Peter Libby works in General / Preventive / Lipids affiliated with Harvard University.
Peter Libby, MD, is a cardiovascular medicine specialist at Brigham and Women’s Hospital and the Mallinckrodt Professor of Medicine at Harvard Medical School. He served as Chief of Cardiovascular Medicine at Brigham and Women’s Hospital from 1998 to 2014. His research focuses on the role of inflammation in atherosclerosis and other vascular diseases.
1,249 pubs · 211,398 cites · h-index 227
MD
University of California, San Diego School of Medicine
1973
BA
University of California, Berkeley
1969
Mallinckrodt Professor of Medicine and Senior Physician
Harvard Medical School / Brigham and Women's Hospital
Chief of Cardiovascular Medicine
Brigham and Women's Hospital · 1998 - 2014
Head of Vascular Medicine and Atherosclerosis Unit
Brigham and Women's Hospital · 1990 - 1997
Consulting Physician
Dana-Farber Cancer Institute
Nilsson et al.review
Hypothesis-generating for anti-oxidized LDL antibodies in coronary inflammation; leaves open clinical efficacy in atherothrombotic disease reduction.
Nature Reviews CardiologyAggarwal et al.Guideline
This International Atherosclerosis Society Consensus Statement outlines the evaluation and management of hypertriglyceridaemia, emphasizing that elevated triglycerides serve as a marker of atherosclerotic risk warranting optimization of modifiable cardiovascular risk factors rather than relying on triglyceride-specific pharmacotherapies to reduce cardiovascular events.
Cardiac Imaging · Harvard University
A calcium score of zero is reassuring, but it does not mean that someone has no risk of a future heart attack. Our study shows that inflammation can reveal risk that calcium scoring alone may miss.
JAMA CardiologyChan et al.
CirculationGupta et al.Original Research
Cardiac Imaging · Boston University
The ancient fight-or-flight responses to injury stimulate immune cell activities that are involved in wound healing. But when the 'wound' is in the heart and caused by atherosclerosis, that increased activity actually accelerates the underlying disease. While most of this work was done in mice, we have hints that something similar may happen in human patients -- for example, we found increased numbers of blood stem cells in the spleens of patients who had died shortly after a heart attack.
NatureDutta et al.
Fang et al.preclinical
Demonstrates that the effects of reduced CCM2 function on atherosclerosis and CAD risk are context- and stage-dependent, shifting from protective in early/baseline states to deleterious in advanced cardiometabolic disease.
JACCLibby et al.Original Research
AtherosclerosisHellinghus et al.Original Research
General / Preventive / Lipids · Brigham and Women's Hospital
Although we believe this expanded indication for statin therapy to be a move in the right direction, it should be noted that this regulatory recommendation was not made on the basis of the trial's prespecified primary endpoint, did not take into account the enrolment criterion in JUPITER that required all participants to have an hsCRP of 2 mg/L or greater, which augmented absolute risk, and does not address most of the patients actually studied.
The LancetRidker et al.
LancetHeusch et al.review
Supports early reperfusion and targeted therapies in CAD and HF; extends mechanistic models to guide future targeted interventions.
General / Preventive / Lipids · Brigham and Women's Hospital
When we designed the main trial, we knew we were going after atherosclerosis and we knew we were going after cancer.
Journal of the American College of CardiologyDonath et al.
JACCPanizzi et al.preclinical
Findings in atherosclerotic mice warrant caution extrapolating to human post-MI care; leaves open whether targeting Ly-6Chi monocytes improves remodeling.
Interventional Cardiology · Boston University
We need to do a better job of phenotyping the artery beyond structure, plaque burden, and fibrous cap thickness.
Journal of the American College of CardiologyJaffer et al.
Small et al.cohort
ASXL1-mutant CHIP was associated with aortic stenosis and calcification; extends prior CHIP observations and leaves IL-1/IL-6 inhibition hypothesis-generating.
JAMA CardiolNordan et al.Cohort Study
Cohort study uncovers an association between loss of chromosome Y and aortic aneurysm risk across anatomical locations, highlighting a potential genetic marker for vascular disease.
CirculationSaba et al.Original Research
CirculationLibbyOriginal Research
CirculationLibbyreview
This historical review traces the paradigm shift in coronary artery disease management from mechanically treating focal luminal stenoses to targeting the underlying inflammatory and biological mechanisms of atherosclerotic plaque destabilization and overall disease burden.
Science Translational MedicineKamineni et al.Original Research
Cohort study reveals links between splenic MRI radiomics and coronary artery disease, highlighting the hematopoietic system's role in cardiovascular risk.
JACCGallone et al.Original Research
This review summarizes recent advances in understanding the residual risk factors for patients following an acute coronary syndrome. It emphasizes the roles of platelets, coagulation, cholesterol, and systemic inflammation in long term secondary prevention. The focus has shifted from single vulnerable plaques toward a more holistic view of the vulnerable patient.
