Donate during COVID-19
Learn more via this medical animation about this minimally-invasive, catheter-based treatment performed to reduce the thickening of the heart muscle, specifically the ventricular septum, for patients with hypertrophic cardiomyopathy (HCM).
CVC physicians Andrew Weintraub, MD, Carey Kimmelstiel, MD and Hassan Rastegar, MD describe this minimally-invasive surgical option for those who have aortic stenosis, or a narrowing of the aortic valve opening.
Guarav Gulati, MD
Cardiology Research Fellow - Class of 2019
"Ever since I was an undergraduate, all my teachers have also been researchers. I have always been drawn to the idea of doing research, but it’s hard to find the motivation if the only time you have for research is at the end of a long workday. I learned the importance of dedicated research time when I was a medical student, when I took a year off to work on several projects related to cardiac and pulmonary physiology. While a resident, I became particularly interested in the physiology and hemodynamics of advanced heart failure. I started working on some projects with Dr. Kiernan as a first and second year fellow, but my productivity was always limited by my busy clinical schedule. I quickly realized that if I wanted to pursue academic medicine seriously, I would need to add two additional features to my fellowship: dedicated time protected from clinical demands to build my research portfolio, and statistical training to give me the skills to carry out my work.
While I was applying for fellowship, I learned about the masters degree program at the Tufts Clinical and Translational Sciences Institute through Dr. Upshaw and Dr. Wessler, both of whom had completed the program while they were cardiology fellows and who are now pursuing careers like the one I want for myself. The masters degree program is a two year program of classwork in statistics and independent research open to post-doctoral applicants interested in academic careers. Early in my second year of fellowship, I worked with my program director, Dr. Huggins, to ensure that it would be possible for me to overlap my third year of fellowship and the first year of the masters program, thereby extending my total fellowship time by one year instead of two. The CTSI also has an NIH-sponsored TL1 grant to provide financial support for a limited number of positions. Applications for the CTSI program and the TL1 grant positions are accepted on a rolling basis, and I was encouraged to submit my application as early as possible. With the support of Dr. Huggins, and the Cardiology department chair, Dr. Udelson, I was fortunate enough to be awarded one of these funded positions.
Once I complete the two year research program, I plan to complete an advanced fellowship in Heart Failure and Transplant Cardiology. Inserting the CTSI program into my training before my AHFTC fellowship year will allow me to generate a cohesive body of work in advanced heart failure and LVAD physiology that I can use to support my application for academic faculty positions. Looking to the future, I plan to use the skills I lean and the research I do in the next two years to position myself to apply for a K-level NIH award so that I can spend the majority of my time as a faculty member researching ways to advance the care of patients with advanced heart failure."
Robert Kung Fellow
Class of 2019
"I received my bachelor’s degree in Biotechnology from the Maharishi Dayanada University, India, moved in 2009 to Germany for master’s in biomedical engineering, and completed masters in March 2011 at the University of Furtwangen, Germany. After completing Masters, I started my graduate studies at Georg August University, Goettingen, Germany. I completed my Ph.D. degree in Molecular Medicine in June 2014 at Georg August University, Goettingen, Germany in the Department of Cardiovascular Physiology on ‘Impact of the oxygen sensors PHD2 and PHD3 for myelo-angiogenic functions’ in the laboratory of Prof Dr. Dörthe Katschinski. I continued working in the same group to complete my studies on ‘Redox Imaging Using Cardiac Myocyte-Specific Transgenic Biosensor Mice’ before moving to USA for my Post-doctoral research studies.
Cardiovascular diseases, including myocardial infarction, cardiac hypertrophy and metabolic heart disease, are associated with changes in the cellular redox status. Ischemia per se and reperfusion induce changes in the cellular redox status. Previous data demonstrates that ischemia/reperfusion not only causes redox stress but also results in activation of specific redox-signaling pathways contributing to pathogenesis. I propose to investigate i) how I/R and redox signaling affect mitochondrial function in heart and ii) to determine ischemia/reperfusion is associated with reactive oxygen species production in cardiomyocytes. Recent advances in generating redox sensitive probes such as redox-sensitive (ro) green fluorescent protein (GFP) 2 in combination with established transgenic mouse models offer new technical opportunities to visualize and measure biological processes in vivo. Using my experience in redox biology and mitochondria, now at Tufts Medical Center as part of my post doctoral research I propose to study the effect of Ischemia Reperfusion on mitochondria redox state and its function in cardiomyocytes in both in-vitro and in-vivo experiments."
Learn more about the Robert Kung IHF Fellowship >
Iris Jaffe, MD, PhD & Navin Kapur, MD
Jan 19: "The Molecular Cardiology Research Institute at Tufts Medical Center: The Impact of 20 Years of Cardiovascular Research"
Marvin Konstam, MD
May 25: "The Future of CV Care: Advanced Technologies, Affordable Care & the Academic Medical Center"
Thomas Deering, MD, MBA
Jun 1: "The Holy Grail of CardioVascular Medicine: Creating Value – Patients, Providers, Processes, Programs"
Roger S. Blumenthal, MD
Jun 15: "The ABC’s of Primary & Secondary Prevention in 2018"
Robert Blanton, Jr., MD is an Assistant Professor, CardioVascular Center, Principal Investigator, Cardiac Biology Research Center, Molecular Cardiology Research Institute; Co-Director, Mouse Physiology Core Laboratory; Tufts Medical Center
The Blanton Lab studies the effect of drugs like Viagra on heart function. Most people have heard of Viagra (generic name sildenafil) and know what it’s used for. But, we now know that Viagra and related drugs can also help the heart, and can keep it from weakening and enlarging too much when stressed. Since heart failure impacts nearly 7 million individuals in the United States alone, identifying new ways to prevent or treat heart failure has broad-reaching implications.
Unfortunately, while drugs like Viagra improve heart failure in lab animals, they have had more mixed results when tested as heart failure treatments for humans. We thought that if we could figure out what Viagra and related drugs actually do to heart muscle cells, then we could identify new clues as to how to treat heart failure. By studying the specific protein that Viagra "turns on," or activates, known as protein kinase G (PKG), our lab has discovered new ways that the heart normally protects itself from weakening (Figure).
The Blanton Laboratory was recently awarded an independent investigator award from the National Institutes of Health (RO1) entitled: Novel Protein Kinase GI Substrates in Cardiac Remodeling and Blood Pressure Control. This NIH RO1 grant will investigate how PKG prevents remodeling of the heart, so that we may find new ways to harness the PKG effect in humans.
The lab will focus on understanding one PKG cooperating molecule we have identified called MLK3, by investigating how MLK3 functions in the heart and the blood vessel to prevent remodeling. The findings from these studies may identify MLK3 as a potential new drug target and could offer novel strategies to target the PKG protective effect in humans with heart failure.
It's time to use a name that is trusted locally and revered nationally.
The one that has been by our side throughout our long journey.
Every person here understands
that we are not just taking care of the child.
We are taking care of the childhood.