With an aim to highlight the work of promising early-career scientists, the Cardiovascular Research Institute of Vermont (CVRI) held the first annual “Viridis Montis Early Career Investigator Challenge in Cardiovascular Disease” competition on February 5, 2020. Four finalists delivered oral abstract presentations before a panel of five invited judges, including University of Vermont Provost Patty Prelock, Ph.D., and distinguished cardiovascular researchers from the Larner College of Medicine faculty. 

The idea for the new merit-based scientific abstract competition was developed by the CVRI Early Career Advisory Committee. 

“Knowing that competition brings out the best in people, and to make it more fun, the committee opted for this challenge format,” said Sherrie Khadanga, M.D., chair of the CVRI Early Career Advisory Committee, assistant professor of medicine, and assistant director of the Cardiac Rehabilitation Program. 

All early-career cardiovascular investigators were eligible to apply, including Ph.D. and master’s degree students, medical students, postdoctoral fellows, residents and clinical fellows, and faculty within five years of their first appointment. Applications were reviewed by the CVRI Board of Directors and scored using American Heart Association abstract guidelines. According to Khadanga, the board reported that the submissions were highly competitive and selecting the four finalists was a difficult process.

“In addition to highlighting cardiovascular research, the application emphasized a personal and professional commitment to good cardiovascular health and service, which all four research finalists embodied,” said Margaret Infeld, M.D., a cardiology fellow and clinical instructor in medicine who co-organized the event with Jonathan Flyer, M.D., assistant professor of medicine. Infeld and Flyer served as co-moderators at the event, which took place in Davis Auditorium at the UVM Medical Center. 

The winner of the Challenge was Zhaojin "Scarlett" Li, M.S., a Neuroscience Graduate Program doctoral degree student working with Professor of Neurological Sciences Marilyn Cipolla, Ph.D., who presented on “Angiotensin Converting Enzyme Inhibition Reverses Vasoconstriction and Impaired Dilateion of Pial Collaterals During Chronic Hypertension.” This work examined how hypertension – or high blood pressure – impacts constriction in a network of small blood vessels called LMAs that connect the branches of the main arteries in the brain. The study used two rodent models – one hypertensive and one with normal blood pressure – to examine the effects of blood pressure-lowering treatments on LMA vasoconstriction. The findings showed that using an ACE inhibitor during chronic hypertension reversed the vascular dysfunction and hyperconstriction of LMAs, indicating a potential treatment that could improve stroke outcome by increasing blood flow in these collateral vessels. 

Li, who also just received the Stroke Basic Science Award at the International Stroke Conference in Los Angeles, Calif., and her mentor each received a cash prize and recognition plaque. 

Among the other finalists presenting at the February 5 event were Abbie Chapman Johnson, Ph.D., assistant professor of neurological sciences, who discussed “Memory Impairment during Chronic Hypertension is Associated with Hippocampal Hypoperfusion and Hippocampal Vascular Dysfunction.” Johnson’s research focuses on the role of hypertension in cerebrovascular diseases like stroke and vascular cognitive impairment and dementia. While scientists have shown that chronic hypertension can lead to cerebrovascular dysfunction in the brain’s outer tissue layer – the cortex – little is known about its effect on the artery branches that deliver blood to the hippocampus, which is located deep in the brain and is responsible for learning and memory. Hippocampal arterioles (HAs) are critical in ensuring that hippocampal neurons get the energy they need, and if this process is affected by chronic hypertension, it results in too little blood supply to the hippocampus, neuronal dysfunction, and impaired memory. Johnson and her colleagues hypothesized that hippocampal-dependent memory would be impaired during chronic hypertension resulting from reduced hippocampal blood flow and HA dysfunction. Their results showed that hippocampal arteriole dysfunction during chronic hypertension restricts blood flow to the hippocampus that may contribute to memory deficits in a rodent model. She and the research team say this information may indicate a potential therapeutic avenue for limiting vascular cognitive impairment. 

Nga-Ling “Teresa” Ko, Ph.D., assistant professor of obstetrics, gynecology and reproductive sciences, presented her work, titled “Venous Hemodynamics in the Gestational Uterine Vascular Remodeling.” The placenta provides oxygen and nutrients to the fetus during pregnancy. To be successful, the uterine blood vessels must be able to constantly adapt in order maintain normal blood flow. To better understand the mechanisms that drive the uterine blood flow process during pregnancy, Ko and her team developed a novel pregnant rodent model with restricted uteroplacental venous blood flow and compared it to a control model. They measured the proteins that were secreted by the placenta, as well as uterine vessel growth and birth outcomes, and discovered that restricting uteroplacental venous blood flow resulted in the secretion of proteins that are also secreted in preeclampsia, as well as reduced vessel growth, decreased placental efficiency and decreased offspring birthweight.

Kramer Wahlberg, M.D., chief medical resident and clinical instructor in medicine, discussed “Effects of a Higher Heart Rate on Quality of Life and Functional Capacity in patient with Left Ventricular Diastolic Dysfunction.” This study sought to determine if a higher-paced resting heart rate would positively impact quality of life and functional status in a group of patients who have diastolic dysfunction and/or heart failure with preserved ejection fraction, a type of heart failure that has no evidence-based treatment. The research involved 22 patients with diastolic dysfunction – a stiffening of the left ventricle’s pump function, which causes shortness of breath, weakness, and other symptoms – and a pre-existing pacemaker, with the lower resting rate of pacemakers typically set at a low rate of 60 beats per minute. Wahlberg and his colleagues assessed quality of life, function, and a biomarker blood test that is elevated in heart failure over a four-week period during which they increased the participants’ pacemaker lower heart rate setting to 80 beats per minute. After four weeks at a higher lower-rate setting, they observed improvement in heart failure symptoms and functional status in all patients, as well as an improvement in the heart failure biomarker for a specific group of patients. After returning the lower-rate setting to the participants’ baseline, they observed a reversal in the changes in symptoms and biomarker that had been observed after being paced at the higher rate.

Learn more about the CVRI.