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Giselle C. Meléndez

Researcher at Wake Forest University

Publications -  24
Citations -  721

Giselle C. Meléndez is an academic researcher from Wake Forest University. The author has contributed to research in topics: Ejection fraction & Heart failure. The author has an hindex of 10, co-authored 24 publications receiving 531 citations.

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Timing hypothesis for postmenopausal hormone therapy: its origin, current status, and future.

TL;DR: Evidence indicating that estrogens administered in the perimenopausal transition or early in menopause are not harmful to the cardiovascular system and, when given for a few years for the treatment of menopausal symptoms, may slow the progression of atherosclerosis and reduce the postmenopausal cardiovascular disease burden seems convincing.
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Anthracycline-Associated T1 Mapping Characteristics Are Elevated Independent of the Presence of Cardiovascular Comorbidities in Cancer Survivors.

TL;DR: Three years after anthracycline-based chemotherapy, elevations in myocardial T1 and ECV occur independent of underlying cancer or cardiovascular comorbidities, suggesting that imaging biomarkers of interstitial fibrosis in cancer survivors are related to prior receipt of a potentially cardiotoxic cancer treatment regimen.
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Left Ventricular Mass Change After Anthracycline Chemotherapy.

TL;DR: Early after Anth-bC, LV mass reductions associate with worsening HF symptomatology independent of LVEF, suggesting an alternative mechanism whereby anthracyclines may contribute to HF symptom atology and raising the possibility that surveillance strategies during Anth- bC should also assess LV mass.
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Automated assessments of circumferential strain from cine CMR correlate with LVEF declines in cancer patients early after receipt of cardio-toxic chemotherapy

TL;DR: These cine derived measures of circumferential strain correlate with early subclinical declines in LVEF, and can be obtained in 6¾ minutes from cine bSSFP LV short-axis images in 98.6% of patients receiving treatment for cancer with potentially cardio-toxic chemotherapy.
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Doxorubicin-Induced Myocardial Fibrosis Involves the Neurokinin-1 Receptor and Direct Effects on Cardiac Fibroblasts

TL;DR: It is demonstrated that cardiac fibrosis induced by Anth-bC can be reduced by NK-1R blockade, and the residual fibrotic response is likely due to direct Dox effects on cardiac fibroblasts to produce collagen.