Cardiovascular Concerns, Cancer Treatment, and Biological and Chronological Aging in Cancer: Family Series.

Cardiovascular disease (CVD) and cancer are leading causes of death globally, particularly among the rapidly growing population of older adults (OAs). CVD is a leading cause of mortality among cancer survivors, often accelerated by cancer treatments associated with short- or long-term cardiotoxicity. Moreover, there is a dynamic relationship among CVD, cancer, and aging, characterized by shared risk factors and biological hallmarks, that plays an important role in caring for OAs, optimizing treatment approaches, and developing preventive strategies.

Cardiovascular Toxicities of Radiation Therapy and Recommended Screening and Surveillance.

Radiation therapy is a key part of treatment for many cancers. Vast advancements in the field of radiation oncology have led to a decrease in malignancy-related mortality, which has uncovered some of the long-term side effects of radiation therapy. Specifically, there has been an increase in research looking into the cardiovascular side effects of chest radiation therapy for cancers of the esophagus, breast, and lung tissue as well as lymphomas.

LVAD therapy as a catalyst to heart failure remission and myocardial recovery.

The management of chronic heart failure over the past decade has witnessed tremendous strides in medical optimization and device therapy including the use of left ventricular assist devices (LVAD). What we once thought of as irreversible damage to the myocardium is now demonstrating signs of reverse remodeling and recovery. Myocardial recovery on the structural, molecular, and hemodynamic level is necessary for sufficient recovery to withstand explant and achieve sustained recovery post-LVAD.

Giant ventral hernia following left ventricular assist device bridge to heart transplantation.

Ventral hernias following left ventricular assist device (LVAD) placement are rare. With the improvement in technology, and miniaturization of devices associated with intrapericardial placement, these complications have largely been abolished. The mere presence of a large ventral hernia should not exclude recipients from being candidates for orthotopic heart transplantation.

Special Considerations in the Care of Women With Advanced Heart Failure.

Advanced heart failure (AHF) is associated with increased morbidity and mortality, and greater healthcare utilization. Recognition requires a thorough clinical assessment and appropriate risk stratification. There are persisting inequities in the allocation of AHF therapies.

Identifying Patients With a Higher Potential for Recovery Post Left Ventricular Assist Device: A Single-Center Experience.

Few patients with a left ventricular assist device (LVAD) achieve functional myocardial recovery to the point of LVAD explantation. The aim of this study was to highlight some of the hemodynamic and echocardiographic parameters we observed in patients who recovered. We conducted a retrospective analysis of 7 patients who received the HeartMate II LVAD (Abbott) at Temple Heart and Vascular Institute and subsequently underwent successful explantation following myocardial recovery.

Healthcare disparities in cardio oncology: patients receive same level of surveillance regardless of race at a safety net hospital.

Background: Cardiotoxicity remains a dreaded complication for patients undergoing chemotherapy with human epidermal growth factor (HER)-2 receptor antagonists and anthracyclines. Though many studies have looked at racial disparities in heart failure patients, minimal data is present for the cardio-oncology population.

Methods: We queried the echocardiogram database at a safety net hospital, defined by a high proportion of patients with Medicaid or no insurance, for patients who received HER2 receptor antagonists and/or anthracyclines from January 2016 to December 2018.

Prior β-blocker treatment decreases leukocyte responsiveness to injury.

Following injury, leukocytes are released from hematopoietic organs and migrate to the site of damage to regulate tissue inflammation and repair, however leukocytes lacking β2-adrenergic receptor (β2AR) expression have marked impairments in these processes. β-blockade is a common strategy for the treatment of many cardiovascular etiologies, therefore the objective of our study was to assess the impact of prior β-blocker treatment on baseline leukocyte parameters and their responsiveness to acute injury. In a temporal and βAR isoform-dependent manner, chronic β-blocker infusion increased splenic vascular cell adhesion molecule-1 (VCAM-1) expression and leukocyte accumulation (monocytes/macrophages, mast cells and neutrophils) and decreased chemokine receptor 2 (CCR2) expression, migration of bone marrow cells (BMC) and peripheral blood leukocytes (PBL), as well as infiltration into the heart following acute cardiac injury.

Whole transcriptome microarrays identify long non-coding RNAs associated with cardiac hypertrophy.

Long non-coding RNAs (lncRNAs) have recently emerged as a novel group of non-coding RNAs able to regulate gene expression. While their role in cardiac disease is only starting to be understood, their involvement in cardiac hypertrophy is poorly known. We studied the association between lncRNAs and left ventricular hypertrophy using whole transcriptome microarrays.

Identification of candidate long noncoding RNAs associated with left ventricular hypertrophy.

Purpose: Long noncoding RNAs (lncRNAs) constitute an emerging group of noncoding RNAs, which regulate gene expression. Their role in cardiac disease is poorly known. Here, we investigated the association between lncRNAs and left ventricular hypertrophy.

Cardioprotection of controlled and cardiac-specific over-expression of A(2A)-adenosine receptor in the pressure overload.

Adenosine binds to three G protein-coupled receptors (R) located on the cardiomyocyte (A(1)-R, A(2A)-R and A(3)-R) and provides cardiac protection during both ischemic and load-induced stress. While the role of adenosine receptor-subtypes has been well defined in the setting of ischemia-reperfusion, far less is known regarding their roles in protecting the heart during other forms of cardiac stress. Because of its ability to increase cardiac contractility and heart rate, we hypothesized that enhanced signaling through A(2A)-R would protect the heart during the stress of transverse aortic constriction (TAC).

Effects of cardiac-restricted overexpression of the A(2A) adenosine receptor on adriamycin-induced cardiotoxicity.

Activation of the A(2A) adenosine receptor (A(2A)R) has been shown to be cardioprotective. We hypothesized that A(2A)R overexpression could protect the heart from adriamycin-induced cardiomyopathy. Transgenic (TG) mice overexpressing the A(2A)R and wild-type mice (WT) were injected with adriamycin (5 mg.