Cardio-oncology最新文献

Background: Immune checkpoint inhibitors (ICIs) have become the standard for treating various cancers. Nevertheless, their use may lead to significant cardiovascular immune-related adverse events (CV irAEs).

Objectives: We aimed to assess whether pre-treatment coronary artery calcium (CAC) deposition predicts CV irAEs in patients treated with ICIs.

Methods: A retrospective single-center cohort of patients treated with ICIs who performed pre-treatment chest computed tomography. A visual CAC assessment was categorized into Positive or Negative calcium deposits. Patients with pre-existing ischemic heart disease were excluded. The primary endpoint was the composite CV irAEs, including myocarditis, acute coronary syndrome, heart failure, and arrhythmias, and the secondary endpoint was all-cause mortality.

Results: The cohort included 240 patients with a median age of 67 (IQR 59-73) years and 47% female. The most prevalent type of cancer was lung cancer (36%), and the prominent ICIs was pembrolizumab (54%). Patients with Positive CAC (38%) were predominantly male, with higher rates of cardiovascular comorbidities. The primary outcome occurred in 36 cases (15%) at a median of 94 (IQR 48-338) days from the first ICIs dose. The Positive CAC group observed a non-significant trend toward a higher hazard for CV irAEs (HR 1.66, 95% CI 0.86-3.21, p = 0.13), with no significant difference in all-cause mortality (HR 1.15, 95% CI 0.88-1.51, p = 0.30).

Conclusion: Pre-treatment CAC deposition did not demonstrate an independent predictive role in assessing the risk of CV irAEs and all-cause mortality in patients treated with ICIs.

Background: Cancer therapy-related cardiac dysfunction (CTRCD) is recognized complication of antineoplastic therapies, and is particularly associated with anthracyclines. Treatment revolves around heart failure management, with limited evidence for other medications. Specifically, the aim of this study is to evaluate the role of glucagon-like peptide-1 receptor agonists (GLP-1RAs) in patients with CTRCD.

Methods: All adult cancer patients with a diagnosis of anthracycline induced CTRCD between 2012 and 2022 were retrieved from the TriNetX Research Network. Baseline characteristics, oncology data, and laboratory parameters were also abstracted. Patients were grouped based on administration of GLP-1RAs, with the development of a propensity matched non-GLP-1RA treatment cohort. Clinical outcomes were compared between the cohorts including all-cause mortality, all cause hospitalizations, acute heart failure events, acute renal failure, new atrial fibrillation, and cardiac arrest.

Results: Overall, 2282 cancer patients with CTRCD were identified. Following propensity matching, a control cohort of 201 patients who did not receive GLP-1RAs were compared to 201 patients receiving GLP-1RAs. Over a mean follow-up of 295.4 ± 109.6 days, patients receiving GLP-1RAs treatment had significantly lower risk of all-cause hospitalization (HR 0.617, 95% CI 0.474-0.803, p < 0.001), acute heart failure events (HR 0.612, 95% CI 0.428-0.875, p = 0.007), and acute renal failure (HR 0.577, 95% CI 0.408-0.815, p = 0.002). There were no significant differences in the risk of all-cause mortality, atrial fibrillation, or cardiac arrest.

Conclusion: In cancer patients with anthracycline induced CTRCD, those treated with GLP-1RAs had significantly lower risk of adverse clinical outcomes.

Background: Fruquintinib is a highly selective tyrosine kinase inhibitor that targets vascular endothelial growth factor receptors (VEGFR) 1, 2, and 3, which play a critical role in angiogenesis and tumor growth. As a novel anti-angiogenic agent, Fruquintinib has demonstrated promising efficacy in the treatment of various advanced malignancies, including metastatic colorectal cancer. However, concerns about its cardiovascular safety have emerged, given that VEGFR inhibition is often associated with cardiovascular adverse events.

Methodology: We conducted a systematic search through PubMed, Scopus, Embase, and Web of Science to identify randomized controlled trials and cohort studies that assessed the safety of Fruquintinib compared with placebo in patients with metastatic colorectal and other cancers. The evaluated outcomes included hypertension, coronary artery disease, cerebrovascular accidents, peripheral artery disease, heart failure, thromboembolism, arrhythmias, aortic dissection, and superior vena cava syndrome. Two independent reviewers screened the titles/abstracts based on predefined inclusion and exclusion criteria, followed by a full-text review of potentially relevant studies. Any disagreements between the reviewers were resolved through consultation with a third reviewer to ensure the accuracy and consistency of the study selection.

Results: Fifteen reports were included in our study. Out of 3832 patients taking Fruquintinib monotherapy, a total of 997 developed hypertension with a pooled estimate incidence of 0.329 (95% CI: 0.248, 0.410; P < 0.001). In comparison to placebo, Fruquintinib was associated with significantly higher odds of developing hypertension (OR: 6.856; 95% CI: 5.071, 9.268; P < 0.001). Compared to Regorafenib, Fruquintinib demonstrated an OR of 1.549 (95% CI: 0.804, 2.983; P = 0.191) for the development of hypertension. Additionally, patients taking Fruquintinib had a pooled estimate incidence of 0.041 (95% CI: 0.021, 0.060, P < 0.001) for thromboembolism development with an OR of 2.092 (95% CI: 0.813, 5.385; P = 0.126) compared to placebo. Other reported cardiovascular side effects included sinus tachycardia, superior vena cava syndrome, peripheral edema, heart failure, myocardial enzymes elevation, and vascular access complications.

Conclusion: Our study found that Fruquintinib is associated with significant cardiovascular risks, with hypertension being the most common adverse event, while thromboembolism did not reach statistical significance. Therefore, close monitoring for treatment-related cardiovascular events should be considered in these patients.

Background: Cardiac Amyloidosis (CA) remains highly underdiagnosed, especially among patients with causes of increased ventricular wall thickness, such as aortic stenosis (AS). The prevalence of CA throughout the spectrum of mild to severe AS is unknown and specific validated diagnostic parameters for this population are lacking. Here, we propose and prospectively evaluate a screening algorithm for CA among patients with mild to severe AS.

Methods: In this prospective, single-center study (NCT05010980), we included patients ≥ 65 years with mild to severe AS, an interventricular septum thickness > 11 mm, and at least one of the following criteria: Sokolow-Lyon-Index to left ventricular mass index ratio < 1.6 or stroke volume index < 35 ml/m2. Participants were prospectively screened for CA according to current guideline recommendations.

Results: After screening 2126 patients of whom 187 were eligible, 57 participants were enrolled and completed the diagnostic work-up. Mean age was 83 ± 0.7 years and 71% were male. 30% of the participants had mild, 37% had moderate and 33% had severe AS, respectively. Overall 26% of participants were diagnosed with CA. The prevalence of CA was higher among patients with mild AS (41%) compared to participants with moderate (24%) or severe AS (16%, p = 0.01). Within this preselected patient population, troponin (AUC:0.9, p < 0.0001) and NT-proBNP (AUC:0.86, p < 0.0001) further improved discrimination of patients with and without CA.

Conclusion: The prevalence of CA among AS patients fulfilling the preselected inclusion criteria was high, especially among those with mild to moderate AS. Implementing these criteria in clinical protocols could improve early diagnosis of CA.

Background: Carcinoid Heart Disease (CHD) primarily affects the right heart valves, while left heart involvement is rare and often associated with a patent foramen ovale (PFO). Early identification of a PFO in CHD can be critical to patient outcomes. A 61-year-old woman with metastatic neuroendocrine tumor presented with worsening breathlessness and hypoxemia. Imaging excluded pulmonary embolism and lung metastases. Transthoracic echocardiography revealed severe tricuspid regurgitation due to carcinoid valve involvement. Persistent hypoxemia prompted transesophageal echocardiography, which demonstrated a right-to-left shunt through a PFO. Right heart catheterization confirmed the findings excluding significant pulmonary hypertension. Percutaneous PFO closure improved oxygenation, but the patient deteriorated due to right ventricular failure and ultimately died from multiorgan failure despite later tricuspid valve replacement.

Conclusion: This case illustrates the importance of early detection of PFO in CHD, as delayed intervention can lead to poor outcomes. Simultaneous PFO closure and valve replacement may be preferable to a staged approach. A multidisciplinary strategy is vital for timely diagnosis and optimal treatment planning in such complex cases.

Aims: Adult survivors of haematological malignancies are at increased risk of long-term cardiovascular sequelae. Several echocardiographic metrics have been tested to detect subclinical myocardial dysfunction before it progresses toward cardiac events. Myocardial work (MW) is a load-independent echocardiographic index that conjugates non-invasive arterial blood pressure and global longitudinal strain (GLS).

Methods: Sixty-three disease-free survivors of Hodgkin Lymphoma (HL) [49% male, median age 42 (33,0-50,5) years], without known cardiovascular disease or reported cardiological symptoms, were included in this observational study. Myocardial work data from cancer survivors were compared with those from healthy subjects recruited in the EACVI NORRE Study.

Results: Mean left ventricular ejection fraction and GLS were, respectively, 57,0% (55,0-60,0) and - 18,0% (-19,2-17,1). Global work efficiency [GWE, 96% (94-97)], global work index (GWI, 1732 ± 340 mmHg%) and global wasted work [GWW, 78 (55-131) mmHg%] did not differ between male and female survivors; however, global constructive work (GCW, 2116 ± 386 mmHg%) was lower in males. Of importance, GWI and GCW were lower in cancer survivors compared to healthy subjects from the EACVI NORRE study (p = 0,0008 and p = 0,0324, respectively). When evaluating associations of MW indices with patients' characteristics, only systolic blood pressure and ejection fraction were independently associated with both GWI and GCW at multivariable analysis.

Conclusion: For the first time, this report provides values of MW indices in asymptomatic HL survivors without cardiovascular disease. GWI and GCW were significantly lower in HL survivors compared to healthy subjects. MW metrics might serve as valuable markers of subclinical cardiac dysfunction in this population.

Background: Patients with primary central nervous system lymphoma (PCNSL) often require high-dose methotrexate (HD-MTX)-based regimens for effective disease control. However, the coexistence of heart failure with a reduced ejection fraction (HFrEF) poses significant challenges due to the increased risk of treatment-related cardiotoxicity and the potential exacerbation of cardiac dysfunction from fluid overload.

Main body: This review explores current PCNSL treatment modalities and their implications for patients with HFrEF. These findings emphasize the importance of multidisciplinary care, the cardiovascular risks associated with HD-MTX and adjunct therapies, and the strategies available to mitigate these risks.

Conclusion: Managing PCNSL in patients with HFrEF requires individualized therapy, vigilant monitoring, and strong collaboration between oncology and cardiology teams. Emerging therapies may reduce cardiotoxicity, but further evidence is needed to guide their safe use in this vulnerable population.

Cardiac fibrosis, a condition characterized by the deposition of excess collagen in the cardiac tissue, is a major complication of various cardiovascular diseases, including myocardial infarction, hypertension, and different types of cardiomyopathies. CAR T-cell therapy, a form of immunotherapy that involves the genetic modification of T cells to recognize and target specific antigens, has shown promise in the treatment of various cancers and autoimmune diseases. The rationale behind using CAR T-cell therapy to treat cardiac fibrosis lies in the fact that fibrosis is often driven by the activation of pro-fibrotic immune cells, such as myofibroblasts. By targeting these pro-fibrotic cells with CAR T-cells, it may be possible to reduce the severity of cardiac fibrosis. Enhancing CAR T-cell therapy through innovative nanoparticle delivery systems provides a comprehensive approach to treating cardiac fibrosis, with experimental evidence indicating potential in reducing fibrosis and improving cardiac function. Despite these benefits, significant challenges such as cardiotoxicity and cardiovascular complications remain. Therefore, this review explores the molecular mechanisms underlying cardiac fibrosis and the effects of CAR T-cell therapy on the heart, elucidating both its antifibrotic properties and associated cardiotoxic effects based on findings from recent studies.

Background: Anti-HER2 receptor monoclonal antibodies like trastuzumab are the mainstay of treatment in HER2-positive breast cancer but can result in cancer therapy-related cardiac dysfunction (CTRCD). Guidelines recommend cardiac surveillance prior to anti-HER2 therapy initiation, every 3 months during therapy, and within 1 year after therapy completion. Resource limitations in safety-net settings without cardio-oncology programs may impact cardiac surveillance and treatment patterns and contribute to disparities in cardiovascular health among patients with cancer. We aimed to characterize and compare patterns of cardiac surveillance and short-term cardiovascular outcomes among patients with breast cancer receiving trastuzumab in a safety-net versus a tertiary care system.

Methods: A retrospective cohort study was conducted on women diagnosed with stage I-III HER2-positive breast cancer between 2018 and 2020 in a safety-net and a tertiary care system. Clinical data from transthoracic echocardiograms, multigated acquisition scans, and cardiac magnetic resonance imaging one year out from trastuzumab initiation were collected. CTRCD was defined by decrements in left ventricular ejection fraction, global longitudinal strain changes, and symptoms of heart failure. Demographics and referral patterns were also assessed.

Results: A total of 235 patients were included (93 safety-net, 142 tertiary care). The safety-net population was 23% Black, 60% Hispanic, and 69% uninsured, while the tertiary care population was 64% White and 3.5% uninsured (p < 0.001). Baseline cardiac surveillance was obtained in 84% of safety-net patients and 89% of tertiary care patients, with mean surveillance interval of approximately 3 months. Only 54% of patients at each site obtained cardiac surveillance post-trastuzumab. CTRCD occurred in 12% of patients in the safety-net system and 19% in the tertiary care system, with most cases being asymptomatic (p = 0.143). High-risk patients were more likely to be referred to cardiology/cardio-oncology in the tertiary care system compared to the safety-net system (67% vs. 6.7%, p < 0.001).

Conclusions: While our data shows similar frequency of cardiac surveillance based on left ventricular ejection fraction at our safety-net and tertiary care center, the utilization of various imaging modalities and cardiology/cardio-oncology services were significantly different between the two institutions. These differences may result in underdiagnosis of CTRCD in vulnerable populations and contribute to inferior long-term cardiovascular outcomes.