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Mitochondrial cytopathies and cardiovascular disease
  1. Elizabeth A Dominic1,
  2. Ali Ramezani1,
  3. Stefan D Anker2,
  4. Mukesh Verma3,
  5. Nehal Mehta4,
  6. Madhumathi Rao5
  1. 1The George Washington School of Medicine, Washington, District of Columbia, USA
  2. 2Applied Cachexia Research, Department of Cardiology, CharitÃ, Campus Virchow-Klinikum, Augustenburger Platz 1, Berlin, Germany
  3. 3Division of Cancer Control and Population Sciences, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, Maryland, USA
  4. 4Section of Inflammation and Cardiometabolic Diseases, National Heart, Lung and Blood Institute, Bethesda, Maryland, USA
  5. 5Department of medicine, Tufts University School of Medicine, Boston, Massachusetts, USA
  1. Correspondence to Dr Ali Ramezani, The George Washington University, Department of Medicine, 2300 I St., NW, Washington, DC 20037, USA; Ramezani{at}


The global epidemic of cardiovascular disease remains the leading cause of death in the USA and across the world. Functional and structural integrity of mitochondria are essential for the physiological function of the cardiovascular system. The metabolic adaptation observed in normal heart is lost in the failing myocardium, which becomes progressively energy depleted leading to impaired myocardial contraction and relaxation. Uncoupling of electron transfer from ATP synthesis leads to excess generation of reactive species, leading to widespread cellular injury and cardiovascular disease. Accumulation of mitochondrial DNA mutation has been linked to ischaemic heart disease, cardiomyopathy and atherosclerotic vascular disease. Mitochondria are known to regulate apoptotic and autophagic pathways that have been shown to play an important role in the development of cardiomyopathy and atherosclerosis. A number of pharmacological and non-pharmacological treatment options have been explored in the management of mitochondrial diseases with variable success.

  • Heart Failure
  • Coronary Artery Disease

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