Faculty Bibliography

BACKGROUND:Extrinsic compression of the pulmonary artery (PA) has been described with mediastinal and other thoracic masses. This compression can lead to acquired pulmonic stenosis and pulmonary hypertension. CASE SUMMARY/METHODS:A 27-year-old woman was diagnosed with Hodgkin lymphoma with a mediastinal mass compressing her PA leading to severe pulmonary hypertension, without hemodynamic compromise. She was treated with chemotherapy and had rapid resolution of the pulmonary artery compression on subsequent transthoracic echocardiogram 1 month after starting treatment. DISCUSSION/CONCLUSIONS:The current literature on the rare entity of extrinsic PA compression includes cases of surgical or percutaneous intervention to relieve compression and cases with resolution of compression based on changes in physical examination or transthoracic echocardiogram several months after initial diagnosis. This case is novel in reporting echocardiographic evidence of complete resolution of PA compression within 1 month of treatment without invasive intervention. TAKE-HOME MESSAGES/CONCLUSIONS:Pulmonary hypertension secondary to extrinsic PA compression from a mediastinal tumor is rare, but this case demonstrates that it may completely and rapidly resolve after initiation of chemotherapy. Short-interval follow-up echocardiography is helpful to reassess the degree of pulmonary hypertension after treatment.

The optimal treatment of patients with diffuse large B-cell lymphoma (DLBCL) or Hodgkin lymphoma (HL) with preexisting cardiomyopathy is uncertain. An anonymous, electronic survey was distributed by e-mail to three US lymphoma cooperative groups, two community hospitals, and twelve academic medical systems, and distributed at one international lymphoma meeting. Fifty hematology-oncology providers caring for patients with lymphoma were included. In response to a vignette of a 67-yo with Stage III DLBCL with LVEF of 40-45%, 15 (30%) would use non-anthracycline regimens, 13 (26%) R-CHOP with liposomal doxorubicin instead of doxorubicin, 11 (22%) R-CHOP without modification and 6 (12%) R-CHOP with a continuous doxorubicin infusion. In a second vignette of a patient with HL in remission after frontline treatment with doxorubicin cumulative dose 300 mg/m², 16 (32%) would order an echocardiogram after treatment. There was substantial variability in preferred treatment regimens with preexisting cardiomyopathy and in cardiac monitoring after anthracycline.

BACKGROUND:Acute decompensated heart failure (HF) can progress to cardiogenic shock, and patients with cancer are at an increased risk of HF compared to patients without cancer. However, limited data exist on outcomes of patients admitted for HF-related cardiogenic shock (HF-CS) with cancer versus without cancer. METHODS:Adult patients admitted for HF-CS between 2014-2020 were identified using the National Readmission Database. Propensity score matching (PSM) was used to match 1 patient with cancer to 10 patients without cancer. Primary outcomes were in-hospital death, major bleeding, and thrombotic complications. Exploratory outcomes were 90-day readmission rates among patients who survived initial hospitalization. Temporal trends were also explored. RESULTS:Of 137,316 admissions for HF-CS, 7,306 (5.3%) had active cancer. After PSM, patients with cancer had increased odds of in-hospital death (OR 1.12, 95% CI 1.06 - 1.18), thrombotic complications (OR 1.12, 95% CI 1.03 - 1.21), and major bleeding (OR 1.23, 95% CI 1.17 - 1.31) compared to patients without cancer, with risks differing by cancer type. In exploratory analyses, rates of readmission were similar for patients with and without cancer. From 2014-2020, patients with cancer had no significant change in in-hospital mortality (ptrend = 0.43), while patients without cancer had decreased mortality over time (ptrend < 0.001). CONCLUSIONS:Among patients admitted for HF-CS, patients with cancer are at increased risk of in-hospital death, thrombotic complications, and major bleeding compared to patients without cancer. Future studies are needed to guide nuanced evaluation and management of this population to improve outcomes.

Heart failure and cancer remain two of the leading causes of morbidity and mortality and the two disease entities are linked in a complex manner. Patients with cancer are at increased risk of cardiovascular complications related to the cancer therapies. The presence of cardiomyopathy or heart failure in a patient with new cancer diagnosis portends a high risk for adverse oncology and cardiovascular outcomes. With the rapid growth of cancer therapies, many of which interfere with cardiovascular homeostasis, heart failure practitioners need to be familiar with prevention, risk stratification, diagnosis, and management strategies in cardio-oncology. This Heart Failure Society of America statement addresses the complexities of heart failure care among patients with active cancer diagnosis and cancer survivors. Risk stratification, monitoring, and management of cardiotoxicity are presented across Stages A through D heart failure, with focused discussion on heart failure preserved ejection fraction and special populations such as survivors of childhood and young adulthood cancers. We provide an overview of the shared risk factors between cancer and heart failure, highlighting heart failure as a form of cardiotoxicity associated with many different cancer therapeutics. Finally, we discuss disparities in the care of patients with cancer and cardiac disease and present a framework for a multidisciplinary team approach and critical collaboration between heart failure, oncology, palliative care, pharmacy, and nursing teams in the management of these complex patients.

The organization of a cardio-oncology clinic and overall program is designed to provide comprehensive cardiovascular care to patients who are at risk of or have developed cardiovascular sequelae during or following cancer treatments. In this article, we summarize the core components of a contemporary cardio-oncology program, including its core members (cardiologists, oncologists, clinical pharmacists, advanced practice providers, nurses, and coordinators), key services (risk assessment, treatment planning, cardiac imaging, intervention, and management), and practical integration within the health care system.

INTRODUCTION/BACKGROUND:Patients with congenital heart disease (CHD) are at increased risk of cancer. In patients with CHD and advanced heart failure, isolated heart transplantation (HT) can be considered. In the overall HT population, immunosuppression after HT increases the risk of post-transplant malignancy (PTM). However, cancer outcomes among adult HT patients with CHD have not been investigated. METHODS:Patients aged ≥ 18 years who received HT between January 1, 2010 and December 31, 2021 were identified using the United Network for Organ Sharing (UNOS) registry. Patients with CHD were compared to those without. T primary outcome was a composite outcome of PTM or death due to malignancy. Multivariable Fine-Gray competing-risk regression was used to estimate the subhazard ratio (SHR) of primary and secondary outcomes. RESULTS:Of the total of 29717 patients with HT were included, 1017 (3.4%) had CHD. Patients with CHD were younger, more likely to be female, and have had prior cardiac surgery. After multivariable competing-risk regression, CHD was associated with a higher risk of the primary outcome (SHR 1.43, 95% CI 1.15-1.80). Among patients who developed PTM, the median time to diagnosis of first PTM (median 36 vs. 46 months, p = 0.027) was shorter in patients with CHD. Among patients with CHD, survival after PTM was significantly lower compared with patients without malignancy (HR 3.32, 95% CI 2.03-5.43). CONCLUSIONS:Among adult patients with HT, CHD was associated with an increased risk of PTM. Further investigation is warranted to identify risk factors and screening strategies for malignancy in this patient population.

Heart failure (HF) in patients with cancer is associated with high morbidity and mortality. The success of cancer therapy has resulted in an exponential rise in the population of cancer survivors, however cardiovascular disease (CVD) is now a major life limiting condition more than 5 years after cancer diagnosis [Sturgeon, Deng, Bluethmann, et al 40(48):3889-3897, 2019]. Prevention and early detection of CVD, including cardiomyopathy (CM) and HF is of paramount importance. The European Society of Cardiology (ESC) published guidelines on Cardio-Oncology (CO) [Lyon, López-Fernández, Couch, et al 43(41):4229-4361, 2022] detailing cardiovascular (CV) risk stratification, prevention, monitoring, diagnosis, and treatment throughout the course and following completion of cancer therapy. Here we utilize a case to summarize aspects of the ESC guideline relevant to HF clinicians, with a focus on risk stratification, early detection, prevention of CM and HF, and the role for guideline directed medical therapy in patients with cancer.

The optimal surveillance and management strategies for breast cancer patients receiving anthracycline therapy are limited by our incomplete understanding of the role of biomarkers heralding the onset of cardiotoxicity. The purpose of this study was to determine whether there is a temporal correlation between cardiac biomarkers and subclinical left ventricular dysfunction in breast cancer patients receiving anthracycline chemotherapy. Thirty-one females between 46 and 55 years old with breast cancer treated with anthracycline chemotherapy were prospectively enrolled. Cardiac biomarkers were correlated with echocardiography with speckle tracking at baseline, post-anthracycline therapy, and 6 months post-anthracycline chemotherapy. Subclinical cardiotoxicity was defined as ≥ 10% reduction in global longitudinal strain (GLS). There was a relative reduction in left ventricular ejection fraction (LVEF) ≥ 10% in 5/30 (17%) and 7/27 (26%) patients post-anthracycline therapy and 6 months post-anthracycline therapy, respectively. Subclinical cardiotoxicity was noted in 8/30 (27%) and 10/26 (38%) patients post-anthracycline and 6 months post-anthracycline therapy, respectively. Baseline N-terminal pro B-type natriuretic peptide (NT-proBNP) was the strongest predictor of LVEF (ρ = -0.45; p = 0.019), with post-therapy NT-proBNP values illustrating similar predictive value (ρ = -0.40; p = 0.038). Interim changes in suppression of tumorigenicity 2 (ST2) and galectin-3 correlated with a 6-month change in LVEF (ρ = -0.48; p = 0.012 and ρ = -0.45; p = 0.018, for ST2 and galectin-3, respectively). Changes in galectin-3 from baseline to mid-therapy paralleled changes in GLS. NT-proBNP, ST2, and galectin-3 correlate with reduced LVEF among breast cancer patients receiving anthracycline therapy. Additional trials focusing on a cardiac biomarker approach may provide guidance in the early diagnosis and management of anthracycline-induced cardiotoxicity.

Amyloidosis is a pathologic and clinical condition resulting from the accumulation of insoluble aggregates of misfolded proteins in tissues. Extracellular deposition of amyloid fibrils in the myocardium leads to cardiac amyloidosis, which is often overlooked as a cause of diastolic heart failure. Although cardiac amyloidosis was previously believed to have a poor prognosis, recent advances in diagnosis and treatment have emphasized the importance of early recognition and changed management of this condition. This article provides an overview of cardiac amyloidosis and summarizes current screening, diagnosis, evaluation, and treatment options.