Equity in Cardio-Oncology Care and Research: A Scientific Statement From the American Heart Association.

Advances in cancer therapeutics have revolutionized survival outcomes in patients with cancer. However, cardiovascular toxicities associated with specific cancer therapeutics adversely affect the outcomes of patients with cancer. Recent studies have uncovered excess risks of these cardiotoxic events, especially in traditionally underrepresented populations. Despite advances in strategies to limit the risks of cardiovascular events among cancer survivors, relatively limited guidance is available to address the rapidly growing problem of disparate cardiotoxic risks among women and underrepresented patient populations. Previously decentralized and sporadic evaluations have led to a lack of consensus on the definitions, investigation, and potential optimal strategies to address disparate cardiotoxicity in contemporary cancer care (eg, with immunotherapy, biologic, or cytotoxic therapies) settings. This scientific statement aims to define the current state of evidence for disparate cardiotoxicity while proposing uniform and novel methodological approaches to inform the identification and mitigation of disparate cardio-oncology outcomes in future clinical trials, registries, and daily clinical care settings. We also propose an evidence-based integrated approach to identify and mitigate disparities in the routine clinical setting. This consensus scientific statement summarizes and clarifies available evidence while providing guidance on addressing inequities in the era of emerging anticancer therapies.

Cardiovascular Imaging in Contemporary Cardio-Oncology: A Scientific Statement From the American Heart Association.

Advances in cancer therapeutics have led to dramatic improvements in survival, now inclusive of nearly 20 million patients and rising. However, cardiovascular toxicities associated with specific cancer therapeutics adversely affect the outcomes of patients with cancer. Advances in cardiovascular imaging have solidified the critical role for robust methods for detecting, monitoring, and prognosticating cardiac risk among patients with cancer. However, decentralized evaluations have led to a lack of consensus on the optimal uses of imaging in contemporary cancer treatment (eg, immunotherapy, targeted, or biological therapy) settings. Similarly, available isolated preclinical and clinical studies have provided incomplete insights into the effectiveness of multiple modalities for cardiovascular imaging in cancer care. The aims of this scientific statement are to define the current state of evidence for cardiovascular imaging in the cancer treatment and survivorship settings and to propose novel methodological approaches to inform the optimal application of cardiovascular imaging in future clinical trials and registries. We also propose an evidence-based integrated approach to the use of cardiovascular imaging in routine clinical settings. This scientific statement summarizes and clarifies available evidence while providing guidance on the optimal uses of multimodality cardiovascular imaging in the era of emerging anticancer therapies.

Microfluidic Digital Immunoassay for Point-of-Care Detection of NT-proBNP from Whole Blood.

The high prevalence and economic burden of heart failure remain a challenge to global health. This lifelong disease leads to a buildup of permanent heart damage, making early detection and frequent monitoring crucial for effective treatment. N-terminal proBNP (NT-proBNP) is an important biomarker for monitoring the disease state, but current commercial and research NT-proBNP assays require phlebotomy and bulky equipment or do not satisfy clinical requirements such as sensitivity and detection thresholds. Here, we report a point-of-care (POC) compatible microfluidic digital immunoassay that can quantify the NT-proBNP concentration in a small volume of whole blood. Our automated microfluidic device takes whole blood samples mixed with biotinylated detection antibodies and passes through a plasma filter to react with a capture antibody-functionalized sensor surface. Streptavidin-coated gold nanoparticles (GNPs) are then released to mark the surface-bound single NT-proBNP immunocomplexes and recorded with bright-field microscopy. NT-proBNP concentrations in the sample are quantified via a hybrid digital/analog calibration curve. Digital counts of bound GNPs are used as readout signal at low concentrations for high sensitivity detection, and GNP pixel occupancies are used at high concentrations for extended dynamic range. With this approach, we detected NT-proBNP in the range of 8.24-10 000 pg/mL from 7 µL of whole blood in 10 min, with a limit of detection of 0.94 pg/mL. Finally, the method was validated with 15 clinical serum samples, showing excellent linear correlation (r = 0.998) with Roche's Elecsys proBNP II assay. This evidence indicates that this method holds promise for decentralized monitoring of heart failure.

Cancer Therapy-Associated Pulmonary Hypertension and Right Ventricular Dysfunction: Etiologies and Prognostic Implications.

Advances in cancer therapies have improved oncologic outcomes but can potentially expose patients to risk of cardiovascular toxicity. While left ventricular (LV) dysfunction is a well-known cardiotoxicity of cancer therapy. Pulmonary hypertension (PH) and right ventricular (RV) dysfunction are seen with several cancer therapies, including alkylating agents, tyrosine kinase inhibitors (TKIs), and immunotherapy, and are associated with significant morbidity and mortality. Awareness and recognition of cancer therapy-associated PH and RV dysfunction is critical to identify underlying etiologies and institute the appropriate therapy. However, gaps exist in the current literature on the epidemiology of PH and RV dysfunction in cancer, underlying pathophysiology and optimal management strategies.

Catheter-based therapy for intermediate or high-risk pulmonary embolism is associated with lower in-hospital mortality in patients with cancer: Insights from the National Inpatient Sample.

BACKGROUND: Pulmonary embolism (PE) is a common complication among patients with cancer and is a significant contributor to morbidity and mortality. Catheter-based therapies (CBT), including catheter-directed thrombolysis (CDT) and mechanical thrombectomy, have been developed and are used in patients with intermediate or high-risk PE. However, there is a paucity of data on outcomes in patients with cancer as most clinical studies exclude this group of patients. AIMS: To characterize outcomes of patients with cancer admitted with intermediate or high-risk PE treated with CBT compared with no CBT. METHODS: Patients with an admission diagnosis of intermediate or high-risk PE and a history of cancer from October 2015 to December 2018 were identified using the National Inpatient Sample. Outcomes of interest were in-hospital death or cardiac arrest (CA) and major bleeding. Inverse probability treatment weighting (IPTW) was utilized to compare outcomes between patients treated with and without CBT. Variables that remained unbalanced after IPTW were adjusted using multivariable logistic regression. RESULTS: A total of 2084 unweighted admissions (10,420 weighted) for intermediate or high-risk PE and cancer were included, of which 136 (6.5%) were treated with CBT. After IPTW, CBT was associated with lower death or CA (aOR 0.54, 95% CI 0.46-0.64) but higher major bleeding (aOR 1.41, 95% CI 1.21-1.65). After stratifying by PE risk type, patients treated with CBT had lower risk of death or CA in both intermediate (aOR 0.52, 95% CI 0.36-0.75) and high-risk PE (aOR 0.48, 95% CI 0.33-0.53). However, patients with CBT were associated with increased risk of major bleeding in intermediate-risk PE (aOR 2.12, 95% CI 1.67-2.69) but not in those with high-risk PE (aOR 0.84, 95% CI 0.66-1.07). CONCLUSIONS: Among patients with cancer hospitalized with intermediate or high-risk PE, treatment with CBT was associated with lower risk of in-hospital death or CA but higher risk of bleeding. Prospective studies and inclusion of patients with cancer in randomized trials are warranted to confirm our findings.

Inflammation in Chemotherapy-Induced Cardiotoxicity.

PURPOSE OF REVIEW: In this review we describe the role of inflammation in chemotherapy-induced cardiotoxicity with a particular focus on anthracycline-induced cardiomyopathy (AIC). First, we discuss inflammation associated with anthracyclines at a cellular level. Next, we discuss the clinical implications of these inflammatory mechanisms for early detection and cardioprotective strategies in patients undergoing anthracycline treatment. RECENT FINDINGS: Key inflammatory pathways identified in AIC include cytokine release, upregulation of the innate immune system via toll-like receptors, and activation of the inflammasome. Emerging evidence suggests a role for inflammatory biomarkers in detecting subclinical AIC. Advanced imaging techniques, such as cardiac PET with novel tracers targeting inflammation, may enhance early detection. Both traditional cardioprotective strategies and novel anti-inflammatory therapies show potential in preventing and treating AIC. Understanding the inflammatory mechanisms involved in AIC provides new opportunities for early detection and targeted cardioprotective strategies in patients undergoing anthracycline treatment and informs our understanding of other forms of chemotherapy-induced cardiotoxicity.

Biomarkers and cardiovascular outcomes in chimeric antigen receptor T-cell therapy recipients.

AIMS: Chimeric antigen receptor T-cell therapy (CAR-T) harnesses a patient's immune system to target cancer. There are sparse existing data characterizing death outcomes after CAR-T-related cardiotoxicity. This study examines the association between CAR-T-related severe cardiovascular events (SCE) and mortality. METHODS AND RESULTS: From a multi-centre registry of 202 patients receiving anti-CD19 CAR-T, covariates including standard baseline cardiovascular and cancer parameters and biomarkers were collected. Severe cardiovascular events were defined as a composite of heart failure, cardiogenic shock, or myocardial infarction. Thirty-three patients experienced SCE, and 108 patients died during a median follow-up of 297 (interquartile range 104-647) days. Those that did and did not die after CAR-T were similar in age, sex, and prior anthracycline use. Those who died had higher peak interleukin (IL)-6 and ferritin levels after CAR-T infusion, and those who experienced SCE had higher peak IL-6, C-reactive protein (CRP), ferritin, and troponin levels. The day-100 and 1-year Kaplan-Meier overall mortality estimates were 18% and 43%, respectively, while the non-relapse mortality (NRM) cumulative incidence rates were 3.5% and 6.7%, respectively. In a Cox model, SCE occurrence following CAR-T was independently associated with increased overall mortality risk [hazard ratio (HR) 2.8, 95% confidence interval (CI) 1.6-4.7] after adjusting for age, cancer type and burden, anthracycline use, cytokine release syndrome grade ≥ 2, pre-existing heart failure, hypertension, and African American ancestry; SCEs were independently associated with increased NRM (HR 3.5, 95% CI 1.4-8.8) after adjusting for cancer burden. CONCLUSION: Chimeric antigen receptor T-cell therapy recipients who experience SCE have higher overall mortality and NRM and higher peak levels of IL-6, CRP, ferritin, and troponin.

Rapid Exclusion of Acute Myocardial Injury and Infarction With a Single High-Sensitivity Cardiac Troponin T in the Emergency Department: A Multicenter United States Evaluation.

BACKGROUND: There are good data to support using a single high-sensitivity cardiac troponin T (hs-cTnT) below the limit of detection of 5 ng/L to exclude acute myocardial infarction. Per the US Food and Drug Administration, hs-cTnT can only report to the limit of quantitation of 6 ng/L, a threshold for which there are limited data. Our goal was to determine whether a single hs-cTnT below the limit of quantitation of 6 ng/L is a safe strategy to identify patients at low risk for acute myocardial injury and infarction. METHODS: The efficacy (proportion identified as low risk based on baseline hs-cTnT<6 ng/L) of identifying low-risk patients was examined in a multicenter (n=22 sites) US cohort study of emergency department patients undergoing at least 1 hs-cTnT (CV Data Mart Biomarker cohort). We then determined the performance of a single hs-cTnT<6 ng/L (biomarker alone) to exclude acute myocardial injury (subsequent hs-cTnT >99th percentile in those with an initial hs-cTnT<6 ng/L). The clinically intended rule-out strategy combining a nonischemic ECG with a baseline hs-cTnT<6 ng/L was subsequently tested in an adjudicated cohort in which the diagnostic performance for ruling out acute myocardial infarction and safety (myocardial infarction or death at 30 days) were evaluated. RESULTS: A total of 85 610 patients were evaluated in the CV Data Mart Biomarker cohort, among which 24 646 (29%) had a baseline hs-cTnT<6 ng/L. Women were more likely than men to have hs-cTnT<6 ng/L (38% versus 20%, P<0.0001). Among 11 962 patients with baseline hs-cTnT<6 ng/L and serial measurements, only 1.2% developed acute myocardial injury, resulting in a negative predictive value of 98.8% (95% CI, 98.6-99.0) and sensitivity of 99.6% (95% CI, 99.5-99.6). In the adjudicated cohort, a nonischemic ECG with hs-cTnT<6 ng/L identified 33% of patients (610/1849) as low risk and resulted in a negative predictive value and sensitivity of 100% and a 30-day rate of 0.2% for myocardial infarction or death. CONCLUSIONS: A single hs-cTnT below the limit of quantitation of 6 ng/L is a safe and rapid method to identify a substantial number of patients at very low risk for acute myocardial injury and infarction.

Interventional Cardio-Oncology: Unique Challenges and Considerations in a High-Risk Population.

OPINION STATEMENT: Patients with cancer are at risk of developing cardiovascular disease (CVD) including atherosclerotic heart disease (AHD), valvular heart disease (VHD), and atrial fibrillation (AF). Advances in percutaneous catheter-based treatments, including percutaneous coronary intervention (PCI) for AHD, percutaneous valve replacement or repair for VHD, and ablation and left atrial appendage occlusion devices (LAAODs) for AF, have provided patients with CVD significant benefit in the recent decades. However, trials and registries investigating outcomes of these procedures often exclude patients with cancer. As a result, patients with cancer are less likely to undergo these therapies despite their benefits. Despite the inclusion of cancer patients in randomized clinical trial data, studies suggest that cancer patients derive similar benefits of percutaneous therapies for CVD compared with patients without cancer. Therefore, percutaneous interventions for CVD should not be withheld in patients with cancer, as they may still benefit from these procedures.

Mechanisms of Myocardial Ischemia in Cancer Patients: A State-of-the-Art Review of Obstructive Versus Non-Obstructive Causes.

In patients with cancer, myocardial infarction (MI) has distinct features and mechanisms compared to the non-oncology population. Triggers of myocardial ischemia specific to the oncology population have been increasingly identified. Coronary plaque disruption, coronary vasospasm, coronary microvascular dysfunction, spontaneous coronary artery dissection, and coronary oxygen supply-demand mismatch are all causes of MI that have been shown to have specific triggers related to either the treatments or complications of cancer. MI can occur in the presence or absence of atherosclerotic coronary artery disease (CAD). MI with nonobstructive CAD (MINOCA) is a heterogeneous syndrome that has distinct pathophysiology and different epidemiology from MI with significant CAD (MI-CAD). Recognition and differentiation of MI-CAD and MINOCA is essential in the oncology population, due to unique etiology and impact on diagnosis, management, and overall outcomes. There are currently no reports in the literature concerning MINOCA as a unified syndrome in oncology patients. The purpose of this review is to analyze the literature for studies related to known triggers of myocardial ischemia in cancer patients, with a focus on MINOCA. We propose that certain cancer treatments can induce MINOCA-like states, and further research is warranted to investigate mechanisms that may be unique to certain cancer states and types of treatment.

Social Media and Cardiovascular Health: Implications for Women.

PURPOSE OF REVIEW: Cardiovascular disease (CVD) is the leading cause of mortality in adult women in the USA, yet CVD is underrecognized in women. Disparities in care are further pronounced in women of racial/ethnic minority backgrounds. In this review, we discuss the role of social media (SoMe) as a tool to (i) promote women's cardiovascular (CV) health and (ii) address and potentially reduce gaps in care, particularly in general cardiology (targeting atherosclerotic cardiovascular disease), cardio-oncology, and cardio-obstetrics. We also briefly discuss women's CV health as a common, although not unique, focus of women in cardiology on SoMe. RECENT FINDINGS: Studies have suggested the utility of social media to help advance subspecialties of cardiology. Leaders within general cardiology, cardio-oncology, and cardio-obstetrics have curated social media strategies to advance their respective fields and call attention to cardiovascular health disparities in female populations and racial/ethnic minorities. In addition to these types of uses, women in cardiology also frequently use SoMe to encourage a career in cardiology and to share experiences, challenges, and resources for support and career advancement as healthcare professionals; men in cardiology and especially those who are allies for sex and racial/ethnic minorities also use SoMe for these means. Herein, we highlight the role and myriad applications of social media in the promotion of women's cardiovascular health. We discuss five primary roles of social media: increasing public awareness, disseminating medical literature in a rapid and accessible fashion, facilitating professional networking, serving as a platform for medical conferences, and empowering patients. These core strategies are discussed through the lens of general cardiology, cardio-oncology, and cardio-obstetrics. We also demonstrate how these applications can be leveraged to increase representation of women in cardiology, also supporting an increased focus on women's cardiovascular health.

NCCN Guidelines® Insights: Survivorship, Version 1.2022.

The NCCN Guidelines for Survivorship are intended to help healthcare professionals who work with survivors to ensure that the survivors' complex and varied needs are addressed. The NCCN Guidelines provide screening, evaluation, and treatment recommendations for the consequences of adult-onset cancer and its treatment; recommendations to help promote physical activity, weight management, and immunizations in survivors; and a framework for care coordination. This article summarizes updates to the NCCN Guidelines pertaining to preventive health for cancer survivors, including recommendations about alcohol consumption and vaccinations.

T-cell Immunotherapy and Cardiovascular Disease: Chimeric Antigen Receptor T-cell and Bispecific T-cell Engager Therapies.

Chimeric antigen receptor (CAR) T-cell and bispecific T-cell engager (BiTE) therapies have revolutionized the treatment of refractory or relapsed leukemia and lymphoma. Increased use of these therapies has revealed signals of significant cardiotoxicity, including cardiomyopathy/heart failure, arrhythmia, myocardial injury, hemodynamic instability, and cardiovascular death mainly in the context of a profound inflammatory response to CAR T-cell antitumor effects known as cytokine release syndrome (CRS). Preexisting cardiovascular risk factors and disease may increase the risk of such cardiotoxicity. High index of suspicion and close monitoring is required for prompt recognition. Supportive hemodynamic care and targeted anti-IL-6 therapy, as well as possibly broader immunosuppression with corticosteroids, are the cornerstones of the management.

Training and Career Development in Cardio-Oncology Translational and Implementation Science.

Cardiovascular disease is a leading cause of death in cancer survivors, after recurrence of the primary tumor or occurrence of a secondary malignancy. Consequently, the interdisciplinary field of cardio-oncology has grown rapidly in recent years to address the cardiovascular care needs of this unique population through clinical care and research initiatives. Here, the authors discuss the ideal infrastructure for training and career development in cardio-oncology translational and implementation science and emphasize the importance of the multidisciplinary cardiovascular team for both research and patient care. Cardio-oncology training opportunities in general cardiology, hematology/oncology, and specialized cardio-oncology clinical and research fellowships are also considered.

Reclassification of Treatment Strategy with Fractional Flow Reserve in Cancer Patients with Coronary Artery Disease.

Background and Objectives: Cancer and coronary artery disease (CAD) often coexist. Compared to quantitative coronary angiography (QCA), fractional flow reserve (FFR) has emerged as a more reliable method of identifying significant coronary stenoses. We aimed to assess the specific management, safety and outcomes of FFR-guided percutaneous coronary intervention (PCI) in cancer patients with stable CAD. Materials and Methods: FFR was used to assess cancer patients that underwent coronary angiography for stable CAD between September 2008 and May 2016, and were found to have ≥50% stenosis by QCA. Patients with lesions with an FFR > 0.75 received medical therapy alone, while those with FFR ≤ 0.75 were revascularized. Procedure-related complications, all-cause mortality, nonfatal myocardial infarction, or urgent revascularizations were analyzed. Results: Fifty-seven patients with stable CAD underwent FFR on 57 lesions. Out of 31 patients with ≥70% stenosis as measured by QCA, 14 (45.1%) had an FFR ≥ 0.75 and lesions were reclassified as moderate and did not receive PCI nor DAPT. Out of 26 patients with <70% stenosis as measured by QCA, 6 (23%) had an FFR < 0.75 and were reclassified as severe and were treated with PCI and associated DAPT. No periprocedural complications, urgent revascularization, acute coronary syndromes, or cardiovascular deaths were noted. There was a 22.8% mortality at 1 year, all cancer related. Patients who received a stent by FFR assessment showed a significant association with decreased risk of all-cause death (HR: 0.37, 95% CI 0.15−0.90, p = 0.03). Conclusions: Further studies are needed to define the optimal therapeutic approach for cancer patients with CAD. Using an FFR cut-off point of 0.75 to guide PCI translates into fewer interventions and can facilitate cancer care. There was an overall reduction in mortality in patients that received a stent, suggesting increased resilience to cancer therapy and progression.

High-Sensitivity Cardiac Troponin T for the Detection of Myocardial Injury and Risk Stratification in COVID-19.

BACKGROUND: Limited data exist on high-sensitivity cardiac troponin (hs-cTn) for risk-stratification in COVID-19. METHODS: We conducted a multicenter, retrospective, observational, US-based study of COVID-19 patients undergoing hs-cTnT. Outcomes included short-term mortality (in-hospital and 30-days post-discharge) and a composite of major adverse events, including respiratory failure requiring mechanical ventilation, cardiac arrest, and shock within the index presentation and/or mortality during the index hospitalization or within 30-days post-discharge. RESULTS: Among 367 COVID-19 patients undergoing hs-cTnT, myocardial injury was identified in 46%. They had a higher risk for mortality (20% vs 12%, P < 0.0001; unadjusted HR 4.44, 95% CI 2.13-9.25, P < 0.001) and major adverse events (35% vs. 11%, P < 0.0001; unadjusted OR 4.29, 95% CI 2.50-7.40, P < 0.0001). Myocardial injury was associated with major adverse events (adjusted OR 3.84, 95% CI 2.00-7.36, P < 0.0001) but not mortality. Baseline (adjusted OR 1.003, 95% CI 1.00-1.007, P = 0.047) and maximum (adjusted OR 1.005, 95% CI 1.001-1.009, P = 0.0012) hs-cTnT were independent predictors of major adverse events. Most (95%) increases were due to myocardial injury, with 5% (n = 8) classified as type 1 or 2 myocardial infarction. A single hs-cTnT <6 ng/L identified 26% of patients without mortality, with a 94.9% (95% CI 87.5-98.6) negative predictive value and 93.1% sensitivity (95% CI 83.3-98.1) for major adverse events in those presenting to the ED. CONCLUSIONS: Myocardial injury is frequent and prognostic in COVID-19. While most hs-cTnT increases are modest and due to myocardial injury, they have important prognostic implications. A single hs-cTnT <6 ng/L at presentation may facilitate the identification of patients with a favorable prognosis.

Left main coronary artery compression in pulmonary hypertension.

Extrinsic compression of the left main coronary artery (LMCA) by a dilated pulmonary artery (PA) in the setting of pulmonary arterial hypertension (PAH) is an increasingly recognized disease entity. LMCA compression has been associated with angina, arrhythmia, heart failure, and sudden cardiac death in patients with PAH. Recent studies suggest that at least 6% of patients with PAH have significant LMCA compression. Screening for LMCA compression can be achieved with computed coronary tomography angiography, with a particular emphasis on assessment of PA size and any associated downward displacement and reduced takeoff angle of the LMCA. Indeed, evidence of a dilated PA (>40 mm), a reduced LMCA takeoff angle (<60°), and/or LMCA stenosis on CCTA imaging should prompt further diagnostic evaluation. Coronary angiography in conjunction with intravascular imaging has proven effective in diagnosing LMCA compression and guiding subsequent treatment. While optimal medical therapy and surgical correction remain in the clinician's arsenal, percutaneous coronary intervention has emerged as an effective treatment for LMCA compression. Given the prevalence of LMCA compression, its associated morbidity, and mortality, and the wide array of successful treatment strategies, maintaining a high degree of suspicion for this condition, and understanding the potential treatment strategies is critical.

Chemotherapy and Radiation-Associated Cardiac Autonomic Dysfunction.

PURPOSE OF REVIEW: Cardiovascular autonomic dysfunction (AD) among cancer survivors is increasingly being recognized. However, the mechanisms and incidence are poorly understood. In this review, the clinical features, diagnostic modalities, proposed mechanisms, and currently available treatments of cardiovascular AD in cancer survivors are described. RECENT FINDINGS: Much of our current understanding of cardiovascular AD is based on disease states such as diabetes, multisystem atrophy, and Parkinson's disease. Several non-invasive tests, measurements, and scoring systems have been developed as surrogates for autonomic function, with some even demonstrating associations with all-cause mortality. The mechanism of cardiovascular AD specifically in the cancer population, however, has not been directly studied. The etiology of cardiovascular AD in cancer survivors is likely multifactorial, and proposed mechanisms include direct nerve damage by chemoradiation, the pro-inflammatory state associated with malignancy, and paraneoplastic syndromes. It may also be that cardiovascular AD is an early marker of global cardiomyopathy rather than its own condition. Current pharmacologic options for cardiovascular AD are extrapolated from how it has been treated in other disease processes, and these agents have not been studied in the cancer population or compared head-to-head. Cardiovascular AD in cancer survivors can cause significant debilitation and may be associated with all-cause mortality. Current diagnostic modalities have several limitations, such as standardization and validity. However, given the nonspecific nature of cardiovascular AD, these tools provide an objective marker for diagnosis and tracking treatment response. While the mechanism of cardiovascular AD in cancer survivors has not been directly studied, it may be useful to evoke mechanisms of cardiovascular AD in other disease states such as diabetes, Parkinson's disease, and multisystem atrophy in addition to identifying unique conditions associated with malignancy like a pro-inflammatory state. Until further studies are performed, management of cardiovascular AD as seen in other disease states may serve as a guide for symptom management in cancer survivors.

National Cardiovascular Data Registry Model Predicts Long-Term Mortality in Patients Undergoing Percutaneous Coronary Interventions.

National Cardiovascular Data Registry (NCDR)-based logistic regression model is available for clinicians to predict in-hospital all-cause mortality after a percutaneous coronary intervention (PCI). However, this model has never been used to predict long-term all-cause mortality after PCI. Therefore, we sought to test the ability of the NCDR model to predict the short- and long-term risk of all-cause mortality in patients undergoing PCI. All patients undergoing PCI in the Mayo Clinic Health System were enrolled in the Mayo Clinic CathPCI registry. Patient-level demographic, clinical, and angiographic data from January 2006 to December 2017 were extracted from the registry. Patients who underwent coronary artery bypass graft surgery (CABG) were excluded. The area under the receiver operator characteristic curve (AUC) was calculated to assess the ability of the NCDR model to predict outcomes of interest (6-month, 1-year, 2-year, and 5-year all-cause mortality) after PCI. A total of 17,356 unique patients were included for the final analysis after excluding 165 patients who underwent CABG surgery. The mean age was 66.9 ± 12.5 years, and 71% were men. The 6-month, 1-year, 2-year, and 5-year all-cause mortality rates were 4.2% (n = 737), 5.8% (n = 1,005), 8.06% (n = 1,399), and 14.2% (n = 2,472), respectively. The AUCs of the NCDR model to predict 6-month, 1-year, 2-year, and 5-year all-cause mortality were 0.84 (95% CI: 0.82-0.86), 0.82 (95% CI: 0.80-0.84), 0.80 (95% CI: 0.79-0.81), and 0.78 (95% CI: 0.77-0.79), respectively. The NCDR model was able to accurately predict both short- and long-term all-cause mortality after PCI.

AngioVac Aspiration Thrombectomy of Right Atrial Thrombus is Safe and Effective in Cancer Patients.

OBJECTIVES: The aim of this study was to test the hypothesis that endovascular aspiration thrombectomy of right atrial thrombus (RAT) using the AngioVac device is as safe and effective in patients with cancer as those without cancer. BACKGROUND: RAT is a uniquely challenging clinical presentation of venous thromboembolism due to its low incidence and historically high-risk of mortality due to thrombus propagation into the pulmonary arteries. There is a lack of consensus regarding management, particularly in high-risk cancer patients. Endovascular aspiration thrombectomy utilizing the AngioVac device is effective in removal of right atrial thrombus and may be a safer option for patients with cancer in whom avoidance of higher-risk intervention is preferred. METHODS: This was an institutional review board-approved retrospective single-center case control study of patients with RAT who underwent AngioVac aspiration thrombectomy between August 2013 and July 2020. Analysis of patient demographics and clinical characteristics, thrombus-related factors, and operative details was performed. Primary endpoints included survival, safety, and technical success. RESULTS: A total of 44 patients met inclusion criteria, 20 of whom with active malignancy. The oncology group had a significantly higher Charlson comorbidity index (P = 0.01). Comparative outcomes between the oncology and non-oncology group showed no difference in survival (P = 0.8) or technical success (OR 3, 95% CI 0.83-10.9). There were 9 complications, including 6 minor, 1 moderate, 1 severe, and 1 death. CONCLUSIONS: AngioVac aspiration thrombectomy of RAT is as safe and effective in patients with cancer as those without cancer.