PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 10453404

BMIPP compared with PET metabolism.

E Tadamura·N Tamaki·T Kudoh·N Hattori·J Konishi
View original source ↗Export metadata ↓

Abstract

I-123 15-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid (BMIPP) was introduced as an approved radiopharmaceutical in Japan in 1993. This article reviews our clinical comparisons between BMIPP and PET metabolism conducted at Kyoto University. BMIPP uptake was suggested to reflect exogenous fatty acid utilization in the myocardium. By the comparison between FDG PET and BMIPP SPECT, reduced uptake of BMIPP relative to thallium was considered metabolically damaged but viable myocardium in ischemic coronary artery disease. In hypertrophic cardiomyopathy, reduction of BMIPP uptake was shown to precede suppression of oxidative or glucose metabolism. Occasionally we encounter subjects with absent myocardial BMIPP uptake. The majority of these subjects showed metabolic switching from normal free fatty acid metabolism to abnormally enhanced glucose metabolism in the fasting state. Thus, BMIPP provides us with the valuable metabolic information which is unattainable using a perfusion tracer.

Explore related subjects

CardiomyopathiesFatty AcidsHeartHumansIodine RadioisotopesIodobenzenesMyocardial IschemiaMyocardiumTomography, Emission-ComputedTomography, Emission-Computed, Single-PhotonComparative StudyJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

E Tadamura, N Tamaki, T Kudoh, N Hattori, J Konishi. 1999. BMIPP compared with PET metabolism.. https://doi.org/10.1023/a%3A1006148619691

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2026

Hypertrophic cardiomyopathy: a genome-wide association meta-analysis and polygenic risk score.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is a heritable trait with marked variability in expression and outcomes. Our aims were to discover new genetic loci associated with HCM and to test the effect of a new polygenic risk score (PRS) on incidence, phenotype and outcomes stratified by genotype status. METHODS: A discovery genome-wide association study (GWAS) was performed on 2284 HCM cases and 4525 controls. Two fixed-effects meta-analyses combined our discovery GWAS with single-trait and multi-trait results from a published study. Discovered loci underwent comprehensive bioinformatic analysis including functional and druggability annotations. A PRS using loci from the two meta-analyses was evaluated for association with HCM diagnosis in 411 213 individuals from UK Biobank (UKBB); imaging phenotypes in individuals without HCM; a composite endpoint (including all-cause mortality and transplantation); and sudden cardiac death (SCD) in 1756 HCM cases. PRS analyses were stratified by genotype status. RESULTS: Three loci were found in the discovery GWAS (BAG3, FHOD3 and novel locus PPP1R3A). In the meta-analyses, 70 unique loci were identified, four novel (MYPN, YWHAE, NOS1AP and OBSCN). Bioinformatic analyses identified NOS1AP as a candidate HCM gene. A new PRS was significantly associated with HCM diagnosis (HR=3.19, 95% CI 2.46 to 4.14 for top 5% vs lower 95%; HR=1.88, 95% CI 1.72 to 2.06 per SD increase). Significant associations were found between PRS and greater left ventricular (LV) wall thickness and higher LV ejection fraction in UKBB participants without HCM. Genotype-negative HCM cases in the top 20% of the PRS distribution had an increased risk of SCD (HR=2.72, 95% CI 1.03 to 7.17). CONCLUSIONS: We report novel HCM loci. A new PRS predicted the risk of HCM development and associated imaging characteristics in the UKBB and outcomes in an HCM cohort.

Cardiomyopathies↗
PubMed2024

Integrative omics analysis identifies biomarkers of septic cardiomyopathy.

Septic Cardiomyopathy (SCM) is a syndrome of acute cardiac dysfunction in septic patients, unrelated to cardiac ischemia. Multiomics studies including transcriptomics and proteomics have provided new insights into the mechanisms of SCM. In here, a rat model of SCM was established by intraperitoneal injection of lipopolysaccharide (LPS). Biomarkers of SCM were characterized via a multi-omics analysis. The differentially expressed (DE) mRNAs predominantly appeared in pathways linked to the immune response, inflammatory response, and the complement and coagulation cascades, while DE proteins were mainly enriched in pathways associated with the complement and coagulation cascades. On this basis, the integrated analysis was performed between transcriptome and proteome. The potential biomarkers were further verified by RT-qPCR and WB. The current proteotranscriptomic research has furnished a valuable dataset and fresh perspectives that will enhance our comprehension of the development of SCM. This, in turn, is expected to expedite the formulation of novel approaches for the prevention and management of SCM in patients.

Cardiomyopathies↗