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Percutaneous Coronary Intervention vs Coronary Artery Bypass Grafting in Patients With Left Main Coronary Artery Stenosis: A Systematic Review and Meta-analysis Transcatheter Aortic Valve Replacement in Low-risk Patients With Bicuspid Aortic Valve Stenosis Aortic Valve Stenosis Treatment Disparities in the Underserved JACC Council Perspectives Usefulness of minimum stent cross sectional area as a predictor of angiographic restenosis after primary percutaneous coronary intervention in acute myocardial infarction (from the HORIZONS-AMI Trial IVUS substudy) Coronary artery imaging with intravascular high-frequency ultrasound Dual Antiplatelet Therapy Duration: Reconciling the Inconsistencies Operator Experience and Outcomes After Left Main Percutaneous Coronary Intervention Simple Electrocardiographic Measures Improve Sudden Arrhythmic Death Prediction in Coronary Disease Antithrombotic Therapy for Atherosclerotic Cardiovascular Disease Risk Mitigation in Patients With Coronary Artery Disease and Diabetes Mellitus Clinical Impact of Valvular Heart Disease in Elderly Patients Admitted for Acute Coronary Syndrome: Insights From the Elderly-ACS 2 Study
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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.

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