectional link: within twelve months of an unprovoked deep vein thrombosis (DVT), 6–15% of patients are diagnosed with occult cancer, a substantial proportion of which are already locally advanced or metastatic at detection. In this context, obesity acts as a dual amplifier of both thrombotic and oncologic risk, making the post-DVT patient with an incidentally diagnosed cancer a paradigmatic candidate for integrated management. Objective: To propose an evidence-based, unifying cardiometabolic and antithrombotic clinical framework that reconciles (i) risk-stratified screening for occult malignancy after unprovoked DVT, (ii) contemporary pharmacotherapy of obesity, and (iii) cancer-associated thrombosis (CAT) management, in the light of evidence published through 2025. Methods: Narrative synthesis based on a structured literature search (PubMed/MEDLINE, Embase, Scopus; 2000–March 2025) of current guidelines (ISTH, ASH, ESC Cardio-Oncology, EASO) and pivotal randomized evidence on GLP-1 and dual GLP-1/GIP receptor agonists (semaglutide, tirzepatide), SGLT2 inhibitors (empagliflozin, dapagliflozin), and direct oral anticoagulants (DOACs), with critical interpretation of recent meta-analytic data on oncologic signals, cardiovascular outcomes, and bleeding safety. Results: Three evidence-based pillars emerge: (1) limited screening complemented by age- and sex-specific testing in patients ≥ 50 years with unprovoked DVT, enhanced by FDG-PET/CT for high-risk phenotypes in which obesity itself degrades the sensitivity of clinical examination and conventional imaging; (2) GLP-1/GIP receptor agonist-based anti-obesity pharmacotherapy, associated in observational cohorts with a 17% relative reduction in overall cancer incidence (HR 0.83; 95% CI 0.76–0.91) and neutral-to-reassuring oncologic signals, but requiring cautious, case-by-case use in patients with active cancer because of the risk of accelerating sarcopenia and cachexia; and (3) apixaban as the preferred DOAC for cancer-associated thrombosis, with a superior efficacy-to-bleeding ratio in network meta-analyses and a reduced-dose extended strategy now validated by the API-CAT trial. Conclusions: Patients with obesity presenting with unprovoked DVT and an incidentally detected cancer embody a cardiometabolic–antithrombotic continuum. A framework integrating structured occult-cancer screening, judicious obesity pharmacotherapy, and apixaban-preferred anticoagulation—coordinated by a multidisciplinary team and illustrated here by a case-based pathway—offers the most rational, evidence-aligned approach. Prospective, dedicated trials in this specific phenotype are urgently warranted. Full article

Cancer and atherosclerotic cardiovascular disease (ASCVD) represent two of the leading causes of death worldwide. Increasingly, these two are being recognized as biologically related conditions rather than entirely segregated disease states. In addition to traditional risk factors such as aging, smoking, and obesity, chronic inflammation may be a key factor connecting the two illnesses. Endothelial dysfunction, oxidative stress, plaque progression, and thrombosis are all facilitated by inflammatory signaling in ASCVD. Similar pathways are known to contribute to cancer growth and invasion. Emerging epidemiologic data demonstrate increased cancer incidence among patients with cardiovascular disease, while cancer survivors and recipients of cardiotoxic therapies exhibit accelerated vascular disease. This narrative review aims to describe the bidirectional relationship between ASCVD and cancer. Targeting shared pathways using statins, colchicine, canakinumab, IL-6 inhibition, and lifestyle modification may provide dual benefits. Future biomarker-guided trials with integrated cardiovascular and oncologic endpoints are needed to clarify causality and optimize prevention and management. Full article

Background: Type 2 diabetes mellitus (T2DM) is associated with subclinical myocardial dysfunction, which may occur despite preserved left ventricular ejection fraction. Left ventricular global longitudinal strain (LV GLS) is a sensitive marker of early systolic impairment and may detect subtle changes in myocardial function before conventional echocardiographic parameters become abnormal. The effect of sodium-glucose cotransporter-2 inhibitors (SGLT2i) on LV GLS in adults with T2DM remains incompletely defined. Objective: To synthesize the available evidence on the effects of SGLT2i therapy on LV GLS or LV strain in adults with T2DM. Methods: Original full-text human studies evaluating SGLT2i therapy in adults with T2DM and reporting LV GLS or LV strain were included. LV GLS was assessed primarily by speckle-tracking echocardiography, while one study used cardiac magnetic resonance feature-tracking. Reviews, conference abstracts, protocols, animal-only studies, and studies without LV strain assessment were excluded. Risk of bias was assessed using RoB 2 for randomized studies and ROBINS-I for non-randomized studies. Results: Twenty-six studies involving more than 2300 participants were included. The studies evaluated dapagliflozin, empagliflozin, ertugliflozin, canagliflozin, or mixed SGLT2i regimens across heterogeneous clinical populations, including patients with preserved ejection fraction, pre-heart failure, diabetes-related cardiomyopathy, chronic heart failure, coronary artery disease, hypertension, non-alcoholic fatty liver disease, and cardio-oncology risk. Most observational and before–after studies reported favorable changes in LV GLS after SGLT2i therapy, whereas randomized and controlled studies showed more variable findings. Several studies also reported improvements in LV remodeling, diastolic function, left atrial function, myocardial work indices, NT-proBNP, cardiometabolic parameters, or epicardial adipose tissue thickness. However, the certainty of evidence was limited by methodological heterogeneity, differences in comparator groups, variable follow-up duration, non-standardized imaging protocols, and risk of bias, particularly in non-randomized and single-arm studies. Conclusions: SGLT2i therapy may be associated with favorable changes in LV GLS in adults with T2DM, suggesting a potential beneficial effect on subclinical left ventricular systolic function. However, current evidence does not definitively establish a consistent treatment effect across all populations. Larger randomized controlled trials with standardized strain imaging protocols, predefined LV GLS endpoints, and clinically relevant follow-up are needed to determine whether SGLT2i-related improvements in LV GLS reflect true myocardial benefit and translate into improved cardiovascular outcomes. Full article

Background/Objectives: Heart failure (HF) and cancers share common molecular and pathophysiological mechanisms. However, the association between HF and the risk of developing cancer remains unclear. This systematic review and meta-analysis evaluates the association between HF and the risk of cancer incidence by pooling data from studies that compared cancer incidence in HF patients with non-HF controls. Additionally, it quantifies pooled hazard ratios (HRs) for site-specific cancers. Methods: A systematic literature search was conducted across four databases until March 2025 (PROSPERO: CRD420251001541). Seven studies involving over 1.6 million participants were included. Three studies provided direct HF versus non-HF comparisons. Pooled HRs and their corresponding 95% confidence intervals (CIs) were calculated utilising random-effects models. Results: The pooled estimate for overall cancer in HF was not significant (HR 1.32; 95% CI: 0.94–1.85; p = 0.11). However, site-specific analyses revealed significantly elevated risks for lung cancer (HR 1.66; 95% CI: 1.27–2.16), urinary tract cancers (HR 1.66; 95% CI: 1.51–1.82), haematological cancers (HR 1.47; 95% CI: 1.12–1.94), and colorectal cancer (HR 1.38; 95% CI: 1.04–1.83). The associations with breast and prostate cancers were not significant. Notably, substantial heterogeneity was observed across most cancer sites (I² = 96–98%), apart from urinary tract cancers (I² = 0%). Conclusions: Although the pooled estimate for overall cancer was not significant, the significant findings for specific cancer sites suggest the need for enhanced cancer surveillance in patients with HF. Future research should focus on standardising definitions of HF, ensuring consistent adjustment for confounders, and stratifying data by HF phenotype. Full article

Background/Objectives: Anthracycline-induced cardiotoxicity remains a major challenge in cancer treatment, and researchers are showing interest in artificial intelligence (AI) to improve the prediction and detection of cancer therapy-related cardiac dysfunction (CTRCD). Current surveillance strategies rely mainly on left ventricular ejection fraction and, more recently, global longitudinal strain. Methods: The present study was designed to evaluate cardiac performance in a rat model of doxorubicin-induced cardiotoxicity and empagliflozin-mediated cardioprotection using a machine learning-based analytical framework. Eighteen adult male Sprague–Dawley rats were assigned to five experimental groups. We aimed to quantify ventricular wall dynamics and contractility using an advanced image-processing and object-detection model that has not been previously used to distinguish normal from impaired cardiac kinetics. During real-time recording, simultaneous electrocardiogram monitoring was performed, enabling direct correlation between deep learning-based ventricular wall motion metrics and cardiac electrical activity. The cardioprotective effects of empagliflozin were further validated by immunofluorescence staining (cTnI, vimentin, α-SMA, and Cx43) of rat cardiomyocytes and paraffin-embedded cardiac tissue, demonstrating attenuation of cellular injury and structural remodeling. Results: The integrated analysis of cardiac kinetic patterns derived via machine learning distinguishes not only extreme cardiotoxicity, but also tracks a graded pattern consistent with ECG-derived severity and treatment-related functional preservation. These findings indicate that the algorithm captures the gradient of empagliflozin’s cardioprotective effect within this internally validated preclinical setting. Additionally, immunofluorescence results validated the benefits of SGLT2 inhibition on myocardial integrity. Conclusions: The novelty of the present work lies at the intersection of advanced cardiac kinetic analysis using AI, preclinical modeling, and SGLT2-mediated cardioprotection in cardio-oncology. Full article

Cardiovascular disease and cancer remain the leading causes of death worldwide. Although numerous cancer therapies have improved survival rates, they also increase the risk of cardiomyopathy, heart failure, and arrhythmias. These cardiovascular complications can limit treatment options and adversely affect the long-term quality of life of cancer survivors. Ca_V1.3, an L-type calcium channel encoded by CACNA1D, emerges as a central molecular mediator linking cardiovascular disease and cancer. It regulates calcium entry into cardiomyocytes and contributes to sinoatrial pacemaking and atrioventricular conduction. It also contributes to proliferation, migration, and therapy resistance in several cancers. Chemotherapy-induced oxidative stress, inflammatory signaling, hypoxia, and transcriptional changes can modulate the expression, gating, splicing, and trafficking of Ca_V1.3 channels. All these changes destabilize diastolic depolarization and impair conduction, thereby promoting arrhythmias in cancer patients. This review focuses on Ca_V1.3 biology in cardio-oncology, along with the mechanisms of chemotherapy-induced cardiotoxicity. It outlines the role of Ca_V1.3 as a key mediator linking cancer therapies to subsequent nodal dysfunction and increased arrhythmia susceptibility. It also expands on how patient-specific induced pluripotent stem cell-derived cardiomyocytes can model Ca_V1.3 dysregulation as well as support the development of targeted therapies. We propose that Ca_V1.3 represents a mechanistic bridge linking cancer therapy, calcium signaling, and cardiac electrophysiology, and that elucidating its pathophysiology may guide the design of targeted strategies in cardio-oncology. Full article

Cancer therapies have significantly improved survival but are frequently limited by cancer therapy-related cardiovascular toxicity (CTR-CVT). Cardiovascular imaging plays a central role in baseline risk stratification, surveillance during therapy and long-term follow-up. Transthoracic echocardiography (TTE) remains the first-line imaging modality; however, conventional parameters such as left ventricular ejection fraction (LVEF) often fail to detect early myocardial injury. Myocardial deformation imaging, particularly global longitudinal strain (GLS), has emerged as a sensitive marker of subclinical dysfunction across multiple cardiotoxic phenotypes. Cardiac magnetic resonance (CMR) further enhances diagnostic accuracy through tissue characterization techniques, enabling the detection of myocardial edema, inflammation, and fibrosis before overt functional decline. Different anticancer therapies induce distinct pathophysiological mechanisms of injury, each associated with characteristic imaging patterns. Emerging imaging biomarkers and multimodality approaches may improve early detection, the spatial characterization of myocardial injury and individualized surveillance strategies. Pediatric patients represent a uniquely vulnerable population due to their myocardial immaturity, altered pharmacokinetics and prolonged post-treatment life expectancy, resulting in a higher cumulative lifetime cardiovascular risk. In conclusion, a mechanism-based multimodality imaging approach integrating echocardiography, CMR and emerging data-driven technologies is essential to optimize early detection, risk stratification and long-term cardiovascular outcomes in both adult and pediatric cardio-oncology populations. Full article

Background: Proteasome inhibitors (PIs) are integral in multiple myeloma (MM) treatment but carry a substantial risk of cardiovascular adverse events (CVAEs). The Heart Failure Association–International Cardio-Oncology Society (HFA-ICOS) risk score was designed to identify patients at risk of cardiotoxicity, but its performance in MM remains uncertain. Methods: We retrospectively evaluated 98 patients with MM or primary amyloidosis treated with PIs between 2019 and 2024 to externally validate and refine this score. Results: CVAEs occurred in 22 patients (22.5%), predominantly heart failure. The original HFA-ICOS model demonstrated modest predictive accuracy (AUC 0.66) and sensitivity (50%), with frequent risk overclassification. Carfilzomib exposure (HR 4.68, 95% CI 1.47–14.90; p = 0.009) and elevated NT-proBNP before cycle 2 (>300 pg/mL; HR 3.13, 95% CI 1.10–8.93; p = 0.033) independently predicted CVAEs. A dynamic model incorporating these parameters and adjusting the age threshold to ≥65 years was associated with improved discrimination (AUC 0.72, p = 0.032), model fit (ΔAIC = −4), and CVAE-free survival stratification (p = 0.026), achieving 90.9% sensitivity. Conclusions: These findings indicate that the original HFA-ICOS score has limited prognostic value in PI-treated MM patients. Incorporating early NT-proBNP monitoring, carfilzomib exposure, and refined age categorization may improve risk prediction and support more personalized cardiovascular surveillance strategies in cardio-oncology. However, this refined dynamic model should be regarded as exploratory and requires validation in larger independent cohorts before it can be considered for clinical application. Full article

The coexistence of cancer and severe aortic stenosis (AS) is increasing as a result of population aging and substantial improvements in cancer survival. Transcatheter aortic valve implantation (TAVI) has transformed the management of AS; however, patients with active malignancy or a history of cancer remain markedly under-represented in pivotal randomized trials. This under-representation has resulted in persistent uncertainty regarding patient selection, risk stratification, and the expected benefit of TAVI in this growing and clinically heterogeneous population. This review provides a comprehensive and contemporary synthesis of the evidence on TAVI in patients with cancer, integrating cardiovascular (CV), oncologic, and geriatric perspectives. Available data on epidemiological overlap, cancer-specific procedural challenges, and short- and long-term outcomes following TAVI are critically examined, with particular emphasis on distinctions between active cancer and cancer survivorship. Key modifiers of risk and benefit—including prior thoracic radiotherapy, competing thrombotic and bleeding risk, immunosuppression, frailty, sarcopenia, and nutritional status—are discussed in detail. Limitations of conventional surgical risk scores in oncology populations are highlighted, underscoring the need for individualized assessment beyond traditional CV metrics. Across registries and meta-analyses, TAVI is associated with high procedural success and comparable short-term outcomes in patients with and without cancer. Excess mortality observed during mid- and long-term follow-up is driven predominantly by non-CV causes related to malignancy rather than valve-related complications. Importantly, patients with cancer in remission demonstrate outcomes similar to those of non-cancer populations, whereas prognosis in active cancer is strongly influenced by disease stage, biology, and competing risks. Overall, cancer diagnosis alone should not preclude consideration of TAVI. Optimal management requires multidisciplinary, goal-oriented decision-making that integrates oncologic prognosis, functional status, and patients’ priorities. As cancer survivorship continues to expand, prospective studies, integrated risk stratification tools, and closer alignment between cardio-oncology and structural heart programs are essential to guide evidence-based and equitable care. Full article

Background: Cancer-associated thrombosis (CAT) is a leading cause of morbidity and mortality in cancer patients. Although international guidelines provide comprehensive recommendations for venous thromboembolism (VTE) prevention and treatment, the degree to which clinicians adhere to these guidelines in routine practice remains unclear, particularly in countries with limited national data such as Turkey. Methods: A cross-sectional, descriptive survey was conducted among oncology specialists (medical oncologists, radiation oncologists, and surgical oncologists) and cardiologists practicing across Turkey. A structured, case-based questionnaire comprising 21 multiple-choice questions was distributed electronically via SurveyMonkey. The questionnaire assessed perioperative VTE prophylaxis approaches, VTE risk assessment practices in ambulatory patients, primary and long-term secondary thromboprophylaxis preferences, acute VTE treatment strategies, and management of special clinical scenarios. Responses were analyzed using descriptive statistics and compared between oncologist and cardiologist groups. Results: A total of 84 physicians participated (34 oncologists [40.5%], 50 cardiologists [59.5%]). Perioperative and inpatient VTE prophylaxis practices were largely concordant with guideline recommendations, with 67.9% individualizing prophylaxis decisions and 66.7% initiating prophylaxis in hospitalized immobile patients when not contraindicated. However, only 33.7% routinely performed VTE risk assessment in ambulatory patients, and 64.6% did not use any validated risk scoring system. Low-molecular-weight heparin (LMWH) was the preferred agent for acute VTE treatment (72.6%), while direct oral anticoagulants (DOACs) gained preference in long-term secondary thromboprophylaxis (42.2%). No statistically significant differences were observed between oncologists and cardiologists across all survey items (all p > 0.05). Notably, 94.1% of respondents expressed a need to update their knowledge regarding CAT management. Conclusions: While oncologists and cardiologists in Turkey demonstrate general awareness of CAT guidelines, significant gaps persist in VTE risk stratification and primary prophylaxis for ambulatory cancer patients. The near-universal self-reported need for knowledge updates highlights the urgency for structured multidisciplinary education programs, integration of validated risk scoring tools into clinical workflows, and development of nationally adapted clinical practice guidelines. These findings reflect self-reported practices and may not fully represent actual clinical behavior; future studies incorporating medical record reviews or prescription data are needed to validate these observations. Full article

Postoperative atrial fibrillation (POAF) is the most frequent post-cardiac surgical arrhythmia and is associated with haemodynamic instability, longer hospital stays, higher healthcare utilisation, stroke and adverse long-term outcomes. Conventional models of POAF focus on advancing age, pre-existing atrial substrate, increasing operative complexity, inflammatory responses related to cardiopulmonary bypass, disturbances in autonomic balance, and acute metabolic insults during the perioperative period. Although these explanations are important, they may be incomplete. Malignancy and the cancer-associated systemic environment involve biological processes potentially relevant to postoperative atrial vulnerability, such as chronic inflammation, oxidative stress, impaired vascular function, hypercoagulability, altered immune response, frailty, and treatment-related myocardial, pericardial, or conduction-system injury. This review assesses whether malignancy should be regarded as an underrecognised modifier of susceptibility rather than as a coincidental comorbidity. Most available data are extrapolated from cardio-oncology and thoracic oncology studies or general studies related to atrial fibrillation (AF) rather than studies focused on cardiac surgery. While malignancy cannot be dismissed as irrelevant to the generation of POAF, it also does not permit causal inference. Future studies should move beyond binary cancer status and incorporate cancer activity, treatment exposures, biomarker profiles, and atrial substrate measures to determine whether malignancy improves perioperative POAF risk stratification. Full article

Background: Cardiovascular complications are increasingly recognized in patients undergoing hematopoietic stem cell transplantation (HSCT). Early detection of subclinical myocardial dysfunction may improve risk stratification, and global longitudinal strain (GLS) is emerging as a sensitive marker of early cardiac impairment. Methods: We conducted a single-center observational cohort study including 518 adult patients undergoing autologous (n = 64) or allogeneic (n = 454) HSCT between 2004 and 2025. Baseline cardiovascular risk factors, transplant characteristics, and echocardiographic parameters—including GLS in a subset—were recorded. Abnormal GLS was defined as less negative than −20%. The primary outcome was the occurrence of cardiovascular events (composite of cardiovascular death, myocardial infarction, stroke, atrial fibrillation/flutter, pericardial effusion, pulmonary embolism, and left ventricular systolic dysfunction). Multivariable logistic regression was used to identify independent predictors. Results: Median age was 53 years; 58% were male. Cardiovascular events were predominantly atrial fibrillation, pericardial effusion, and reduced left ventricular function, whereas ischemic events were rare. Over 90% of events occurred within 100 days post-transplant. Multivariable analysis identified older age (OR 1.28 per 10-year increment; 95% CI 1.10–1.48; p = 0.002), chronic kidney disease (OR 2.44; 95% CI 1.18–5.02; p = 0.01), pre-transplant atrial fibrillation (OR 2.12; 95% CI 1.04–4.31; p = 0.03), and abnormal baseline GLS (OR 1.89; 95% CI 1.02–3.52; p = 0.04) as independent predictors. Importantly, the prognostic value of GLS remained significant after excluding clinically insignificant pericardial effusions from the composite endpoint. GLS deterioration during follow-up occurred more frequently in patients receiving reduced-intensity conditioning compared with myeloablative conditioning (25% vs. 12.7%; p = 0.006). Conclusions: Subclinical myocardial dysfunction detected by GLS identifies HSCT recipients at increased cardiovascular risk. These findings support the incorporation of strain imaging into routine pre- and post-transplant cardiovascular evaluation to enable earlier detection and guide targeted interventions. Full article

Background/Objectives: Carvedilol is an adrenergic blocker FDA-approved to improve outcomes in heart failure with reduced ejection fraction. Clinical trials examining whether carvedilol may be cardioprotective in the setting of cancer therapy-induced heart failure have generated mixed results that may depend on the cancer regimen, tumor, or comorbidities. Methods: To investigate the therapeutic potential of carvedilol to mitigate doxorubicin cardiotoxicity in cardiomyocytes, myocardial tissue, and in vivo, independent of confounding factors in clinical studies, we utilized disease-free cardiac slices and cardiomyocytes from mice, dogs, and human in vitro, and in wildtype mice injected with doxorubicin in vivo. We further evaluated the impact of carvedilol in dogs with cancer receiving doxorubicin. Results: In primary canine and murine cardiac slices, carvedilol treatment restored autophagy and prevented apoptosis from doxorubicin. Carvedilol restored mitochondrial energetics in human, canine, and murine models. In wildtype mice challenged with doxorubicin, carvedilol prevented declines in cardiac function and alterations in cardiac structure. In pet dogs with cancer and undergoing doxorubicin treatment, carvedilol was beneficial in preserving cardiac function and structure. Conclusions: Carvedilol activates cardioprotective autophagy, arrests doxorubicin-induced cell death, and improves energetics and cardiac structure and function across species. Full article

Immune checkpoint inhibitors (ICIs) have transformed the therapeutic landscape of oncology but are increasingly associated with cardiovascular immune-related adverse events (irAEs), including myocarditis, heart failure, arrhythmias, and vascular complications. Among these, ICI-associated myocarditis represents the most severe manifestation, often characterized by high mortality and challenging early diagnosis. Detecting subclinical myocardial injury before irreversible cardiomyocyte necrosis occurs remains a major unmet need in contemporary cardio-oncology. This narrative expert review critically examines the biological rationale, preclinical evidence, and emerging clinical data supporting the potential role of heart-type fatty acid-binding protein (H-FABP) as an adjunctive biomarker of early immune-mediated myocardial injury during ICI therapy. H-FABP is a small cytosolic lipid chaperone abundantly expressed in cardiomyocytes and rapidly released into the circulation following subtle membrane destabilization and metabolic stress, frequently preceding detectable troponin elevation in other forms of myocardial injury. Experimental studies support a mechanistic association between H-FABP release, inflammasome activation, cytokine amplification, mitochondrial dysfunction, and immune–metabolic cardiomyocyte stress. Preliminary clinical observations further suggest that H-FABP elevations may occur during ICI treatment even in the absence of overt myocarditis or concomitant increases in high-sensitivity cardiac troponins (hs-cTns). Although H-FABP cannot replace hs-cTn, which remains the cornerstone biomarker for the diagnosis of clinically significant ICI-associated myocarditis, its rapid kinetics and sensitivity to early metabolic membrane injury support its potential role as an investigational adjunctive biomarker for early surveillance and risk stratification. This approach may be particularly relevant in patients receiving high-risk combination ICI regimens or in individuals with pre-existing cardiovascular disease. However, current evidence remains limited, and large prospective multicenter studies integrating H-FABP with hs-cTns, natriuretic peptides, cardiac magnetic resonance imaging, and clinical outcomes are required before routine clinical implementation can be considered. Full article