Since arriving at MGH for my medical residency training in 1999 I have had the privilege of teaching as a chief resident in internal medicine and as a cardiology attending, providing clinical care to patients with a broad range of cardiovascular diseases, and conducting research. As an investigator at MGH I have published over 20 manuscripts in fields ranging from the evaluation of novel therapies for heart failure to mechanisms of exercise intolerance in cardiovascular disease and metabolic response patterns to exercise. I am particularly interested in the role of the lung circulation in mediating exercise intolerance in patients with heart failure. Our team of investigators is also interested in understanding the molecular mechanisms of exercise adaptation through mass spectrometry-based metabolic profiling through several ongoing projects in collaboration with the Broad Institute and Dr. Robert Gerszten. My clinical interests parallel my research interests and focus on improving cardiac performance in patients with a variety of cardiovascular diseases. As a staff member in the recently established Cardiac Performance Program I look forward to offering state of the art cardiopulmonary exercise testing to a broad spectrum of individuals- from patients with heart failure to athletes- in an effort to further understand and improve cardiac performance.
As an investigator I combine my background in biochemistry and metabolomics with physiologic phenotyping of myocardial ischemia and heart failure. I worked with Dr. Marc Semigran to test the hypothesis that selective pulmonary vasodilation with the phosphodiesterase 5 inhibitor, sildenafil, would augment exercise performance in patients with heart failure (HF). We found that both one-time administration of sildenafil and 12-weeks of treatment improved peak VO2 proportionate to pulmonary vasodilation (see Circulation manuscripts, 2007). This work is currently being extended to HF with preserved ejection fraction (HFpEF) in an NIH-Heart Failure Network trial to determine if sildenafil improves peak VO2 in HFpEF. Our group is currently pursuing several other studies using CPx to characterize HF.
In parallel, complimentary work, I have been working at the Broad Institute since 2005 where I helped to establish a >200-component liquid-chromatography mass-spectrometry based platform to measure small molecules in human plasma. This methodology was described in 3 first author publications in 2008-2010, including a manuscript in JCI on metabolic profiling of myocardial injury and a study in Science Translational Medicine describing metabolic changes induced by exercise in more and less fit individuals. My NIH K23 Career Development Award focuses on the application of metabolic profiling to define metabolic signatures of myocardial injury and heart failure. My ultimate goal is to define metabolic signatures of ischemia and heart failure that will guide strategies to redress metabolic derangements.
Please see Pubmed for a complete list
Lewis GD, Shah R, Shahzad K, et al. Sildenafil Improves Exercise Capacity and Quality of Life in Patients with Systolic Heart Failure and Secondary Pulmonary Hypertension. Circulation. 2007.116:1555-1562.
Lewis GD, Gona P, Benjamin EJ, et al. Exercise Blood Pressure and the Risk of Incident Cardiovascular Disease: The Framingham Heart Study. Am J Cardiol 2008, Jun 1;101(11):1614-20
Lewis GD, Shah RV, Systrom DM, et al. Determinants of Ventilatiory Efficiency in Heart Failure. Circulation Heart Failure, 2008; 1: 227-233
Lewis GD, Farrell L, Wood MJ, et al. Metabolic Signatures of Exercise in Human Plasma. Science Translational Medicine. 2010;2(33)
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