Etiopathologies Associated with Intercostal Muscle Hypermetabolism and Prominent Right Ventricle Visualization on 2-Deoxy-2[F-18]fluoro-d-glucose-Positron Emission Tomography: Significance of an Incidental Finding and in the Setting of a Known Pulmonary Disease

Basu, Sandip; Alzeair, Saad; Li, Geming; Dadparvar, Simin; Alavi, Abass

doi:10.1007/s11307-007-0102-7

Cited by 18 publications

(15 citation statements)

References 3 publications

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“…One study discussed similar findings but used only non-attenuation-corrected PET images, not PET/ CT (16). Another study assessed both obstructive and restric- tive lung diseases (17). Both studies had a smaller sample size, and neither correlated with spirometry.…”

Section: Discussionmentioning

confidence: 99%

Does 18F-FDG Uptake by Respiratory Muscles on PET/CT Correlate with Chronic Obstructive Pulmonary Disease?

Osman¹,

Tran²,

Muzaffar³

et al. 2011

Journal of Nuclear Medicine Technology

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Section: Discussionmentioning

confidence: 99%

Does 18F-FDG Uptake by Respiratory Muscles on PET/CT Correlate with Chronic Obstructive Pulmonary Disease?

Osman¹,

Tran²,

Muzaffar³

et al. 2011

Journal of Nuclear Medicine Technology

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“…A clue to the cause of electrical remodeling in RVH comes from positron emission tomography (PET) studies of small groups of PAH patients. Increased 2-fluoro-2-deoxy-D-glucose (FDG) uptake occurs in the RV in PAH[13, 14]. This suggests the RV may be glycolytic, moreover mild hyperoxia can improve experimental RVH, again suggesting that glucose oxidation may be impaired in RVH[15].…”

Section: Introductionmentioning

confidence: 99%

The inhibition of pyruvate dehydrogenase kinase improves impaired cardiac function and electrical remodeling in two models of right ventricular hypertrophy: resuscitating the hibernating right ventricle

et al. 2009

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Background Right ventricular hypertrophy (RVH) and RV failure contribute to morbidity and mortality in pulmonary arterial hypertension (PAH). The cause of RV dysfunction and the feasibility of therapeutically targeting the RV are uncertain. We hypothesized that RV dysfunction and electrical remodeling in RVH result, in part, from a glycolytic-shift in the myocyte, caused by activation of pyruvate dehydrogenase kinase (PDK). Methods and Results We studied 2 complementary rat models: RVH+PAH (induced by monocrotaline) and RVH+without PAH (induced by pulmonary artery banding, PAB). Monocrotaline-RVH reduced RV O2-consumption and enhanced glycolysis. RV 2-fluoro-2-deoxy-glucose uptake, Glut-1 expression and pyruvate dehydrogenase phosphorylation increased in monocrotaline-RVH. The RV monophasic action potential duration and QTc-interval were prolonged due to decreased expression of repolarizing voltage-gated K+ channels (Kv1.5, Kv4.2). In the RV working-heart model, the PDK inhibitor, dichloroacetate, acutely increased glucose oxidation and cardiac work in monocrotaline-RVH. Chronic dichloroacetate therapy improved RV repolarization and RV function in vivo and in the RV Langendorff model. In PAB-induced RVH, a similar reduction in cardiac output and glycolytic shift occurred and it too improved with dichloroacetate. In PAB-RVH the benefit of dichloroacetate on cardiac output was ~1/3 that in monocrotaline-RVH. The larger effects in monocrotaline-RVH likely reflect dichloroacetate’s dual metabolic benefits in that model: regression of vascular disease and direct effects on the RV. Conclusion Reduction in RV function and electrical remodeling in 2 models of RVH relevant to human disease (PAH and pulmonic stenosis) result, in part, from a PDK-mediated glycolytic shift in the RV. PDK inhibition partially restores RV function and regresses RVH by restoring RV repolarization and enhancing glucose oxidation. Recognition that a PDK-mediated metabolic shift contributes to contractile and ionic dysfunction in RVH offers insight into the pathophysiology and treatment of RVH.

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“…CTalso demonstrated marked dilation of the right ventricle in proportion to the left ventricle and bowing of the interventricular septum, a known secondary sign of elevated right heart pressure (31). An increase in right ventricular myocardial FDG uptake has been described in association with pulmonary arterial hypertension (32)(33)(34). Therefore, the finding of increased right ventricular wall uptake in this patient likely reflects acutely increased pulmonary arterial and right heart pressure because of the massive PE.…”

Section: Discussionmentioning

confidence: 65%

The Incidence of Pulmonary Embolism and Associated FDG-PET Findings in IV Contrast-Enhanced PET/CT

et al. 2014

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Rationale and Objectives: Most fluorine-18 fluorodeoxyglucose (FDG)-positron emission tomography with computed tomography (PET/ CT) studies are performed on cancer patients. These patients are at increased risk of pulmonary embolism (PE). In this retrospective review, we determined the rate of PE, and the prevalence of associated FDG-PET findings on intravenous (IV) contrast-enhanced PET/CT. Materials and Methods:We identified all PET/CT studies performed at our institution with a reported finding of PE between January 2005 and October 2012. The medical record was reviewed for symptoms, which were identified after the diagnosis of PE, and whether the patients received treatment. The prevalence of associated FDG-PET findings was determined.Results: A total of 65 total cases of PE (of 182,72 total PET/CT examinations) were identified of which 59 were previously unknown. This gives an incidental PE (IPE) rate of 0.32%. Of the patients where sufficient clinical information was available, 34 of 36 (94%) were treated either with therapeutic anticoagulation or inferior vena cava filter, and 30 of 36 (83%) were asymptomatic in retrospect. Of the patients with IPE, we found nine (15.2%) with associated focal pulmonary artery hypermetabolism, three (5.1%) with hypermetabolic pulmonary infarction, and one with increased isolated right ventricular FDG uptake (1.7%). One case of chronic PE demonstrated a focal hypometabolic filling defect in a pulmonary artery on PET. Conclusions:We found IPE in 0.32% of PET/CT scans. Focal pulmonary artery hypermetabolism or hypometabolism, and hypermetabolic pulmonary artery infarction with the ''rim sign'' were uncommonly associated with PE. These findings could raise the possibility of IPE in non-IV contrast-enhanced PET/CT studies.

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Etiopathologies Associated with Intercostal Muscle Hypermetabolism and Prominent Right Ventricle Visualization on 2-Deoxy-2[F-18]fluoro-d-glucose-Positron Emission Tomography: Significance of an Incidental Finding and in the Setting of a Known Pulmonary Disease

Cited by 18 publications

References 3 publications

Does 18F-FDG Uptake by Respiratory Muscles on PET/CT Correlate with Chronic Obstructive Pulmonary Disease?

Does 18F-FDG Uptake by Respiratory Muscles on PET/CT Correlate with Chronic Obstructive Pulmonary Disease?

The inhibition of pyruvate dehydrogenase kinase improves impaired cardiac function and electrical remodeling in two models of right ventricular hypertrophy: resuscitating the hibernating right ventricle

The Incidence of Pulmonary Embolism and Associated FDG-PET Findings in IV Contrast-Enhanced PET/CT

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