Peter Libby

General / Preventive / Lipids

Harvard University

About

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.

Research focus

AtherosclerosisInflammation in vascular diseasePreventive cardiologyVascular biologyClonal hematopoiesis of indeterminate potential

Impact

1,249 pubs · 211,398 cites · h-index 227

Training

MD
University of California, San Diego School of Medicine
1973
BA
University of California, Berkeley
1969

Affiliations

Work Experience

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

Publications

Nature Reviews CardiologyAggarwal et al.Guideline

Cardiovascular risk, evaluation and management in patients with hypertriglyceridaemia: a Consensus Statement from the International Atherosclerosis Society

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.

Dr. Kenneth Chan

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.

Assessment of Coronary Inflammatory Risk From Noncontrast Cardiac Computed Tomography

JAMA CardiologyChan et al.Nov 2026

CirculationGupta et al.Original Research

The Scientific Synthesis that Modernized Cardiology: A Perspective on the Formative NIH Years of Dr Eugene Braunwald (1955–1970)

Matthias Nahrendorf

Cardiac Imaging · Boston University

11d

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.

Myocardial infarction accelerates atherosclerosis

NatureDutta et al.Jun 2012

Fang et al.preclinical

CCM2 deficiency shows stage-dependent atherosclerosis effects, reducing early lesions but worsening late-stage disease burden.

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

Seeking the Sweet Spot in Targeting Cardiovascular Inflammation

AtherosclerosisHellinghus et al.Original Research

A Quantitative Model to Estimate Free Il-6 Levels Among Participants Treated With the Il-6 Ligand Inhibitor Ziltivekimab: Implications for the Zeus, Hermes, and Artemis Trials

Paul M Ridker

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.

Reduction in C-reactive protein and LDL cholesterol and cardiovascular event rates after initiation of rosuvastatin: a prospective study of the JUPITER trial

The LancetRidker et al.Mar 2009

LancetHeusch et al.review

Early reperfusion and targeted medical therapies mitigate adverse cardiovascular remodelling in CAD and heart failure.

Supports early reperfusion and targeted therapies in CAD and HF; extends mechanistic models to guide future targeted interventions.

Paul Ridker

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.

Anti-Inflammatory Therapy With Canakinumab for the Prevention and Management of Diabetes

Journal of the American College of CardiologyDonath et al.Mar 2018

JACCPanizzi et al.preclinical

Atherosclerosis drives ~13-fold higher post-MI inflammatory monocytes, worsening infarct healing and LV dilation.

Findings in atherosclerotic mice warrant caution extrapolating to human post-MI care; leaves open whether targeting Ly-6Chi monocytes improves remodeling.

Farouc Jaffer

Interventional Cardiology · Boston University

We need to do a better job of phenotyping the artery beyond structure, plaque burden, and fibrous cap thickness.

Two-Dimensional Intravascular Near-Infrared Fluorescence Molecular Imaging of Inflammation in Atherosclerosis and Stent-Induced Vascular Injury

Journal of the American College of CardiologyJaffer et al.Jun 2011

Small et al.cohort

ASXL1-mutant clonal hematopoiesis linked to incident aortic stenosis and accelerated valvular calcification.

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

Loss of chromosome Y is linked to an increased risk of abdominal aortic aneurysm.

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

Hemorrhage Within Atherosclerotic Plaques: From Binary Marker to Dynamic Process

CirculationLibbyOriginal Research

Current Concepts of the Pathogenesis of the Acute Coronary Syndromes

CirculationLibbyreview

Disease-modifying therapies targeting plaque biology and inflammation substantially reduce acute coronary syndrome events despite producing only modest improvements in coronary luminal caliber.

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

Machine learning–driven spleen imaging and genomics uncover a splenic connection to coronary artery disease

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

A review summarizes evolving medical therapies to address residual risk after an acute coronary syndrome.

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.

JACCForman et al.review

Gerotherapeutics show potential to boost molecular resilience and transform cardiovascular care in older adults.

Geroscience and gerotherapeutics offer a novel paradigm to address age-related molecular damage, potentially transforming the management of cardiovascular disease in older adults with multimorbidity and frailty.

All publications →

About

Peter Libby works in General / Preventive / Lipids affiliated with Harvard University.

Research focus

AtherosclerosisInflammation in vascular diseasePreventive cardiologyVascular biologyClonal hematopoiesis of indeterminate potential

Impact

1,249 pubs · 211,398 cites · h-index 227

Training

MD
University of California, San Diego School of Medicine
1973
BA
University of California, Berkeley
1969

Work Experience

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

Publications

Nature Reviews CardiologyAggarwal et al.Guideline

Cardiovascular risk, evaluation and management in patients with hypertriglyceridaemia: a Consensus Statement from the International Atherosclerosis Society

Dr. Kenneth Chan

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.

Assessment of Coronary Inflammatory Risk From Noncontrast Cardiac Computed Tomography

JAMA CardiologyChan et al.Nov 2026

CirculationGupta et al.Original Research

The Scientific Synthesis that Modernized Cardiology: A Perspective on the Formative NIH Years of Dr Eugene Braunwald (1955–1970)

Matthias Nahrendorf

Cardiac Imaging · Boston University

11d

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.

Myocardial infarction accelerates atherosclerosis

NatureDutta et al.Jun 2012

Fang et al.preclinical

CCM2 deficiency shows stage-dependent atherosclerosis effects, reducing early lesions but worsening late-stage disease burden.

JACCLibby et al.Original Research

Seeking the Sweet Spot in Targeting Cardiovascular Inflammation

AtherosclerosisHellinghus et al.Original Research

A Quantitative Model to Estimate Free Il-6 Levels Among Participants Treated With the Il-6 Ligand Inhibitor Ziltivekimab: Implications for the Zeus, Hermes, and Artemis Trials

Paul M Ridker

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.

Reduction in C-reactive protein and LDL cholesterol and cardiovascular event rates after initiation of rosuvastatin: a prospective study of the JUPITER trial

The LancetRidker et al.Mar 2009

LancetHeusch et al.review

Early reperfusion and targeted medical therapies mitigate adverse cardiovascular remodelling in CAD and heart failure.

Supports early reperfusion and targeted therapies in CAD and HF; extends mechanistic models to guide future targeted interventions.

Paul Ridker

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.

Anti-Inflammatory Therapy With Canakinumab for the Prevention and Management of Diabetes

Journal of the American College of CardiologyDonath et al.Mar 2018

JACCPanizzi et al.preclinical

Atherosclerosis drives ~13-fold higher post-MI inflammatory monocytes, worsening infarct healing and LV dilation.

Findings in atherosclerotic mice warrant caution extrapolating to human post-MI care; leaves open whether targeting Ly-6Chi monocytes improves remodeling.

Farouc Jaffer

Interventional Cardiology · Boston University

We need to do a better job of phenotyping the artery beyond structure, plaque burden, and fibrous cap thickness.

Two-Dimensional Intravascular Near-Infrared Fluorescence Molecular Imaging of Inflammation in Atherosclerosis and Stent-Induced Vascular Injury

Journal of the American College of CardiologyJaffer et al.Jun 2011

Small et al.cohort

Disease-modifying therapies targeting plaque biology and inflammation substantially reduce acute coronary syndrome events despite producing only modest improvements in coronary luminal caliber.

Science Translational MedicineKamineni et al.Original Research