Associate Professor of Medicine, Brigham and Women's Hospital
Cardiology
Dr. Jane A. Leopold, MD
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Jane A. Leopold, MD works in the field of Cardiology. He went to medical school at Boston University School of Medicine. Boston University School of Medicine is ranked 30 in research and 52 in primary care medicine He received 2 awards: "Meaningful Use Stage 1 Certification" and "Fellow (FACC)". Jane Leopold is a published doctor and has 54 publications published. The lastest was: 'Elevated pulmonary arterial and systemic plasma aldosterone levels associate with impaired cardiac reserve capacity during exercise in left ventricular systolic heart ...' He is registered with Medicare.
Publications
- Elevated Pulmonary arterial and systemic plasma aldosterone levels associate with impaired cardiac reserve capacity during exercise in left ventricular systolic heart ...
- Antioxidants and Coronary artery disease: from pathophysiology to preventive therapy.
- Characterization of right ventricular remodeling and failure in a Chronic pulmonary hypertension model.
- Multivessel giant coronary artery aneurysms in an adult with an Acute coronary syndrome: latent finding of kawasaki disease.
- The role of the renin-angiotensin-aldosterone system in the pathobiology of Pulmonary arterial hypertension (2013 Grover Conference series).
- Microvascular dysfunction: genetic polymorphisms suggest sex-specific differences in Disease phenotype.
- Cellular and molecular mechanisms of arterial stiffness associated with obesity.
- Systems analysis of oxidant stress in the vasculature.
- Effectiveness of Spironolactone Plus Ambrisentan for Treatment of Pulmonary Arterial Hypertension (from the [ARIES] Study 1 and 2 Trials).
- Therapeutic Efficacy of AAV1.SERCA2a in Monocrotaline-Induced Pulmonary Arterial Hypertension.
- Tumor necrosis factor-α-mediated suppression of dual-specificity phosphatase 4: crosstalk between NFκB and MAPK regulates endothelial cell survival.
- Plasma aldosterone levels are elevated in patients with Pulmonary arterial hypertension in the absence of left ventricular heart failure: a pilot study.
- Bone morphogenetic protein-2 decreases microRNA-30b and microRNA-30c to promote vascular smooth muscle cell calcification.
- Increasing glucose 6-phosphate dehydrogenase activity restores redox balance in vascular endothelial cells exposed to high glucose.
- Aldosterone, mineralocorticoid receptor activation, and cardiovascular remodeling.
- Bone morphogenetic protein-2 activates NADPH oxidase to increase endoplasmic reticulum stress and human Coronary artery smooth muscle cell calcification.
- Glutathione Peroxidase-1 (GPx-1) deficiency augments pro-inflammatory cytokine-induced redox signaling and human endothelial cell activation.
- Glutathione peroxidase-3 deficiency promotes platelet-dependent thrombosis in vivo.
- Equalization of Right- and Left-Sided Intracardiac Pressures: Is it Constriction?
- Viral-derived Serp-1 as an adjunctive therapy for percutaneous Coronary intervention: another not ready for prime time player?
- Redox Pioneer: Professor Joseph Loscalzo.
- Glutathione peroxidase-1 modulates lipopolysaccharide-induced adhesion molecule expression in endothelial cells by altering CD14 expression.
- SERCA2a gene transfer enhances eNOS expression and activity in endothelial cells.
- High glucose inhibits glucose-6-phosphate dehydrogenase, leading to increased oxidative stress and beta-cell apoptosis.
- Aldosterone receptor antagonists: effective but often forgotten.
- Glucose-6-phosphate dehydrogenase-deficient mice have increased renal oxidative stress and increased albuminuria.
- Oxidative risk for atherothrombotic cardiovascular Disease.
- Rapid aldosterone signaling and vascular reactivity: relax or don't do it.
- Glutathione peroxidase-1 regulates mitochondrial function to modulate redox-dependent cellular responses.
- Balancing role of nitric oxide in complement-mediated activation of platelets from mCd59a and mCd59b double-knockout mice.
- Aldosterone increases oxidant stress to impair guanylyl cyclase activity by cysteinyl thiol oxidation in vascular smooth muscle cells.
- Does thrombolytic therapy facilitate or foil primary PCI?
- Oxidative mechanisms and atherothrombotic cardiovascular Disease.
- How to solve three puzzles.
- Human alpha B-crystallin mutation causes oxido-reductive stress and protein aggregation Cardiomyopathy in mice.
- Aldosterone impairs vascular reactivity by decreasing glucose-6-phosphate dehydrogenase activity.
- Vascular calcification: pathobiological mechanisms and clinical implications.
- Small-molecule glycoprotein IIb/IIIa antagonists and bleeding risk in women: too much of a good thing?
- Glucose-6-phosphate dehydrogenase deficiency decreases vascular superoxide and atherosclerotic lesions in apolipoprotein E(-/-) mice.
- Impaired angiogenesis in glutathione peroxidase-1-deficient mice is associated with endothelial progenitor cell dysfunction.
- Xanthine oxidase inhibition and Heart failure: novel therapeutic strategy for ventricular dysfunction?
- Glucose-6 phosphate dehydrogenase deficiency decreases the vascular response to angiotensin II.
- Oxidative enzymopathies and vascular Disease.
- Dual antiplatelet therapy for Coronary stenting: a clear path for a research agenda.
- Increased Myocardial dysfunction after ischemia-reperfusion in mice lacking glucose-6-phosphate dehydrogenase.
- Hypoxia potentiates nitric oxide-mediated apoptosis in endothelial cells via peroxynitrite-induced activation of mitochondria-dependent and -independent pathways.
- Glucose-6-phosphate dehydrogenase modulates vascular endothelial growth factor-mediated angiogenesis.
- Glucose-6-phosphate dehydrogenase modulates cytosolic redox status and contractile phenotype in adult cardiomyocytes.
- Cardiogenic shock caused by right ventricular Infarction: a report from the SHOCK registry.
- Glucose-6-phosphate dehydrogenase overexpression decreases endothelial cell oxidant stress and increases bioavailable nitric oxide.
- Vasoactive substances: nitric oxide and endothelial dysfunction in atherosclerosis.
- Atherothrombosis: plaque instability and thrombogenesis.
- MicroRNAs Regulate Vascular Medial Calcification.
Schools
Boston University School Of Medicine
Beth Israel Hospital
Boston Med Center
Procedures Preformed
- Cardiac Catheterization (incl. Coronary Angiography)
- Cardiac Imaging
- Cardioversion, Elective
- Cardioverter-Defibrillator or Pacemaker Insertion, Removal or Repair
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Conditions Treated
- Angina and Acute Coronary Syndrome
- Aortic Aneurysm
- Aortic Valve Disease
- Arrhythmias (incl. Atrial Fibrillation)
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Doctors Specialties
- Cardiology
- Interventional Cardiology
Accepted Insurances
- Aetna HMO
- Choice Plus POS II
- Blue Card PPO
- BlueConnect HMO
- Blue with Managed Care Behavioral Health HMO
- Preferred Blue PPO
- Cigna HMO
- Great West Healthcare-Cigna PPO
- Commercial Insurance Company
- Fallon Community Health Plan
- First Health (Coventry Health Care) PPO
- Humana
- Medicare MCR
- MultiPlan PPO
- PHCS Network PPO
- Tufts PPO
- Choice Plus POS
- Navigate HMO
- Navigate POS
- Options PPO
Awards
- Meaningful Use Stage 1 Certification
- Fellow (FACC)
Education
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Boston University Medical Center -
Beth Israel Deaconess Medical Center -
Boston University School of Medicine
Hospital
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Brigham and Women's Hospital
Drug Facts
| NPI NUMBER | 1851358162 | |
| NPPES Provider LastName | LEOPOLD | |
| NPPES Provider FirstName | JANE | |
| NPPES Provider ZIPCode | 02115 | |
| NPPES Provider State | MA | |
| Specialty Description | Cardiology | |
| Total Claim Count | 48.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1851358162 |
| Last Name Of The Provider | LEOPOLD |
| First Name Of The Provider | JANE |
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