Cardio-oncology最新文献

Purpose: Chimeric antigen receptor (CAR) T-cell therapy is a new revolutionary method for treating refractory or relapsed hematologic malignancies, CAR T-cell therapy has been associated with cytokine release syndrome (CRS) and cardiotoxicity. We directed a systematic review and meta-analysis to determine the incidence and predictors of cardiovascular events (CVE) with CAR T-cell therapy.

Methods: We investigated PubMed, Embase, Cochrane Library, and ClinicalTrials.gov for studies reporting cardiovascular outcomes in CAR-T cell recipients. The study protocol was listed in the International Prospective Register of Systematic Reviews (PROSPERO ID: CRD42023478602). Twenty-three studies were included in this study.

Results: The pooled incidence of CVE was 54% for arrhythmias, 30% for heart failure, 20% for cardiomyopathy, 10% for acute coronary syndrome, and 7% for cardiac arrest. Patients with CVE had a higher incidence of cytokine release syndrome grade ≥ 2 (RR 2.36, 95% CI 1.86-2.99). The incidence of cardiac mortality in our meta-analysis was 2% (95% CI: 1%-3%). Left ventricular ejection fraction decline was greater in the CVE group (-9.4% versus -1.5%, p < 0.001). Cardiac biomarkers like BNP, CRP, creatinine, and ferritin were also elevated.

Conclusions: CAR T-cell therapy commonly leads to cardiotoxicity, mediated by cytokine release syndrome. Vigilant monitoring and tailored treatments are crucial to mitigate these effects. Importantly, there's no significant difference in cardiac mortality between groups, suggesting insights for optimizing preventive interventions and reducing risks after CAR T-cell therapy.

The landscape of cancer survivorship is increasingly populated by individuals facing a spectrum of cardiometabolic risks, attributed to both their oncological history and treatment regimens. This manuscript synthesizes findings from various studies, highlighting the prevalence of traditional risk factors-hypertension, dyslipidemia, diabetes-as well as emergent concerns like obesity and metabolic syndrome among survivors. The impact of demographic variables, specific cancer types, and treatment modalities on cardiometabolic health is explored. Through a lens of multidisciplinary management and future research directives, we advocate for an integrative approach to cardiometabolic health in cancer survivors, aiming to ensure their victory over cancer extends into long-term well-being. Furthermore, we discuss the outcome implications of these cardiometabolic risk factors on cardiovascular disease development, future cardiovascular events, and overall survival, supported by studies showing improved outcomes through exercise and risk factor control.

Background: Fludarabine is a chemotherapeutic agent with lymphodepleting effects that is increasingly used as part of a conditioning regimen prior to allogeneic stem cell transplantation. Fludarabine is generally considered a relatively safe medication with only rare cases of cardiotoxic side effects.

Case presentation: Here, we present a case of a 30-year-old woman who was undergoing conditioning for a haploidentical cell transplantation for treatment of Fanconi anemia with a 5-day course of daily fludarabine infusion. After her second fludarabine infusion, she was noted to have ectopic atrial bradycardia that resolved with supportive therapy and completion of fludarabine infusion.

Conclusion: We report the first case of ectopic atrial bradycardia associated with fludarabine. Although rare and transient, clinicians should recognize this rare cardiotoxic side effect of fludarabine.

Background: Cardiac sarcoidosis though in itself, a rare entity, very rarely presents primarily with conduction abnormalities as the primary manifestation in the spectrum of presentations accounted by this chronic granulomatous systemic disease. Sarcoidosis presenting as intra-atrial masses is virtually unheard of.

Case: A middle aged female presented with progressive conduction system disease was found to have right atrial masses of unclear etiologic on relevant imaging. Over the course of 3 months she underwent a dual-chamber ICD implant for her eventual complete heart block and a surgical resection following an inconclusive biopsy of the right atrial free wall mass. She was then diagnosed with cardiac sarcoidosis and started on immunosupressants almost instantaneously as a part of her treatment.

Conclusion: This is an entirely new and unreported presentation of cardiac sarcoidosis as an intra-atrial mass. Through this case we bring light to cardiac sarcoidosis as a potential differential for intra-cardiac masses and how with available data do we go about treating it.

Atrial fibrillation (AF) is more common in patients with malignancies than in general population. The pathophysiological processes include the pro-inflammatory condition and the exaggerated inflammatory reaction to chemotherapy, radiotherapy, and surgery interventions. Thus, it is pivotal to decrease morbidity and mortality in this group by providing appropriate care and prevention. In this subset, the risk of thromboembolic and bleeding events is high and the common risk score such as CHA2DS2-VASc and HAS-BLED employed in non-oncologic patients have limited evidence in cancer patients. A paucity of evidence in the setting in individuals having both malignancies and atrial fibrillation entangle the clinician when it comes to therapeutic management. Tailored management is recommended of anticoagulation treatment could be difficult, and there is. In this review, we try to explain the mechanism of AF in cancer patients as well as its management in this setting.

Background: Within cardio-oncology, emerging epidemiologic studies have demonstrated a bi-directional relationship between heart failure (HF) and cancer. In the current study, we aimed to further explore this relationship and investigate the underlying pathophysiological pathways that connect these two disease entities.

Methods: We conducted a post-hoc analysis in which we identified 24 Gene Ontology (GO) processes associated with the hallmarks of cancer based on 92 biomarkers in 1960 patients with HF. We performed Spearman's correlations and Cox-regression analyses to evaluate associations with HF biomarkers, severity and all-cause mortality.

Results: Out of a total of 24 GO processes, 9 biological processes were significantly associated with adverse clinical outcome. Positive regulation of mononuclear cell proliferation demonstrated the highest hazard for reaching the clinical endpoint, even after adjusting for confounders: all-cause mortality HR 2.00 (95% CI 1.17-3.42), p = 0.012. In contrast, negative regulation of apoptotic process was consistently associated with a lower hazard of reaching the clinical outcome, even after adjusting for confounders: all-cause mortality HR 0.74 (95% CI 0.59-0.95), p = 0.016. All processes significantly correlated with HF biomarkers, renal function and HF severity.

Conclusions: In patients with HF, GO processes associated with hallmarks of cancer are associated with HF biomarkers, severity and all-cause mortality.

Background: Participation in cardio-oncological rehabilitation is low, and the effects incline to decrease after the initial rehabilitation term. Home-based exercise has the potential to enhance involvement in cardio-oncology rehabilitation and was demonstrated to be feasible, safe, and helpful in increasing short-term cardiorespiratory fitness. The lasting effects on cardiorespiratory fitness and physical activity are uncertain. Hence, a novel approach via telehealth management based on objectively measured exercise at home was proposed.

Objectives: To improve self-monitoring, such as self-confidence, behavioral change, and goal setting for individual exercise, and afterward, increase long-term effects concerning cardiorespiratory fitness.

Design: This randomized controlled trial compares a 12-week guided home exercise telehealth intervention with a center-based exercise intervention of the same duration and intensity of exercise in lymphoma cancer survivors entering cardio-oncology rehabilitation after treatment. Participants will be instructed to exercise gradually at 60-85% of their maximum heart rate for 30-50 min 3 times a week. Participants will receive individual remote guidance (feedback about frequency, duration, and exercise intensity) by preferred contact (phone call, text message) once a week based on shared exercise data through the web platform. The primary outcome is a change in cardiorespiratory fitness expressed as maximal oxygen uptake assessed through cardiopulmonary exercise test at baseline, 12 weeks, and 1 year. Secondary objectives are quality of life, muscle strength, body composition, incidence of adverse events, and exercise adherence. This study will determine whether a telehealth model is effective and safe compared to a center-based model in cancer survivors and whether exercise prescriptions are followed by participants. Additionally, an overview of the long-term effectiveness of telehealth cardio-oncology rehabilitation will be provided. This approach aligns with the trend of moving non-complex healthcare services into the patients' home environment.

Trial registration: ClinicalTrials.Gov Identifier: NCT05779605.

Background: Cardiac angiosarcoma is a very rare and aggressive primary cardiac tumor associated with poor prognosis. Diagnosis is often delayed due to non-specific symptoms, with most cases involving metastases at the time of diagnosis. We describe a unique case of apparent tumor regression of cardiac angiosarcoma post percutaneous biopsy.

Case presentation: A young male was admitted with suspected pericarditis. Echocardiogram revealed a pericardial mass. Cardiovascular magnetic resonance (CMR) suggested primary cardiac malignancy. Percutaneous biopsy was inconclusive, with subsequent CMR demonstrating apparent tumor regression. Interval imaging revealed further tumor growth, and surgical biopsy revealed primary cardiac angiosarcoma (PCAS). Causes of tumor regression following percutaneous biopsy are discussed.

Conclusions: Cases of suspected primary cardiac malignancy require careful follow up with serial multimodality imaging. Percutaneous biopsy effects should be considered in cases of tumor regression, and serial imaging should be planned afterwards.

Background: Trastuzumab treatment for salivary gland, gastric, and breast cancer commonly causes cancer treatment-related cardiac dysfunction (CTRCD). CTRCD incidence by sex has not been well studied.

Methods: This retrospective cohort study investigated frequency of and sex differences in CTRCD in patients with salivary gland cancer treated with trastuzumab at our hospital from April 2017 to March 2022. All patients underwent echocardiography at baseline and after the first, third, and sixth trastuzumab courses. We measured changes in global and regional longitudinal strain (LS) after trastuzumab administration. CTRCD was defined by left ventricular ejection fraction (LVEF) or global LS (GLS). The results were compared by sex.

Results: We recorded clinical data of 49 patients (median age [IQR], 65 [55-71] years; males [75.5%]). The median follow-up period after the sixth trastuzumab course was 120 (111-128) days. One female patient and no male patient had CTRCD defined by LVEF, and two female patients (16.7%) and seven male patients (18.9%) had CTRCD, defined by GLS. The Kaplan-Meier curves showed no significant difference in CTRCD frequency, defined by GLS (log-rank, p = 0.88), between female and male patients. In the univariate analysis, sex was not associated with CTRCD, defined by GLS. A significant difference in apical LS was observed between baseline and the third follow-up results of male patients.

Conclusions: In this study, CTRCD incidence was not significantly different between male and female patients with salivary gland cancer treated with trastuzumab. Although most previous studies have looked at female patients with breast cancer, a male patient may be found to be at similar risk of myocardial damage.

Aims: Cancer therapy-related cardiac dysfunction (CTRCD) is a dreaded complication of anthracycline therapy. CTRCD most frequently appears in patients with cardiovascular risk factors (CVR) or known cardiovascular disease. However, limited data exist on incidence and course of anthracycline-induced CTRCD in patients without preexisting risk factors. We therefore aimed to longitudinally investigate a cohort of young women on anthracycline treatment due to breast cancer without cardiovascular risk factors or known cardiovascular disease (NCT03940625).

Methods and results: We enrolled 59 women with primary breast cancer and scheduled anthracycline-based therapy, but without CVR or preexisting cardiovascular disease. We conducted a longitudinal assessment before, immediately and 12 months after cancer therapy with general laboratory, electrocardiograms, echocardiography and cardiovascular magnetic resonance (CMR), including myocardial relaxometry with T1, T2 and extracellular volume mapping. Every single patient experienced a drop in CMR-measured left ventricular ejection fraction (LVEF) of 6 ± 3% immediately after cancer therapy. According to the novel definition 32 patients (54.2%) developed CTRCD after 12 months defined by reduction in LVEF, global longitudinal strain (GLS) and/or biomarkers elevation, two of them were symptomatic. Global myocardial T2 relaxation times as well as myocardial mass increased coincidently with a decline in wall-thickening. While T2 values and myocardial mass normalized after 12 months, LVEF and GLS remained impaired.

Conclusion: In every single patient anthracyclines induce a decline of myocardial contractility, even among patients without pre-existing risk factors for CTRCD. Our data suggest to thoroughly evaluate whether this may lead to an increased risk of future cardiovascular events.