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Revascularization in Patients With Left Main Coronary Artery Disease and Left Ventricular Dysfunction 3-Year Outcomes of the ULTIMATE Trial Comparing Intravascular Ultrasound Versus Angiography-Guided Drug-Eluting Stent Implantation Comparison of inhospital mortality, length of hospitalization, costs, and vascular complications of percutaneous coronary interventions guided by ultrasound versus angiography Contribution of stent underexpansion to recurrence after sirolimus-eluting stent implantation for in-stent restenosis Successful bailout stenting strategy against lethal coronary dissection involving left main bifurcation Criteria for Iron Deficiency in Patients With Heart Failure Transcatheter Aortic Valve Replacement vs Surgical Replacement in Patients With Pure Aortic Insufficiency Genotyping to Guide Clopidogrel Treatment: An In-Depth Analysis of the TAILOR-PCI Trial Longitudinal Assessment of Vascular Function With Sunitinib in Patients With Metastatic Renal Cell Carcinoma Why and How to Measure Aortic Valve Calcification in Patients With Aortic Stenosis
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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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