Abstract
BACKGROUND: Anti-HER2 targeted therapy has significantly reduced the recurrence and death of HER2-overexpressing breast cancer patients, but might lead to cardiotoxicity. Some patients with normal myocardial function may suffer from subclinical myocardial dysfunction after anti-HER2 targeted therapy. We sought to evaluate earlier the subclinical myocardial dysfunction in breast cancer patients after single or dual anti-HER2 targeted therapy, and identify the risk factors related to subclinical myocardiotoxicity. METHODS: In our study, 40 breast cancer patients after single anti-HER2 targeted therapy, and 40 breast cancer patients after dual anti-HER2 targeted therapy were enrolled. Global longitudinal strain (GLS) was measured through echocardiography. RESULTS: Seven patients in single anti-HER2 therapy group and eight patients in dual anti-HER2 therapy group had GLS lower than - 18%, suggesting subclinical myocardial dysfunction, but no difference between these two groups. Furthermore, we found that increased BMI was associated with reduction of GLS in breast cancer patients after anti-HER2 targeted therapy. Increased BMI (OR 2.683; 95% CI 1.225-5.879) was a risk factor of subclinical cardiotoxicity in dual anti-HER2 targeted therapy group. In addition, the patients with BMI ≥ 25 were more prone to have subclinical myocardial dysfunction in dual anti-HER2 therapy group compared with those with BMI ≥ 25 in single anti-HER2 therapy group. CONCLUSION: Our results indicate dual anti-HER2 therapy does not increase the risk of subclinical myocardial dysfunction for breast cancer patients, compared with single anti-HER2 therapy. Patients with BMI ≥ 25 are more prone to have subclinical cardiotoxicity after dual anti-HER2 therapy than after single anti-HER2 therapy. Weight reduction should be the major measure to prevent subclinical myocardial dysfunction for these patients.