Breast cancer is the most common malignancy affecting females, with over 260,000 new cases annually and over 3.1 million survivors in the United States alone. Exposure to potentially cardiotoxic therapies, including anthracyclines, trastuzumab, and radiation therapy, coupled with host factors, place patients at increased risk for the development of cardiovascular disease (CVD) compared to non-cancer controls. Overall survival outcomes are significantly worse in patients who develop CVD, and in certain breast cancer populations, cardiovascular death exceeds the risk of cancer death in the long-term. In order to mitigate the risk of CVD, there is a growing interest in the use of cardioprotective strategies at the time of cancer therapy initiation. In this review, we present a detailed evaluation of the evidence from recently completed as well as ongoing cardiooncology clinical trials in pharmacologic cardioprotection in breast cancer patients. We focus primarily on the potential role of dexrazoxane, alterations in anthracycline dosing or formulation, neurohormonal antagonists, beta-blockers, and combination therapy. We also discuss ongoing studies in statin cardioprotection, radiation delivery strategies, use of risk-guided strategies and the study of specific cancer populations. We close with a discussion of the ongoing needs in the field of cardio-oncology in order to advance the clinical care of patients with rigorous, evidence-based medicine.
Introduction Health care demand is increasing due to greater longevity of patients with chronic comorbidities. This increasing demand is occurring in a setting of resource scarcity. To address these changes, high‐value care initiatives, such as telemedicine, are valuable resource‐preservation strategies. This study introduces the Roth score as a telemedicine tool that uses patient counting times to accurately risk‐stratify dyspnea severity in terms of hypoxia. Hypothesis The Roth score has correlation with dyspnea severity. Methods This is a prospective, controlled‐cohort study. Roth score index is measured by having the patient count from 1 to 30 in their native language, in a single breath, as rapidly as possible. The primary result of the Roth score is the duration of time and the highest number reached. Results There was a strongly positive correlation between pulse oximetry and both maximal count achieved in 1 breath (r = 0.67; P < 0.001) and counting time (r = 0.59; P < 0.001). For oxygen saturation <95%, the maximal count number area under the curve is 0.828 and counting time area under the curve is 0.764. Counting time >8 seconds had a sensitivity of 78% and specificity of 73% for pulse oximetry <95%. Conclusions The Roth score has strong correlation with dyspnea severity as determined by hypoxia. This tool is reproducible, low resource‐utilization, and amenable to telemedicine. It is not intended to replace full clinical workup and diagnosis of respiratory distress, but it is useful in risk‐stratifying severity of dyspnea that warrants further clinical evaluation.
Background Glucocorticoid treatment remains the cornerstone of therapy for immune checkpoint inhibitor (ICI) myocarditis, but data supporting the use of additional immunotherapy for steroid refractory cases remains limited. We investigate the safety and efficacy of infliximab in patients with ICI myocarditis who are refractory to corticosteroids. Additionally, we highlight the importance of a multi-disciplinary approach in the care for these complex patients. Methods We retrospectively identified consecutive patients who developed ICI myocarditis at our institution between January 2017 and January 2020. Baseline characteristics, laboratory data and clinical outcomes were compared between patients who received infliximab and those who did not. Results Of a total of 11 patients who developed ICI myocarditis, 4 were treated with infliximab. Aside from age, there were no significant differences in baseline patient characteristics between the two groups including total number of ICI doses received and duration from initial ICI dose to onset of symptoms. The time to troponin normalization was 58 vs. 151.5 days (p = 0.25). The duration of prednisone taper was longer in the infliximab group (90 vs. 150 days p = 0.32). All patients survived initial hospital admission. Over a median follow-up period of 287 days, two of the 4 patients died from sepsis 2 and 3 months after initial treatment of their myocarditis; one of these patients was on a steroid taper and the other patient had just completed a steroid taper. Conclusions Infliximab, despite its black box warning in patients with heart failure, may be a safe and effective treatment for ICI myocarditis.
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