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Purpose Cardiotoxicity affects 5–16% of cancer patients who receive anthracyclines and/or trastuzumab. Limited research has examined interventions to mitigate cardiotoxicity. We examined the role of statins in mitigating cardiotoxicity by performing a systematic review and meta-analysis of published studies. Methods A literature search was conducted using PubMed, Embase, Web of Science, ClinicalTrials.gov, and Cochrane Central. A random-effect model was used to assess summary relative risks (RR), weighted mean differences (WMD), and corresponding 95% confidence intervals. Testing for heterogeneity between the studies was performed using Cochran’s Q test and the I 2 test. Results Two randomized controlled trials (RCTs) with a total of 117 patients and four observational cohort studies with a total of 813 patients contributed to the analysis. Pooled results indicate significant mitigation of cardiotoxicity after anthracycline and/or trastuzumab exposure among statin users in cohort studies [RR = 0.46, 95% CI (0.27–0.78), p  = 0.004, I 2  = 0.0%] and a non-significant decrease in cardiotoxicity risk among statin users in RCTs [RR = 0.49, 95% CI (0.17–1.45), p  = 0.20, I 2  = 5.6%]. Those who used statins were also significantly more likely to maintain left ventricular ejection fraction compared to baseline after anthracycline and/or trastuzumab therapy in both cohort studies [weighted mean difference (WMD) = 6.14%, 95% CI (2.75–9.52), p  < 0.001, I 2  = 74.7%] and RCTs [WMD = 6.25%, 95% CI (0.82–11.68, p  = 0.024, I 2  = 80.9%]. We were unable to explore publication bias due to the small number of studies. Conclusion This meta-analysis suggests that there is an association between statin use and decreased risk of cardiotoxicity after anthracycline and/or trastuzumab exposure. Larger well-conducted RCTs are needed to determine whether statins decrease risk of cardiotoxicity from anthracyclines and/or trastuzumab. Trial Registration Number and Date of Registration PROSPERO: CRD42020140352 on 7/6/2020.

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. Summary 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.

BackgroundThere are limited data on the occurrence, associations and outcomes of pericardial effusions and pericarditis on or after treatment with immune checkpoint inhibitors (ICIs).MethodsThis was a retrospective study at a single academic center that compared 2842 consecutive patients who received ICIs with 2699 age- and cancer-type matched patients with metastatic disease who did not receive ICI. A pericardial event was defined as a composite outcome of pericarditis and new or worsening moderate or large pericardial effusion. The endpoints were obtained through chart review and were blindly adjudicated. To identify risk factors associated with a pericardial event, we compared patients who developed an event on an ICI with patients treated with an ICI who did not develop a pericardial event. Cox proportional-hazard model and logistical regression analysis were performed to study the association between ICI use and pericardial disease as well as pericardial disease and mortality. An additional 6-week landmark analysis was performed to account for lead-time bias.ResultsThere were 42 pericardial events in the patients treated with ICI (n=2842) over 193 days (IQR: 64–411), yielding an incidence rate of 1.57 events per 100 person-years. There was a more than fourfold increase in risk of pericarditis or a pericardial effusion among patients on an ICI compared with controls not treated with ICI after adjusting for potential confounders (HR 4.37, 95% CI 2.09 to 9.14, p<0.001). Patients who developed pericardial disease while on an ICI had a trend for increased all-cause mortality compared with patients who did not develop a pericardial event (HR 1.53, 95% CI 0.99 to 2.36, p=0.05). When comparing those who developed pericardial disease after ICI treatment with those who did not, a higher dose of corticosteroid pre-ICI (>0.7 mg/kg prednisone) was associated with increased risk of pericardial disease (HR 2.56, 95% CI 1.00 to 6.57, p=0.049).ConclusionsICI use was associated with an increased risk of development of pericardial disease among patients with cancer and a pericardial event on an ICI was associated with a trend towards increase in mortality.

A 71-year-old woman with a history of locoregional recurrent breast cancer and a remote and recent history of radiation therapy presented with new, progressive dyspnea on exertion that had developed during the previous week.

Background Cardiotoxicity associated with anthracycline-based chemotherapies has limited their use in patients with preexisting cardiomyopathy or heart failure. Dexrazoxane protects against the cardiotoxic effects of anthracyclines, but in the USA and some European countries, its use had been restricted to adults with advanced breast cancer receiving a cumulative doxorubicin (an anthracycline) dose > 300 mg/m 2 . We evaluated the off-label use of dexrazoxane as a cardioprotectant in adult patients with preexisting cardiomyopathy, undergoing anthracycline chemotherapy. Methods Between July 2015 and June 2017, five consecutive patients, with preexisting, asymptomatic, systolic left ventricular (LV) dysfunction who required anthracycline-based chemotherapy, were concomitantly treated with off-label dexrazoxane, administered 30 min before each anthracycline dose, regardless of cancer type or stage. Demographic, cardiovascular, and cancer-related outcomes were compared to those of three consecutive patients with asymptomatic cardiomyopathy treated earlier at the same hospital without dexrazoxane. Results Mean age of the five dexrazoxane-treated patients and three patients treated without dexrazoxane was 70.6 and 72.6 years, respectively. All five dexrazoxane-treated patients successfully completed their planned chemotherapy (doxorubicin, 280 to 300 mg/m 2 ). With dexrazoxane therapy, changes in LV systolic function were minimal with mean left ventricular ejection fraction (LVEF) decreasing from 39% at baseline to 34% after chemotherapy. None of the dexrazoxane-treated patients experienced symptomatic heart failure or elevated biomarkers (cardiac troponin I or brain natriuretic peptide). Of the three patients treated without dexrazoxane, two received doxorubicin (mean dose, 210 mg/m 2 ), and one received daunorubicin (540 mg/m 2 ). Anthracycline therapy resulted in a marked reduction in LVEF from 42.5% at baseline to 18%. All three developed symptomatic heart failure requiring hospitalization and intravenous diuretic therapy. Two of them died from cardiogenic shock and multi-organ failure. Conclusion The concomitant administration of dexrazoxane in patients with preexisting cardiomyopathy permitted successful delivery of anthracycline-based chemotherapy without cardiac decompensation. Larger prospective trials are warranted to examine the use of dexrazoxane as a cardioprotectant in patients with preexisting cardiomyopathy who require anthracyclines.

Background Though the incidence of atrial fibrillation (AF) is increased in patients with cancer, the effectiveness of catheter ablation (CA) for AF in patients with cancer is not well studied. Methods We conducted a retrospective cohort study of patients who underwent CA for AF. Patients with a history of cancer within 5-years prior to, or those with an exposure to anthracyclines and/or thoracic radiation at any time prior to the index ablation were compared to patients without a history of cancer who underwent AF ablation. The primary outcome was freedom from AF [with or without anti-arrhythmic drugs (AADs), or need for repeat CA at 12-months post-ablation]. Secondary endpoints included freedom from AF at 12 months post-ablation with AADs and without AADs. Safety endpoints included bleeding, pulmonary vein stenosis, stroke, and cardiac tamponade. Multivariable regression analysis was performed to identify independent risk predictors of the primary outcome. Results Among 502 patients included in the study, 251 (50%) had a history of cancer. Freedom from AF at 12 months did not differ between patients with and without cancer (83.3% vs 72.5%, p 0.28). The need for repeat ablation was also similar between groups (20.7% vs 27.5%, p 0.29). Multivariable regression analysis did not identify a history of cancer or cancer-related therapy as independent predictors of recurrent AF after ablation. There was no difference in safety endpoints between groups. Conclusion CA is a safe and effective treatment for AF in patients with a history of cancer and those with exposure to potentially cardiotoxic therapy.

The morbidity and mortality associated with heart failure (HF) represents a significant public health challenge. Stage D HF identifies a distinct subgroup of advanced HF patients characterized by adverse clinical and hemodynamic factors which warrant evaluation for specialized advanced management strategies and/or consideration of palliative care in tandem with the same recommendations for goal-directed optimal medical therapy as earlier stages of HF. In fact, one of the inherent markers of progression to stage D disease is the need to withdraw previously tolerated neurohormonal agents in the setting of systemic circulatory limitations or renal dysfunction. Furthermore, the requirement for aggressive diuresis in the setting of borderline blood pressures and renal insufficiency is often complicated by worsening renal impairment. Assessment of the appropriate need for inotropic support, given the significant complications associated with their use, is also a frequently encountered challenge complicating the medical management of Stage D HF. This review outlines some of the most relevant challenges of pharmacological therapy in stage D HF and describes current and future strategies that may be employed to overcome some of these obstacles.

Purpose of ReviewBreast cancer therapies, such as anthracyclines, trastuzumab, and chest irradiation, have well-established cardiotoxicities that lead to adverse outcomes. Here, we will review strategies to mitigate these cardiotoxicities.Recent FindingsRecent consensus guidelines have established criteria for the identification and surveillance of breast cancer patients at increased risk of cardiotoxicity. Dose reduction, liposomal doxorubicin, and dexrazoxane may be considered in high-risk patients receiving anthracyclines. Anthracycline-free regimens should be considered in high-risk patients with HER-2+ breast cancer, if appropriate. Data to support the routine use of concomitant neurohormonal blockade or statins to prevent anthracycline- and trastuzumab-induced cardiomyopathy is not yet available. Strategies that minimize radiation dose to the heart such as deep inspiration and intensity-modulated radiation are recommended to prevent radiation-induced cardiotoxicity.SummaryIdentification of high-risk patients, aggressive management of underlying cardiovascular risk factors, consideration of cardioprotective strategies, and routine surveillance of left ventricular function before and after therapy are recommended to reduce breast cancer treatment-associated cardiotoxicities.