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Open sesame technique in percutaneous coronary intervention for ST-elevation myocardial infarction From Early Pharmacology to Recent Pharmacology Interventions in Acute Coronary Syndromes Pharmacotherapy in the Management of Anxiety and Pain During Acute Coronary Syndromes and the Risk of Developing Symptoms of Posttraumatic Stress Disorder Epidemiology and Clinical Outcomes of Patients With Inflammatory Bowel Disease Presenting With Acute Coronary Syndrome The Prognostic Significance of Periprocedural Infarction in the Era of Potent Antithrombotic Therapy: The PRAGUE-18 Substudy Transition of Macrophages to Fibroblast-Like Cells in Healing Myocardial Infarction Linking Spontaneous Coronary Artery Dissection, Cervical Artery Dissection, and Fibromuscular Dysplasia: Heart, Brain, and Kidneys Comparative Effectiveness of β-Blocker Use Beyond 3 Years After Myocardial Infarction and Long-Term Outcomes Among Elderly Patients Intensive Care Utilization in Stable Patients With ST-Segment Elevation Myocardial Infarction Treated With Rapid Reperfusion Percutaneous coronary intervention for coronary bifurcation disease: 11th consensus document from the European Bifurcation Club

Clinical Trial2018 Apr-Jun;8(2):2045894018768290.

JOURNAL:Pulm Circ. Article Link

Skeletal muscle mitochondrial oxidative phosphorylation function in idiopathic pulmonary arterial hypertension: in vivo and in vitro study

Sithamparanathan S, Rocha MC, Parikh JD et al. Keywords: exercise; oxygen utilization; peripheral muscle

ABSTRACT


Mitochondrial dysfunction within the pulmonary vessels has been shown to contribute to the pathology of idiopathic pulmonary arterial hypertension (IPAH). We investigated the hypothesis of whether impaired exercise capacity observed in IPAH patients is in part due to primary mitochondrial oxidative phosphorylation (OXPHOS) dysfunction in skeletal muscle. This could lead to potentially new avenues of treatment beyond targeting the pulmonary vessels. Nine clinically stable participants with IPAH underwent cardiopulmonary exercise testing, in vivo and in vitro assessment of mitochondrial function by 31P-magnetic resonance spectroscopy (31P-MRS) and laboratory muscle biopsy analysis. 31P-MRS showed abnormal skeletal muscle bioenergetics with prolonged recovery times of phosphocreatine and abnormal muscle pH handling. Histochemistry and quadruple immunofluorescence performed on muscle biopsies showed normal function and subunit protein abundance of the complexes within the OXPHOS system. Our findings suggest that there is no primary mitochondrial OXPHOS dysfunction but raises the possibility of impaired oxygen delivery to the mitochondria affecting skeletal muscle bioenergetics during exercise.