Kerryn Reding
Progression to heart failure (HF) after breast cancer is a substantial cause of morbidity and mortality. One feature of this is progression to Stage C HF, of which a predominant symptom is reduced exercise capacity.… Diminished exercise capacity, manifesting as shortness of breath, in those receiving treatment for breast cancer is prevalent (occurs in 1/3 of women), contributes to reduced quality of life, threatens to offset recent improvement in cancer related survival, and has an unclear relationship to body composition due to limitations of prior research study designs. To date, research into the etiology of reduced exercise capacity among BCa survivors has focused on the role of cardiac changes, e.g., left ventricular (LV) dysfunction, because of the known association between anthracycline chemotherapy and reductions in LV ejection fraction. The role of body fat has mostly been examined via body mass index (BMI), but results inconsistently predict diminished exercise capacity and LV ejection fractions (LVEF) declines. This may be due to the inability of BMI to distinguish body fat depots that do or do not associate with decreased exercise capacity. Recently in 2 studies, our team showed that central adiposity (specifically, elevated intraperitoneal [IP] fat) and fat accumulating within SM (i.e., intermuscular fat [IMF]) were associated with progression to HF, including demonstration of associations with reduced exercise capacity, fatigue, LV dysfunction, and HF symptoms (including dyspnea and exertional limitations) among women treated for breast cancer. Interestingly, in these studies, we did not observe associations between these events and BMI or subcutaneous (SQ) fat. These observations raise the possibility that excess fat accumulation within IMF and IP depots (which incidentally are modifiable) contribute to diminished exercise capacity experienced by women treated for breast cancer.
