Myocardial adaptation and weight fluctuation of seven college wrestlers was examined during a competitive season. Standard M-mode measurements were used to determine left ventricular (LV) end diastolic and end systolic dimensions, fractional shortening, LV diastolic posterior wall thickness (DPW), diastolic interventricular septal thickness (DIVS), and LV mass (LVM) during preseason (test 1) and four months later at the season's end (test 2). The wrestlers' qualifying weights ranged from 53.6 to 80.5 kg and each competed in an average of 17 meets. Systolic and diastolic blood pressure, heart rate, and body weight (BW) were measured at both tests. Daily weight records and qualifying weights were used to calculate seasonal weight fluctuation as a percentage of the highest weight attained between each meet and the wrestler's subsequent qualifying weight. Paired t-tests were used to determine differences between tests 1 and 2. DPW, DIVS and LVM increased from 8.8 +/- 1.0 to 10.3 +/- 1.0 mm, 7.9 +/- 1.5 to 9.9 +/- 0.6 mm, and 171.2 +/- 24.3 to 209.7 +/- 12.9 mm3 respectively while BW declined from 70.3 +/- 9.2 to 67.1 +/- 9.4 (X +/- SD, p < .01) from test 1 to 2. The other variables remained constant across tests. The wrestlers' mean % weight fluctuation throughout the season was 7.5 +/- 1.5 ranging from 4.4 to 9.1%. These findings suggest that significant increases in myocardial mass occur over the course of a competitive wrestling season resulting from increased LV wall thickness. The magnitude and cyclic method of weight loss used by wrestlers does not appear to prevent myocardial hypertrophy.
Background Contemporary patients with heart failure with reduced ejection fraction (HFrEF) are older and have a higher prevalence of cognitive impairment than those studied in trials. The risk/benefit trade‐off of routine beta‐blocker (BB) use in patients with HFrEF and Alzheimer's disease and related dementias (ADRD) has not been explored. This study aimed to determine the association between BB use and outcomes among patients with HFrEF and ADRD. Methods Using a random 40% sample of Medicare Parts A, B, and D data we identified patients with ≥1 hospitalization for HFrEF between 2008 and 2018. Each patient was classified based on BB use prior to admission and after discharge. Outcomes include 90‐day and 1‐year mortality and readmission. Results Between 2008 and 2018, we identified 357,030 patients hospitalized with HFrEF; 12.7% had ADRD. Patients with HFrEF and ADRD had higher 90‐day and 1‐year mortality compared to patients with HFrEF‐only. Among patients admitted on a BB, 60.5% of patients with HFrEF‐only were continued on therapy after discharge, compared to 56.8% of patients with HFrEF and ADRD. Discontinuing BB was associated with a 2.2‐fold higher risk of 90‐day mortality (p < 0.001) among patients with HF‐only and a 2.‐ fold higher risk of 90‐day mortality (p < 0.001) among patients with HFrEF + ADRD. Not starting a BB was associated with a 1.8‐fold higher risk of 90‐day mortality (p < 0.001) among patients with HFrEF‐only and a 1.7‐fold higher risk of 90‐day mortality (p < 0.001) among patients with HFrEF + ADRD. Similar risks were seen at 1 year. Conclusions BB therapy is associated with significantly lower short and long‐term mortality rates among all patients with HFrEF; the magnitude of these associated benefits appear at least as large in patients with HFrEF and ADRD compared to patients with HFrEF‐only.
Background: Immune checkpoint inhibitors (ICIs), including programmed cell death-1 (PD-1), programmed cell death ligand-1 (PD-L1) and cytotoxic lymphocyte antigen-4 (CTLA-4) inhibitors, are increasingly used in treatment of advanced stage cancers due to a well-established mortality benefit. ICI therapy is associated with immune mediated toxicity which may impact any organ system. Cardiovascular toxicities are rare based on existing data, but associated with high mortality rates. Objectives: The aim of this study is to determine whether preexisting cardiac conditions and/or cardiac therapies are associated with an increased or decreased risk of developing cardiotoxicity after ICI exposure. Methods: All patients treated with ICI therapy from March 2011 through October 2019 at our institution were identified. Demographic information, treatment dates, pre-treatment cardiac conditions and comorbidities, cancer types, pre-treatment cardiac biomarkers, and pre-treatment cardio-protective medication use were determined for each patient. New cardiac diagnoses after ICI exposure were identified in the medical record. Multivariate logistic regression was used determine the association between preexisting cardiac conditions and/or cardiac therapies and the development of cardiotoxicity after ICI exposure. Results: There were 902 patients identified with 1071 ICI exposures. The majority of exposures were to a PD-1 inhibitor (70%), with the most common drugs being pembrolizumab (42.8%) and nivolumab (26.5%). Eighty-nine new cardiac diagnoses were coded after initiation of ICI therapy. Sixteen events occurred within 30 days of initial exposure to an ICI and likely represent new cases of immune checkpoint inhibitor associated cardiotoxicity (incidence 1.5%). Of these events, one was confirmed as myocarditis, seven were heart failure without confirmation of myocarditis, three were arrhythmia, one was pericarditis, three were myocardial infarction and one was ventricular tachyarrhythmia/sudden cardiac death, without confirmed myocarditis or heart failure. There was an additional case of myocarditis identified within 90 days of initial exposure to ICI therapy, and a third case identified 115 days following exposure. All three patients who developed myocarditis died, consistent with the known high mortality rate of ICI associated myocarditis. One of the patients who developed myocarditis received pembrolizumab, one nivolumab and one cemiplimab (all PD-1 inhibitors). A history of heart failure increased the odds of developing a cardiac toxicity by 2.3 fold (95% CI 1.4 to 3.3, p<0.001) and prior beta-blocker exposure decreased the odds by 1.8 fold (95% -2.9 to -0.7, p=0.002). Conclusion: A history of heart failure is associated with an increased odds of developing cardiotoxicity after ICI exposure while prior beta blocker exposure appears to be protective.
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