The Sam Laboratory investigates mechanisms that mediate heart failure in cardiac diseases and cardiomyopathies.

Our research is mechanistically centered on how the heart remodels in cardiac hypertrophy, hypertension and heart failure.  We study mechanisms that mediate HFpEF (heart failure with preserved ejection fraction, previously known as “diastolic heart failure”) and “HFrEF” (heart failure with reduced ejection fraction, or systolic heart failure).

A major focus of study in our lab is HFpEF since there are no evidence based therapies for these patients to reduce morbidity or mortality. Therapy is relegated to symptom control and management of associated comorbidities. Yet the prevalence of HFpEF continues to increase worldwide. HFpEF is a clinical disease characterized by the inability of the heart to fill with blood because it is thick or stiff.  Risk factors and comorbidities (such as hypertension, obesity, atrial fibrillation, aging etc) are associated with HFpEF but the pathophysiological mechanisms underlying HFpEF remain uncertain. We are exploring the role of inter-tissue communications, including inflammatory cells-heart, and adipose tissue-heart crosstalk, in HFpEF.

We are also investigating the role of the matrix in human subjects with cardiac amyloid and scleroderma who often present with heart failure which resembles HFpEF.



  • Andreaa Bujor, MD  (BU)
  • Gheorghe Doros, PhD (BU)
  • Matthias Nahrendorf, MD PhD (MGH)
  • David R. Pimental, MD (BU)
  • Philipp Scherer, PhD (UT Southwestern)