Ventricular assist device support for children with chemotherapy-induced cardiomyopathy and advanced heart failure: Perspectives gained from a single-center experience.

BACKGROUND: Guidance and data on ventricular assist device (VAD) support for children with chemotherapy-induced cardiomyopathy, particularly within the first 2 years after chemotherapy, are limited. METHODS: We performed a single-center retrospective case series, reviewing medical records of children <18 years of age with chemotherapy-induced cardiomyopathy and advanced heart failure (HF) who received durable VAD support. RESULTS: Six patients met inclusion criteria-5 HeartWare™ HVAD, 1 Berlin Heart EXCOR® . Median age at cancer diagnosis was 6 years (IQR 4.5-10 years). Median dose of anthracycline received was 540 mg/m2 (IQR 450-630 mg/m2 ). All patients developed HF within 1 year after initiation of cancer treatment (median 8 months, IQR 6-11.5 months) and were initiated on durable VAD support at a median of 8 months after completion of cancer treatment (IQR 3.3-43.5 months). Four patients had significant right ventricular dysfunction needing oral pulmonary vasodilator therapy, one patient had a major bleeding complication, and two patients had thromboembolic strokes while on VAD support. Median duration of VAD support was 7.5 months (IQR 3-11.3 months). Two patients underwent VAD explant due to recovery of LV function, one died due to cancer progression, and three underwent heart transplantation. CONCLUSIONS: Durable VAD support should be considered as a therapeutic option for children who have advanced HF due to chemotherapy-induced cardiomyopathy, even within 2 years of completing cancer treatment. A multi-disciplinary approach is essential for appropriate patient selection prior to implant and to ensure comprehensive care throughout the duration of VAD support.

Cardiovascular disease in women: insights from magnetic resonance imaging.

The presentation and identification of cardiovascular disease in women pose unique diagnostic challenges compared to men, and underrecognized conditions in this patient population may lead to clinical mismanagement.This article reviews the sex differences in cardiovascular disease, explores the diagnostic and prognostic role of cardiovascular magnetic resonance (CMR) in the spectrum of cardiovascular disorders in women, and proposes the added value of CMR compared to other imaging modalities. In addition, this article specifically reviews the role of CMR in cardiovascular diseases occurring more frequently or exclusively in female patients, including Takotsubo cardiomyopathy, connective tissue disorders, primary pulmonary arterial hypertension and peripartum cardiomyopathy. Gaps in knowledge and opportunities for further investigation of sex-specific cardiovascular differences by CMR are also highlighted.

Proteasome Inhibitor-Related Cardiotoxicity: Mechanisms, Diagnosis, and Management.

PURPOSE OF REVIEW: Multiple myeloma is the second most common hematologic malignancy in the USA, with over 32,000 new cases and nearly 13,000 deaths expected in 2019. The past few decades in myeloma research have yielded significant advances, leading to the expansion of novel anti-myeloma agents. This review describes the incidence and mechanisms of cardiotoxicity for the FDA-approved proteasome inhibitors in myeloma and proposes strategies to assess and manage resultant cardiovascular adverse events. RECENT FINDINGS: Proteasome inhibition precipitates protein aggregation and alters transcriptional activation of NF-κB targets which contributes to a pro-apoptotic signaling cascade in myeloma cells. Similar effects in cardiomyocytes and vascular smooth muscle endothelium, along with off-target downregulation of autophagy and signaling alterations of nitric oxide homeostasis, may be linked to observed cardiotoxic effects. There is preliminary evidence for cardioprotective potential for rutin, dexrazoxane, and apremilast that could have clinical applicability in the future. Of the proteasome inhibitors used in clinical practice, carfilzomib is the most strongly associated with cardiotoxicity. Patients with anticipated carfilzomib treatment should undergo assessment and optimization of baseline cardiovascular risk, with close monitoring during treatment. Previous clinical trials were not specifically designed to assess proteasome inhibitor-related cardiotoxicity, creating a need for future studies to identify and risk stratify vulnerable individuals and to develop potential cardioprotective strategies in attenuating cardiac injury.

Chemotherapy-induced cardiomyopathy caused by Pemetrexed.

Chemotherapy-related cardiac toxicity is a rare but serious adverse event in patients with cancer. Thus far, no case of serious cardiac toxicity of pemetrexed has been reported. We describe the case of a patient with advanced lung cancer and cardiomyopathy due to pemetrexed. A 59-year-old woman visited our hospital, and we found abnormal findings on a chest radiograph. She was diagnosed as having stage IV lung adenocarcinoma. Chemotherapy with cisplatin and pemetrexed every 3 weeks was initiated. After four cycles of chemotherapy, maintenance chemotherapy with pemetrexed was administered every 3 weeks. During the seventeenth cycle of pemetrexed, she had shortness of breath in her daily life. A chest radiograph showed an enlarged cardiothoracic ratio (66%), and the transthoracic echocardiogram demonstrated expansion of the left ventricle (diastolic diameter, 67 mm), severe global hypokinesis, and reduced left ventricular ejection fraction (28%). The coronary angiogram showed no coronary constriction. There was no delayed accumulation on the contrast-enhanced cardiac magnetic resonance imaging scan. After right heart catheterization, pathological results of a myocardial biopsy from the ventricular septum indicated no cardiac muscle hypertrophy, cardiac fibrosis, inflammatory cell infiltration, or myocyte disarray. Eventually, she was diagnosed as having pemetrexed-induced cardiomyopathy. Pemetrexed was discontinued, and furosemide, enalapril, and carvedilol were started. Then her symptoms and cardiac function improved. Early detection and discontinuation of causative agents are the most important treatment strategies in similar patients. Diuretics, angiotensin-conversion enzyme inhibitors, and beta-blockers may be effective for treating heart failure.

Pharmacogenetics of Chemotherapy-Induced Cardiotoxicity.

PURPOSE OF REVIEW: The goal of this review is to summarize current understanding of pharmacogenetics and pharmacogenomics in chemotherapy-induced cardiotoxicity. RECENT FINDINGS: Most of the studies rely on in vitro cytotoxic assays. There have been several smaller scale candidate gene approaches and a handful of genome-wide studies linking genetic variation to susceptibility to chemotherapy-induced cardiotoxicity. Currently, pharmacogenomic testing of all childhood cancer patients with an indication for doxorubicin or daunorubicin therapy for RARG rs2229774, SLC28A3 rs7853758, and UGT1A6*4 rs17863783 variants is recommended. There is no recommendation regarding testing in adults. There is clear evidence pointing to the role of pharmacogenetics and pharmacogenomics in cardiotoxicity susceptibility to chemotherapeutic agents. Larger scale studies are needed to further identify susceptibility markers and to develop pharmacogenomics-based risk profiling to improve quality of life and life expectancy in cancer survivors.

Case report and review of the literature: the utilisation of a ventricular assist device as bridge to recovery for anthracycline-induced ventricular dysfunction.

Ventricular assist devices are used in children with heart failure as a bridge to myocardial recovery or cardiac transplantation. Anthracyclines cause cardiac toxicity and may result in acute or long-term cardiac failure. We describe the use of a ventricular assist device as a bridge to recovery in a child with severe acute anthracycline-induced cardiomyopathy, and we review the associated literature. A 6-year-old girl was treated for acute myeloblastic leukaemia with daunorubicin and mitoxantrone. After 2 weeks her final dose of chemotherapy, her Left Ventricular Ejection Fraction decreased to 21%. Despite initiation of medical therapy, she had continued deterioration of left ventricular function and developed evidence of poor end-organ perfusion. She was not a candidate for cardiac transplantation, as the post-transplant immune suppression therapy would put her at risk for recurrence of her malignancy. We placed her on a short-term ventricular assist device as a bridge to ultimately placing her on a long-term ventricular assist device versus continuing medical therapy. Her left ventricular ejection fraction improved to 55% 24 days after ventricular assist device insertion. She was separated from the ventricular assist device 26 days after its insertion. She was discharged home 29 days later and is now 28 months after ventricular assist device implantation with stable ventricular function, as documented by a left ventricular ejection fraction of 55%, and normal end organ function. This case is one of the only reports known describing successful use of a short-term ventricular assist device as a bridge to recovery in a child with severe acute anthracycline-induced cardiotoxicity.

Management of Cancer Therapeutics-Related Cardiac Dysfunction.

Improvements in detection and treatment of cancer have resulted in a significant increase in cancer survivors. However, cancer survivorship comes with long-term risk of adverse effects of cancer therapies, including cardiomyopathy, heart failure, arrhythmias, ischemic heart disease, atherosclerosis, thrombosis, and hypertension. There is a renewed interest in understanding the pathophysiology of cancer therapeuticserelated cardiac dysfunction. In recent years, efforts have been directed to the management of cancer therapeuticserelated cardiac dysfunction. This article discusses the pathophysiology and molecular mechanisms that contribute to cancer therapeutics-related cardiac dysfunction and presents an napproach to the evaluation and treatment of these patients.

Cancer recurrence and mortality after pediatric heart transplantation for anthracycline cardiomyopathy: A report from the Pediatric Heart Transplant Study (PHTS) group.

We aimed to determine whether malignancy after pediatric HTx for ACM affects overall post-HTx survival. Patients <18y listed for HTx for ACM in the PHTS database between 1993 and 2014 were compared to those with DCM. A 2:1 matched DCM cohort was also compared. Wait-list and post-HTx survival, along with freedom from common HTx complications, were compared. Eighty subjects were listed due to ACM, whereas 1985 were listed for DCM. Although wait-list survival was higher in the ACM group, post-HTx survival was lower for the ACM cohort. Neither difference persisted in the matched cohort analysis. Primary cause of death in the ACM group was infection, which was higher than the DCM group. Malignancy rates were not different. All ACM malignancies were due to PTLD without primary cancer recurrence or SMN. Long-term graft survival after pediatric HTx for ACM is no different than for matched DCM peers, nor is there an increased risk of any malignancy. However, risk of infection and death from infection after HTx are higher in the ACM group. Further studies are needed to assess the effects of prior chemotherapy on susceptibility to infection in this group.

Prevention of Chemotherapy Induced Cardiomyopathy.

PURPOSE OF REVIEW: Cardiomyopathy is a significant complication of various cancer treatments and has been best studied in patients receiving anthracyclines and trastuzumab. This paper evaluates strategies to prevent chemotherapy-induced cardiotoxicity. RECENT FINDINGS: Increasing cumulative anthracycline dose, use of ≥2 cardiotoxic therapies, extremes of age, and pre-existing cardiovascular risk factors, or established cardiovascular disease, heighten the risk of developing chemotherapy-induced cardiomyopathy. Continuous rather than bolus anthracycline infusions, liposomal doxorubicin, or concomitant dexrazoxane reduces chemotherapy-induced cardiotoxicity. Treatment with neurohormonal antagonists or statins and exercise training during chemotherapy are promising, but as yet unproven, cardioprotective strategies. Identification of high-risk patients and optimization of their underlying cardiovascular risk factors/disease are essential to prevent cardiotoxicity. In patients requiring high-dose anthracyclines, continuous infusions, liposomal doxorubicin, or dexrazoxane should be considered to mitigate cardiotoxicity. Current data do not support the routine use of neurohormonal antagonists or statins as cardioprotective agents in patients treated with cardiotoxic chemotherapies.

Advanced Heart Failure Therapies for Cancer Therapeutics-Related Cardiac Dysfunction.

End-stage heart failure in cancer survivors may result from cardiotoxic chemotherapy and/or chest radiation and require advanced therapies, including left ventricular assist devices (LVADs) and transplantation. Traditionally, such therapies have been underutilized in cancer survivors owing to lack of experience and perceived risk of cancer recurrence. Recent data from large registries, however, have shown excellent outcomes of LVADs and transplantation in cancer survivors, albeit subject to careful selection and special considerations. This article summarizes all aspects of advanced heart failure therapies in patients with cancer therapy-related cardiac dysfunction and underscores the need for careful selection of these candidates.

Heart Failure Therapies for End-Stage Chemotherapy-Induced Cardiomyopathy.

With ongoing advancements in cancer-related treatments, the number of cancer survivors continues to grow globally, with numbers in the United States predicted to reach 18 million by 2020. As a result, it is expected that a greater number of patients will present with chemotherapy-related side effects. One entity in particular, chemotherapy-related cardiomyopathy (CCMP), is a known cardiotoxic manifestation associated with agents such as anthracyclines, trastuzumab, and tyrosine kinase inhibitors. Although such effects have been described in the medical literature for decades, concrete strategies for screening, prevention, and management of CCMP continue to be elusive owing to limited studies. Late recognition of CCMP is associated with a poorer prognosis, including a lack of clinical response to pharmacologic therapy, and end-stage heart failure. A number of advanced cardiac therapies, including cardiac resynchronization therapy, ventricular assist devices, and orthotopic cardiac transplantation, are available to for end-stage heart failure; however, the role of these therapies in CCMP is unclear. In this review, management of end-stage CCMP with the use of advanced therapies and their respective effectiveness are discussed, as well as clinical characteristics of patients undergoing these treatments. The relative paucity of data in this field highlights the importance and need for larger-scale longitudinal studies and long-term registries tracking the outcomes of cancer survivors who have received cardiotoxic cancer therapy to determine the overall incidence of end-stage CCMP, as well as prognostic factors that will ultimately guide such patients toward receiving appropriate end-stage care.

Therapeutic potential of extracellular vesicles derived from cardiac progenitor cells in rodent models of chemotherapy-induced cardiomyopathy.

Background: Current treatments of chemotherapy-induced cardiomyopathy (CCM) are of limited efficacy. We assessed whether repeated intravenous injections of human extracellular vesicles from cardiac progenitor cells (EV-CPC) could represent a new therapeutic option and whether EV manufacturing according to a Good Manufacturing Practices (GMP)-compatible process did not impair their bioactivity. Methods: Immuno-competent mice received intra-peritoneal injections (IP) of doxorubicin (DOX) (4 mg/kg each; cumulative dose: 12 mg/kg) and were then intravenously (IV) injected three times with EV-CPC (total dose: 30 billion). Cardiac function was assessed 9-11 weeks later by cardiac magnetic resonance imaging (CMR) using strain as the primary end point. Then, immuno-competent rats received 5 IP injections of DOX (3 mg/kg each; cumulative dose 15 mg/kg) followed by 3 equal IV injections of GMP-EV (total dose: 100 billion). Cardiac function was assessed by two dimensional-echocardiography. Results: In the chronic mouse model of CCM, DOX + placebo-injected hearts incurred a significant decline in basal (global, epi- and endocardial) circumferential strain compared with sham DOX-untreated mice (p = 0.043, p = 0.042, p = 0.048 respectively) while EV-CPC preserved these indices. Global longitudinal strain followed a similar pattern. In the rat model, IV injections of GMP-EV also preserved left ventricular end-systolic and end-diastolic volumes compared with untreated controls. Conclusions: Intravenously-injected extracellular vesicles derived from CPC have cardio-protective effects which may make them an attractive user-friendly option for the treatment of CCM.

Clinical characterization and natural history of chemotherapy-induced dilated cardiomyopathy.

AIMS: Chemotherapy-induced dilated cardiomyopathy (CI-DCM) is a well-recognized phenotype of non-ischemic dilated cardiomyopathy (DCM), characterized by poor outcomes. However, a detailed comparison between idiopathic DCM (iDCM) and CI-DCM is still lacking. METHODS AND RESULTS: All consecutive DCM patients enrolled in the Trieste Muscle Heart Disease Registry were analysed. CI-DCM and iDCM were defined according to current recommendations. The primary study outcome measure was all-mortality death and secondary outcomes were a) a composite of cardiovascular death/heart-transplantation/ventricular-assist-device implantation, and b) major ventricular arrhythmias. The study included 551 patients (499 iDCM and 52 CI-DCM). At enrolment, compared with iDCM, CI-DCM patients were older (51 ± 14 years vs. 58 ± 3 years, respectively, P < 0.001) and had a higher left ventricular ejection fraction (32% ± 9 vs. 35% ± 10, respectively, P = 0.03). Over a median follow-up of 90 months (IQR 54-140 months), CI-DCM patients had a higher incidence of all-cause mortality compared with iDCM (36.5% vs. 8.4% in CI-DCM and iDCM respectively, P < 0.001), while the incidence of major ventricular arrhythmias was higher in the iDCM group compared with CI-DCM (4% vs. 0%, in CI-DCM and iDCM respectively, P = 0.03). The risk of the composite outcome was comparable between the two groups (P = 0.91). At Cox multivariable analysis, the diagnosis of CI-DCM emerged as independently associated to primary outcome (HR 6.42, 95% C.I. 2.52-16.31, P < 0.001). CONCLUSIONS: In a well-selected DCM cohort, patients with a chemotherapy-induced aetiology had a higher incidence of all-cause mortality compared with iDCM. Conversely, the incidence of life-threatening ventricular arrhythmic events was higher among patients with iDCM.

Management of Advanced Heart Failure in Children with Cancer Therapy-Related Cardiac Dysfunction.

The evolution of cancer therapies has led to marked improvement in survival of those affected by childhood malignancies, while also increasing the recognition of early and late toxicities associated with cancer therapies. Cardiotoxicity can include cardiomyopathy/heart failure, coronary artery disease, stroke, pericardial disease, arrhythmias, and valvular and vascular dysfunction as a result of exposure to chemotherapy and/or radiation. Anthracyclines remain the most common cause of chemotherapy-induced cardiomyopathy (CCM) with varying clinical presentations including: acute, early onset, and late-onset. Many individuals develop cardiac dysfunction over the long-term, ranging from subclinical cardiac dysfunction to end-stage symptomatic heart failure. The focus of this review is on characterization of symptomatic heart failure in children with cancer therapy-related cardiac dysfunction (CTRCD) primarily due to CCM and utilization of advanced heart failure therapies, including ventricular assist device (VAD) support and heart transplantation, with consideration of unique patient-related factors.

Statin Use Can Attenuate the Decline in Left Ventricular Ejection Fraction and the Incidence of Cardiomyopathy in Cardiotoxic Chemotherapy Recipients: A Systematic Review and Meta-Analysis.

There is insufficient evidence about the cardioprotective effects of statins against chemotherapy-induced cardiomyopathy. The MEDLINE and EMBASE databases were searched from inception to March 2021 for studies that reported the mean left ventricular ejection fraction (LVEF) before and after chemotherapy and the incidence of chemotherapy-induced cardiotoxicity in patients who received concurrent statin therapy and those who received chemotherapy alone. A random effects meta-analysis was performed to obtain the pooled weighted mean difference (WMD) and the 95% confidence interval (CI) for the mean final LVEF and the mean LVEF change, and the pooled odds ratio (OR) and the 95% CI of the incidence of chemotherapy-induced cardiomyopathy. Seven studies with 3042 patients were included in this meta-analysis (statin group: 1382 patients received concurrent statin with chemotherapy; control group: 1660 patients received chemotherapy alone). Patients in the control group had a more significant decline in LVEF (WMD = -6.08%, 95% CI: -8.55 to -3.61, p < 0.001) compared to those in the statin group. Additionally, the statin group had a significantly lower incidence of chemotherapy-induced cardiomyopathy compared to the control group (OR = 0.41, 95% CI = 0.28-0.60, p < 0.001). Consequently, our study showed a significant reduction in the incidence of chemotherapy-induced cardiomyopathy and the degree of LVEF decline in patients in the statin group compared to those in the control group.

Incidence and outcomes of cancer treatment-related cardiomyopathy among referrals for advanced heart failure.

BACKGROUND: Approximately 2-3% of patients undergoing advanced heart failure therapies such as left ventricular assist devices (LVAD) and orthotropic heart transplantation (OHT) have chemotherapy-related cardiomyopathy, according to analyses of large databases such as United Network for Organ Sharing (UNOS) or Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) registries. While these studies have shown similar survival outcomes post-interventions, these databases by definition exclude patients referred for advanced therapies but do not receive them, and thus there is little data on overall outcomes of such patients. Given the lack of nuance in the diagnoses in large registries and the possibility that many cancer treatment-related cardiomyopathy (CCMP) patients might be misclassified by the generic "non-ischemic" or "dilated" cardiomyopathies, we investigated the incidence and clinical outcomes of CCMP patients among advanced heart failure (HF) referrals at a single high volume institution. METHODS: All referrals from 2013 to 2016 were evaluated for type of cardiomyopathy, with careful chart review. Outcomes such as LVAD, OHT and death were compared between CCMP and other cardiomyopathies. RESULTS: Of 553 referrals for advanced HF, 19 (3.4%) were for CCMP. There was a higher percentage of patients receiving advanced therapies in the CCMP vs. non-ischemic cardiomyopathy (NICMP) and ischemic cardiomyopathy (ICMP) (42.1% vs 30.2% vs 33.6%, not significant). Of the CCMP patients, 3 had OHT directly, 2 had LVAD followed by OHT, and 3 had LVADs as bridge to candidacy or destination therapy. Fifty-eight percent of the CCMP did not receive LVAD or OHT compared to 69.8% and 66.3 of the NICMP and ICMP, respectively (p = 0.0388). Independent of type of advanced therapy, survival was significantly higher in the CCMP group compared to NICMP and ICMP (93.3% vs 84.8% vs 73.8%, respectively P = 0.0021 for 1 year, 93.3% vs 76.2% vs 58.3%, respectively, P = < 0.0001 for 3 year). CONCLUSIONS: In a single institution, CCMP accounts for more than 3% of all referrals for advanced HF therapies and almost 8% of NICMP. Contrary to concerns for previous cancer and sequelae of cancer treatment excluding patients for advanced therapies, a higher percentage of CCMP underwent advanced HF therapies and with similar outcomes. This is the first study to show that among patients referred for advanced therapies, CCMP patients do not have inferior outcomes compared to other cardiomyopathies regardless of the selected management strategy.

Rates and risk of arrhythmias in cancer survivors with chemotherapy-induced cardiomyopathy compared with patients with other cardiomyopathies.

Objectives: There is little information about arrhythmia burden in cancer survivors with chemotherapy-induced cardiomyopathy (CIC). We hypothesise that the rates and risk of arrhythmias will be similar in CIC when compared with other non-ischaemic cardiomyopathy (NICMO) aetiologies. Methods: We retrospectively identified nine patients with CIC and an implantable defibrillator and 18 age and sex-matched control patients (nine patients with NICMO and nine patients with ischaemic cardiomyopathy (ICMO)). Rates and odds of arrhythmias were calculated by type of cardiomyopathy, adjusting for days since implantable cardioverter defibrillator implantation, history of atrial fibrillation and length of follow-up using logistic regression analysis. Results: Compared with patients with NICMO, rates and adjusted odds were similar for patients with CIC for atrial arrhythmias (44.4% vs 33.3%; adjusted OR=1.89; 95% CI0.17 to 21.03; P=0.61), non-sustained ventricular tachycardia (NSVT) (44.4% vs 33.3%; OR=2.10; 95% CI 0.21 to 20.56; P=0.53), and the combined outcome of NSVT, sustained ventricular tachycardia and/or ventricular fibrillation (44.4% vs 44.4%; OR=2.70; 95% CI 0.25 to 29.48; P=0.42). Conversely, compared with patients with NICMO, patients with ICMO demonstrated higher rates and adjusted odds of the combined outcome (88.9% vs 44.4%; OR=28.60; 95% CI 1.26 to 648.2; P=0.04) and NSVT (77.8% vs 33.3%; OR=8.95; 95% CI 0.90 to 88.94; P=0.06). Conclusions: While tentative based on sample size, rates of arrhythmias in patients with CIC appear to be similar to those experienced by patients with other forms of NICMO.

The Use of Cardiac Resynchronization Therapy in Cancer Patients with Heart Failure.

OBJECTIVES: Investigate the use of cardiac resynchronization therapy (CRT) in cancer patients with heart failure (HF); assess factors associated with ischemic and non-ischemic HF. BACKGROUND: Many newer cancer therapies are cardiotoxic; thus, the incidence of HF has been increasing in this high-risk patient population. CRT has beneficial effects on morbidity, mortality, and left ventricular function in patients with non-ischemic cardiomyopathy, yet cancer patients and survivors who develop severe HF and are eligible for CRT often do not receive it. METHODS: Review of 2 years of echocardiography and electrocardiography data from cancer patients. RESULTS: Of 272 patients meeting inclusion criteria for CRT placement (LVEF ≤35%, QRS duration ≥120 ms), 131 (48.2%) had HF with ischemic etiology and 141 (51.8%) had HF with non-ischemic etiology. Most patients had solid tumors, including breast, lung, sarcoma, and lymphoma (73.2%, n=199). Only 21.3% (58/272; 27 ischemic; 31 non-ischemic) underwent CRT placement, who were mostly women and those with solid tumors. Non-ischemic HF was significantly associated with younger age (<65 years) (OR=0.91; 95% CI=0.87-0.95) and female sex (OR=2.5; 95% CI=1.1-6.0). As expected, ischemic HF was significantly associated with history of myocardial infarction, diabetes, and cardiovascular disease. CONCLUSIONS: CRT is underutilized in cancer patients with HF. Most of the cancer patients who did not receive CRT had non-ischemic HF secondary to chemotherapy. CRT may be less utilized in those patients due to shortened life expectancy, yet evidence suggests that CRT has beneficial effects on morbidity, mortality, and left ventricular function. Its use may improve patient quality of life and allow oncologists to continue cancer treatments that could prolong survival.

The Crossroads of Geriatric Cardiology and Cardio-Oncology.

Cancer and cardiovascular disease (CVD) are two major causes of mortality in older adults. With improved survival and outcomes from cancer and CVD, the role of the geriatrician is evolving. Geriatricians provide key skills to facilitate patient-centered and value-based care in the growing older population of cancer patients (and survivors). Cancer treatment in older adults is particularly injurious with respect to complications stemming from cancer therapy and as well as to CVD related to cancer therapy in the context of physiologic aging. To best meet their natural potential as caregiving leaders, geriatricians must hone skills and insights pertaining to oncologic and cardiovascular care, insights that can inform and enhance key management expertise. In this paper, we will review common chemotherapy and radiation-induced cardiovascular complications, screening recommendations, and advance the concept of a geriatric, cardiology, and oncology collaboration. We assert that geriatricians are well suited to a leadership role in the care of older cardio-oncology patients and in the education of primary care physicians and subspecialists on geriatric principles.