Literature DB >> 8480584

31P MR spectroscopy in hypertrophic cardiomyopathy: comparison with Tl-201 myocardial perfusion imaging.

H Sakuma1, K Takeda, T Tagami, T Nakagawa, S Okamoto, T Konishi, T Nakano.   

Abstract

Abnormal phosphate metabolism of the myocardium was evaluated in patients with hypertrophic cardiomyopathy (HCM) using 31P magnetic resonance (MR) spectroscopy. The results were compared with those from left ventricular function and thallium 201 (Tl-201) perfusion scintigraphy. Six normal volunteers and 19 patients with HCM were studied with a 1.5 T MR system. The spectra were localized to the myocardium using volume selection with the depth-resolved surface coil spectroscopy (DRESS) technique. Peak areas of 2,3-diphosphoglycerate (DPG), phosphodiesters (PDE), phosphocreatine (PCr), and beta-ATP were determined by fitting Gaussian functions to the phased spectra. The peak areas were corrected for contamination of blood adenosine triphosphate (ATP) and PDE. The corrected PCr/beta-ATP ratio in patients (1.07 +/- 0.10, mean +/- SE) was significantly lower compared with that in normal volunteers (1.71 +/- 0.13, p < .01). The PCr/beta-ATP ratio showed an abnormal decrease (< mean -2 SD of the controls) in 11 (58%) of 19 patients. The averaged PCr/beta-ATP ratio in 15 patients with normal left ventricular ejection fraction (LVEF) was 1.14 +/- 0.10, significantly lower than in healthy subjects. By contrast, the corrected PDE/PCr ratio in HCM did not differ significantly compared with that in healthy subjects (0.46 +/- 0.09 vs 0.36 +/- 0.09). The PDE/PCr ratio was abnormally elevated (> mean + 2 SD of the controls) in only four (21%) of the patients. On Tl-201 myocardial single-photon emission computed tomography (SPECT) imaging, the perfusion of the left ventricular wall looked normal in 6 and abnormal in 5 of 11 HCM patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Entities:  

Mesh:

Substances:

Year:  1993        PMID: 8480584     DOI: 10.1016/0002-8703(93)91002-v

Source DB:  PubMed          Journal:  Am Heart J        ISSN: 0002-8703            Impact factor:   4.749


  6 in total

1.  Can an energy-deficient heart grow bigger and stronger?

Authors:  Robert Roberts; Ali J Marian
Journal:  J Am Coll Cardiol       Date:  2003-05-21       Impact factor: 24.094

2.  31P-MR spectroscopic imaging in hypertensive heart disease.

Authors:  J-P Heyne; R Rzanny; A Hansch; U Leder; J R Reichenbach; W A Kaiser
Journal:  Eur Radiol       Date:  2006-03-02       Impact factor: 5.315

3.  Determinants of myocardial energetics and efficiency in symptomatic hypertrophic cardiomyopathy.

Authors:  Stefan A J Timmer; Tjeerd Germans; Marco J W Götte; Iris K Rüssel; Pieter A Dijkmans; Mark Lubberink; Jurrien M ten Berg; Folkert J ten Cate; Adriaan A Lammertsma; Paul Knaapen; Albert C van Rossum
Journal:  Eur J Nucl Med Mol Imaging       Date:  2010-01-13       Impact factor: 9.236

4.  Reduced myocardial creatine kinase flux in human myocardial infarction: an in vivo phosphorus magnetic resonance spectroscopy study.

Authors:  Paul A Bottomley; Katherine C Wu; Gary Gerstenblith; Steven P Schulman; Angela Steinberg; Robert G Weiss
Journal:  Circulation       Date:  2009-03-30       Impact factor: 29.690

5.  Cellular hypertrophy in cardiomyopathic patients is associated with lower creatine-stimulated mitochondrial respiration.

Authors:  M Popovich; S Kostin; T Branishte; V Kobets; V Kapelko
Journal:  Mol Cell Biochem       Date:  1995-02-09       Impact factor: 3.396

Review 6.  Expert consensus document: Mitochondrial function as a therapeutic target in heart failure.

Authors:  David A Brown; Justin B Perry; Mitchell E Allen; Hani N Sabbah; Brian L Stauffer; Saame Raza Shaikh; John G F Cleland; Wilson S Colucci; Javed Butler; Adriaan A Voors; Stefan D Anker; Bertram Pitt; Burkert Pieske; Gerasimos Filippatos; Stephen J Greene; Mihai Gheorghiade
Journal:  Nat Rev Cardiol       Date:  2016-12-22       Impact factor: 32.419

  6 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.