Payman Zamani
VerifiedUniversity of Pennsylvania · Rehabilitation Medicine
Active 2006–2026
About
Payman Zamani, MD, MTR, is an Assistant Professor of Medicine in the Department of Cardiovascular Medicine at the Hospital of the University of Pennsylvania. He completed his undergraduate studies at Dartmouth College in 2001, earned his MD from Harvard Medical School in 2007, and obtained a Master of Science of Translational Research from the University of Pennsylvania in 2015. His clinical expertise focuses on heart failure with reduced ejection fraction and heart failure with preserved ejection fraction, as well as exercise physiology. His research interests include exercise and cardiovascular health, with a particular emphasis on innovative imaging methods, biological specimen analysis, and therapeutic interventions in heart failure. Dr. Zamani has contributed to numerous studies exploring the physiological and molecular mechanisms underlying heart failure and exercise tolerance, and his work involves investigating novel diagnostic and treatment strategies for cardiovascular diseases.
Research topics
- Medicine
- Internal medicine
- Cardiology
Selected publications
The Lancet Neurology · 2026-04-17 · 1 citations
articleOpen accessBACKGROUND: precursor supplementation with nicotinamide riboside, which have each shown benefits in animal and early clinical studies, on cardiopulmonary fitness in individuals with Friedreich's ataxia. METHODS: . Stage 1 analysis tested the difference between each active treatment versus the control group, and stage 2 analysis (if combination therapy was effective) tested the difference between combination treatment and exercise alone; family-wise type 1 error was maintained <0·05. Analyses were by intention-to-treat. Adverse events were recorded systematically. This trial is registered with ClinicalTrials.gov (NCT04192136) and is complete. FINDINGS: =0·0299) for nicotinamide riboside and exercise in combination. Combination therapy was not statistically different from exercise alone (difference -0·05 ([95% CI -0·10 to 0·21]; p=0·49). Adverse events were all mild or moderate, and included gastrointestinal symptoms, falls, upper respiratory infections, and skin rashes. At least one moderate adverse event of interest in these categories was reported by seven (41%) participants in the control group; six (35%) in the nicotinamide riboside and no exercise group; three (19%) in the placebo and exercise group; and four (25%) in the nicotinamide plus exercise group. INTERPRETATION: The combination of nicotinamide riboside plus exercise for 12 weeks was safe and increased cardiopulmonary fitness in children and adults with Friedreich's ataxia. Longer studies are needed to establish whether adding nicotinamide riboside to exercise could be considered as part of a long-term, comprehensive treatment approach. FUNDING: US National Institutes of Health and Friedreich's Ataxia Research Alliance.
International Journal of Obesity · 2026-01-09
articleOpen accessAbstract The Physiology Of the WEight Reduced State (POWERS) study is a multi-center NIH-funded clinical trial designed to determine the physiological basis for variability in weight loss maintenance among adults with obesity following participation in a behavioral weight loss program. Two hundred and five healthy adults, aged 25–<60 years, with body mass index 30–<40 kg/m 2 complete up to four serial assessments (before weight loss; after ≥7% weight loss; and four and 12 months later). This report, one in a five-part series on the POWERS study design, provides the rationale for and description of behavioral measures. Standardized laboratory meals are used to measure energy intake and eating-related behaviors. Behavioral and neurocognitive factors related to eating (e.g., food-choice decision making, taste preferences, reward, self-control) are assessed via computer-based tasks and self-report questionnaires. Functional and structural neuroimaging augment the behavioral assessments by identifying underlying neural circuitry. Psychological factors related to weight regulation (e.g., self-monitoring, stigma, self-efficacy) are assessed via self-report questionnaires. Free-living physical activity and sleep are measured via accelerometry, polysomnography and self-report questionnaires. We will evaluate how changes, integrated values and patterns in these predictors and components of energy intake and energy expenditure contribute to individual variability in weight change during the 12 months following weight loss. We anticipate that extensive phenotyping using sophisticated eating behavior paradigms and assessments of critical components of energy expenditure before and after weight loss will lead to improved predictions of successful weight loss maintenance. This, in turn, will inform more effective treatments for long-term sustained weight loss.
UNC Libraries · 2026-01-22
articleOpen accessDephospho-Uncarboxylated Matrix Gla-Protein Is Associated With Adverse Outcomes in Heart Failure
Circulation Heart Failure · 2026-01-28
articleOpen accessBACKGROUND: MGP (matrix Gla-protein), a known inhibitor of vascular calcification, becomes biologically active by vitamin K–dependent carboxylation. Circulating levels of dpucMGP (dephospho-uncarboxylated matrix Gla-protein), the inactive form of MGP, have been associated with large artery stiffening and reduced skeletal muscle mass in heart failure (HF). Whether dpucMGP is related to adverse outcomes in patients with HF is unknown. METHODS: In this cohort study, we measured plasma dpucMGP among 2247 PHFS (Penn HF Study) participants. We examined the relationship between dpucMGP and ≈5000 other proteins (SomaScan assay) to identify biological pathways associated with dpucMGP. We assessed the association between dpucMGP levels and (1) death or HF-related hospital admission; (2) all-cause death. RESULTS: Participants’ median age was 61 years (interquartile range, 53–70 years), 64% were male, and 71% were White. dpucMGP exhibited prominent proteomic associations with acute phase response, coagulation, complement system, fibrosis, cell signaling, and metabolic pathways. Greater dpucMGP was associated with older age, renal dysfunction, and warfarin use, whereas Black ethnicity was associated with lower dpucMGP. Increased dpucMGP levels were associated with an increased risk of death or HF-related hospital admission (standardized hazard ratio, 1.23 [95% CI, 1.17–1.28]; P <0.0001) and all-cause death (standardized hazard ratio, 1.32 [95% CI, 1.25–1.40]; P <0.0001), particularly among participants with nonischemic HF. Associations between dpucMGP and outcomes were dependent on warfarin use, and higher dpucMGP levels were found to mediate the association between warfarin use and adverse outcomes (death [total effect: P =0.005; indirect effect: P <0.001] and death or HF-related hospital admission [total effect: P <0.001; indirect effect: P =0.002]). CONCLUSIONS: Higher dpucMGP is associated with multiple biological pathways and with an increased risk for adverse outcomes in HF. Greater dpucMGP levels mediated the relationship between warfarin use and adverse outcomes. Further studies are required to determine the role of therapeutic interventions to reduce dpucMGP levels in this patient population.
International Journal of Obesity · 2026-02-05
articleOpen accessAbstract The Physiology Of the WEight Reduced State (POWERS) study is a multi-center clinical trial designed to understand the physiological basis for observed variability in weight regain following intentional weight loss among US adults. The primary dependent variable is weight regain over one year following a 7% or greater supervised weight loss. The overarching design and study organization, along with rationale and history of the POWERS study and outcomes measures are described in accompanying papers. This paper provides the rationale for and description of biospecimens samples that will ultimately inform on the molecular and cellular basis of the physiological variability that contributes to the regulation of energy balance in the weight reduced state. Participants will be 205 healthy adults ( n = 205), aged 25–59 years, with body mass index (BMI) 30- ≤ 40 kg/m 2 . Biospecimens will be collected prior to weight loss (baseline, BL), immediately following weight loss via lifestyle intervention (T0), and then four (T4) and twelve (T12) months after weight loss. Blood will be collected in the fasting state and following a meal challenge designed to induce hormones related to satiety. Weight change from T0 to T12 will be the primary outcome variable. Biospecimens to be collected include plasma, serum, peripheral blood mononuclear cells (PBMCs), DNA, urine, feces, adipose and skeletal muscle tissue. All samples will be biobanked at each site. This manuscript describes the rationale for the biospecimens chosen to assess contributors to homeostatic mechanisms that drive observed variability of weight regain after weight loss.
SSRN Electronic Journal · 2025-01-01
preprintOpen accessCirculation Heart Failure · 2025-05-13 · 6 citations
articleOpen accessBACKGROUND: Exercise intolerance is a hallmark of heart failure with preserved ejection fraction (HFpEF) and is characterized by skeletal muscle (SkM) dysfunction with impaired oxidative capacity. To maintain oxidative capacity, the SkM secretes myokines such as musclin, which has been shown to potentiate NP (natriuretic peptide) signaling and induce PGC-1α (peroxisome proliferator-activated receptor-γ coactivator-1 alpha) signaling. We sought to investigate the role of musclin in SkM dysfunction in HFpEF. For this study, we selected the oxidative-predominant SkM soleus in HFpEF mice and vastus lateralis from patients with HFpEF. METHODS: Using the SAUNA model, mice underwent HFpEF induction by uninephrectomy, d-aldosterone infusion, and 1% sodium chloride drinking water for 4 weeks. Exogenous musclin was given to HFpEF mice every 2 days during the last 2 weeks of HFpEF induction. Molecular analyses were conducted on blood samples and SkM from HFpEF mice and patients with HFpEF. RESULTS: In HFpEF mice and patients with HFpEF, increased musclin expression was accompanied by decreased cyclic guanosine monophosphate levels and PGC-1α expression in SkM, suggesting impaired NP signaling. Exogenous administration of musclin in mice with HFpEF demonstrated augmented circulating musclin levels and potentiated NP signaling in SkM as shown by increased PKG1 (protein kinase G1) activity and PGC-1α expression. This was associated with a transition from type-2A to type-1 fiber (type-1 has more endurance) and increased succinate dehydrogenase activity, hindlimb blood flow, and capillary density in the soleus muscle. Exogenous musclin also mitigated cardiac hypertrophy without affecting blood pressure or diastolic function. Most importantly, HFpEF mice treated with musclin demonstrated improved functional and exercise capacity. CONCLUSIONS: Musclin mediates beneficial effects in SkM and heart with improved exercise capacity likely by improving oxidative capacity in SkM. Future studies are warranted to address the therapeutic efficacy of exogenous musclin in humans with HFpEF.
International Journal of Obesity · 2025-09-25 · 1 citations
articleOpen accessIntentional weight loss is often followed by unintentional weight regain. The causes of weight regain are uncertain but may include a myriad of responses that result in increased hunger and decreased energy expenditure. An individual's psychological state and social and physical environments are also thought to influence weight regain in ways that can either support or derail weight loss maintenance. Funded by the National Institutes of Health, the Physiology of the WEight Reduced State (POWERS) study is a multi-center clinical trial aimed at describing the molecular, cellular, physiological, behavioral, environmental and psychosocial factors that may be associated with an individual's ability to maintain their new weight after weight loss. This report provides the rationale for and describes the environmental, psychological and social determinants of health measures used in the POWERS study.
Circulation Heart Failure · 2025-01-20 · 16 citations
articleOpen accessBACKGROUND: Iron deficiency (ID) is currently defined as a serum ferritin level <100 or 100 to 299 ng/mL with transferrin saturation (TSAT) <20%. Serum ferritin and TSAT are currently used to define absolute and functional ID. However, individual markers of iron metabolism may be more informative than current arbitrary definitions of ID. METHODS: We assessed prognostic associations of ferritin, serum iron, and TSAT among 2050 participants with heart failure (HF) with reduced/mid-range (n=1821) or preserved (n=229) left ventricular ejection fraction enrolled in the PHFS (Penn HF Study), a prospective cohort study. We measured 4928 plasma proteins using an aptamer-based assay (SOMAScanv4) and assessed prognostic and proteomic associations of markers of iron metabolism. RESULTS: Ferritin concentrations were not associated with outcomes, whereas low TSAT and serum iron were associated with the risk of all-cause death (TSAT: standardized hazard ratio, 0.84 [95% CI, 0.76–0.93]; P =0.001; serum iron: standardized hazard ratio, 0.87 [95% CI, 0.79–0.96]; P =0.007). Similarly, TSAT was associated with the risk of death or HF-related admission (standardized hazard ratio, 0.89 [95% CI, 0.83–0.95]; P =0.0006). Significant interactions between TSAT and HF with preserved ejection fraction status were found such that TSAT was more strongly associated with the risk of death and death or HF-related admission in HF with preserved ejection fraction. We identified 359 proteins associated with TSAT, including TFRC (transferrin receptor protein; β, −0.455; P <0.0001) and CRP (C-reactive protein; β, −0.355; P <0.0001). Pathway analyses demonstrated associations with lipid metabolism, complement activation, and inflammation. In contrast to the robust associations between TSAT and outcomes, ID and absolute ID defined by current criteria were not associated with death or death or HF-related admission. TSAT was associated with outcomes regardless of the presence of functional versus absolute ID. CONCLUSIONS: Low TSAT, but not ferritin concentrations, is significantly associated with adverse outcomes in HF. Low TSAT is more strongly associated with outcomes in HF with preserved ejection fraction. Pathways related to inflammation and lipid metabolism are associated with low TSAT in HF.
American Journal of Transplantation · 2025-08-01
article
Recent grants
HFpEF: more than just the heart - Why the mitochondria and capillaries matter
NIH · $699k · 2016–2020
Frequent coauthors
- 464 shared
Julio A. Chirinos
University of Pennsylvania
- 340 shared
Raymond R. Townsend
- 309 shared
Patrick Segers
Ghent University Hospital
- 275 shared
Scott Lilly
The Ohio State University
- 273 shared
David R. Jacobs
University of Minnesota
- 272 shared
Daniel Duprez
University of Minnesota
- 271 shared
Richard A. Kronmal
University of Washington
- 270 shared
João A.C. Lima
Johns Hopkins Medicine
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