Dr. Fahed earned her medical degree from the American University of Beirut (AUB) in Lebanon. She graduated at the top of her class and was recognized for her outstanding academic achievements and compassionate patient care. Over the course of her medical studies, Dr. Fahed concentrated her research on understanding the pathophysiology behind endothelial dysfunction, hypertension and the metabolic syndrome. As a postdoctoral scholar in the Stanford Cardiovascular Institute, she now focuses on left ventricular diastolic dysfunction and early diagnosis of genetic cardiomyopathy, with a specific focus on transthyretin cardiac amyloidosis, a serious yet often overlooked cause of heart failure. Dr. Fahed aims to devise clinical algorithms to enhance diagnostic care and improve cardiovascular outcomes, while also considering the epidemiological factors at play.
Honors & Awards
Alpha Omega Alpha (AOA) Medical Honor Society, American University of Beirut (2023)
Member at large, Sigma Xi Scientific Research Honor Society (2023)
Gold Humanism Honor Society (GHHS), American University of Beirut (2022)
The Lung Microbiota and Lung Cancer: A Growing Relationship.
2022; 14 (19)
The lung is home to a dynamic microbial population crucial to modulating immune balance. Interest in the role of the lung microbiota in disease pathogenesis and treatment has exponentially increased. In lung cancer, early studies suggested an important role of dysbiosis in tumor initiation and progression. These results have helped accelerate research into the lung microbiota as a potential diagnostic marker and therapeutic target. Microbiota signatures could represent diagnostic biomarkers of early-stage disease. Lung microbiota research is in its infancy with a limited number of studies and only single-center studies with a significant methodological variation. Large, multicenter longitudinal studies are needed to establish the clinical potential of this exciting field.
View details for DOI 10.3390/cancers14194813
View details for PubMedID 36230736
View details for PubMedCentralID PMC9563611
Mechanisms underlying the effects of caloric restriction on hypertension.
2022; 200: 115035
Hypertension is a major risk factor for cardiovascular disease (CVD) as well as a major contributor to all-cause mortality and disability worldwide. The pathophysiology of hypertension is highly attributed to a dysfunctional endothelium and vascular remodeling. Despite the wide use of pharmacological therapies that modulate these pathways, a large percentage of patients continue to have uncontrolled hypertension, and the use of non-pharmacological interventions is increasingly investigated. Among these, caloric restriction (CR) appears to be a promising nutritional intervention for the management of hypertension. However, the mechanisms behind this effect are not yet fully understood, although an evolving view supports a significant impact of CR on vascular structure and function, specifically at the level of vascular endothelial cells, vascular smooth muscle cells along with their extracellular matrix (ECM). Accumulating evidence suggests that CR promotes endothelium-dependent vasodilation through activating eNOS and increasing nitric oxide (NO) levels through multiple cascades involving modulation of oxidative stress, autophagy, and inflammation. Indeed, CR diminishes phenotypic shift, and suppresses proliferation and migration of VSMCs via pathways involving NO and mTOR. By regulating transforming growth factor-β and matrix metalloproteinases, CR appears to reduce ECM and collagen deposition in vascular walls. Here, we offer a detailed discussion of how these mechanisms contribute to CR's influence on reducing blood pressure. Such mechanisms could then provide a valuable foundation on which to base new therapeutic interventions for hypertension.
View details for DOI 10.1016/j.bcp.2022.115035
View details for PubMedID 35427570
Metabolic Syndrome: Updates on Pathophysiology and Management in 2021.
International journal of molecular sciences
2022; 23 (2)
Metabolic syndrome (MetS) forms a cluster of metabolic dysregulations including insulin resistance, atherogenic dyslipidemia, central obesity, and hypertension. The pathogenesis of MetS encompasses multiple genetic and acquired entities that fall under the umbrella of insulin resistance and chronic low-grade inflammation. If left untreated, MetS is significantly associated with an increased risk of developing diabetes and cardiovascular diseases (CVDs). Given that CVDs constitute by far the leading cause of morbidity and mortality worldwide, it has become essential to investigate the role played by MetS in this context to reduce the heavy burden of the disease. As such, and while MetS relatively constitutes a novel clinical entity, the extent of research about the disease has been exponentially growing in the past few decades. However, many aspects of this clinical entity are still not completely understood, and many questions remain unanswered to date. In this review, we provide a historical background and highlight the epidemiology of MetS. We also discuss the current and latest knowledge about the histopathology and pathophysiology of the disease. Finally, we summarize the most recent updates about the management and the prevention of this clinical syndrome.
View details for DOI 10.3390/ijms23020786
View details for PubMedID 35054972
View details for PubMedCentralID PMC8775991
- Analysis of Antiplatelet/Anticoagulant Agents Exposure in Patients With Positive Fecal DNA Test LIPPINCOTT WILLIAMS & WILKINS. 2019: S144-S145
- What Differences Are There Between Early and Delayed Colonoscopy Following a Positive Stool DNA Test? LIPPINCOTT WILLIAMS & WILKINS. 2019: S169
- Colonoscopy Outcome Similarities and Differences Between GI Providers and Non-GI Providers in Patients Who Undergo Colonoscopy Following a Positive Stool DNA Test LIPPINCOTT WILLIAMS & WILKINS. 2019: S167-S168
- Real Life Impact of Physician Awareness of a Positive Stool DNA Test on Subsequent Colonoscopy Outcome in Colorectal Cancer Screening LIPPINCOTT WILLIAMS & WILKINS. 2019: S1561
- Is Stool DNA Test More Specific for Proximal or Distal Neoplasia? LIPPINCOTT WILLIAMS & WILKINS. 2019: S145
Real-Life Experience with More Than 20,000 Stool Dna Tests May Change Your Mind
View details for DOI 10.1016/S0016-5085(19)38978-4