scholarly journals Eplerenone prevents an increase in serum carboxy‐terminal propeptide of procollagen type I after myocardial infarction complicated by left ventricular dysfunction and/or heart failure

2020 ◽  
Vol 22 (5) ◽  
pp. 901-903
Author(s):  
Susan Stienen ◽  
João Pedro Ferreira ◽  
Bertram Pitt ◽  
John G. Cleland ◽  
Pierpaolo Pellicori ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Type I ◽  
Procollagen Type ◽  
Procollagen Type I ◽  
Carboxy Terminal

scholarly journals Increased Serum Procollagen Type I C-terminal Propeptide Levels are Associated with Subclinical Left Ventricular Dysfunction in Patients with Breast Cancer Treated with Anthracycline-Based Cancer Chemotherapy

2020 ◽  
Author(s):  
Ana de la Fuente ◽  
Marta Santisteban ◽  
Josep Lupón ◽  
José Manuel Aramendía ◽  
Agnes Díaz ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Chemotherapy ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Troponin T ◽  
Left Ventricular ◽  
Relative Reduction ◽  
Type I ◽  
Procollagen Type ◽  
Procollagen Type I

Abstract Background Anthracycline-based cancer chemotherapy (ACC) has been related to myocardial interstitial fibrosis (MIF), a lesion contributing to left ventricular dysfunction (LVD). We investigated whether biomarker-assessed MIF was associated with LVD in patients with breast cancer receiving ACC and in patients with ACC-induced heart failure (ACC-HF). Moreover, chemotherapy agent’s pro-fibrotic activity was evaluated in human cardiac fibroblasts (HCFs). Methods Echocardiography, serum biomarkers of collagen deposition (procollagen type-I C-terminal-propeptide [PICP]) and crosslinking (collagen type-I C-terminal-telopeptide/matrix metalloproteinase-1 ratio), and biomarkers of myocardial and vascular stress (galectin-3, sST2, amino-terminal pro-brain natriuretic peptide [NT-proBNP], hs-troponin-T and vascular cell adhesion molecule-1 [VCAM-1]) were assessed in 70 breast cancer patients at baseline, and during ACC at 3 and 6 months. Subclinical cardiotoxicity was defined as global longitudinal strain (GLS) relative reduction>15%. In addition, PICP and NT-proBNP were determined in 347 patients with different HF etiologies, 37 with ACC-HF (of whom 65% had been diagnosed with breast cancer) and 12-month-follow-up LVEF assessment. HCFs activation was examined after incubation with doxorubicin, cyclophosphamide, paclitaxel and trastuzumab for 24 hours. Results In patients with breast cancer, six-months-ACC reduced GLS and upregulated PICP, hs-troponin-T, NT-proBNP and VCAM-1 (P<0.01) versus baseline. At 6 months, elevation of PICP was higher in patients with subclinical cardiotoxicity versus the remaining patients (P for interaction<0.001). PICP levels were directly and independently associated with a relative reduction in GLS (P<0.001). In ACC-HF patients, baseline LVEF was inversely associated with PICP and NT-proBNP (P<0.01). After 12 months, LVEF did not change in patients with higher basal PICP (3rd tertile) but improved in the remaining patients (P<0.001). Doxorubicin, cyclophosphamide and trastuzumab stimulated collagen synthesis in HCFs. Conclusion These results indicate that biomarker-assessed MIF associates with early LVD in ACC-treated patients with breast cancer. In addition, these findings suggest that MIF may be associated with established LVD in ACC-HF patients, hindering LV functional improvement after 12 months. Finally, chemotherapy can directly activate collagen metabolism in HCFs.

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