1998
DOI: 10.1016/s0002-9149(98)00399-3
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Metabolic changes in hibernating myocardium after percutaneous transluminal coronary angioplasty and the relation between recovery in left ventricular function and free fatty acid metabolism

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Cited by 15 publications
(6 citation statements)
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“…Myocardial 201 Tl and 123 I-BMIPP dual scintigraphy enable simultaneous assessment of myocardial flow and fatty acid metabolism [11]. The areas exhibiting a flow-metabolism mismatch, defined as a larger defect on 123 I-BMIPP than that on 201 Tl, correspond to impaired but viable myocardium after AMI [12,13], and are considered to be where further improvements in myocardial function will be [14][15][16][17]. On the other hand, AMI patients showing a concordant defect on 201 Tl/ 123 I-BMIPP dual single-photon emission computed tomography (SPECT) have a worse outcome than those without it [17][18][19][20].…”
Section: Introductionmentioning
confidence: 99%
“…Myocardial 201 Tl and 123 I-BMIPP dual scintigraphy enable simultaneous assessment of myocardial flow and fatty acid metabolism [11]. The areas exhibiting a flow-metabolism mismatch, defined as a larger defect on 123 I-BMIPP than that on 201 Tl, correspond to impaired but viable myocardium after AMI [12,13], and are considered to be where further improvements in myocardial function will be [14][15][16][17]. On the other hand, AMI patients showing a concordant defect on 201 Tl/ 123 I-BMIPP dual single-photon emission computed tomography (SPECT) have a worse outcome than those without it [17][18][19][20].…”
Section: Introductionmentioning
confidence: 99%
“…[8][9][10][11] This also reflects a state brought about by continuing fatty acid metabolism impairment mainly due to persistent myocardial ischemia or memory imaging. 9,11) It has been suggested that these mechanisms are due to severe culprit lesions and infarct-related artery occlusion or stenosis, and a sustained tissuelevel perfusion injury and impaired myocardial reperfusion of the microvascular level in patients with no significant coronary artery stenosis.…”
Section: Discussionmentioning
confidence: 99%
“…The importance of this approach, using exogenous short chain fatty acids to bypass LCFA utilization, 13 is that if a direct measure of LCFA were performed, we would only demonstrate the known reduction in LCFA oxidation. [1][2][3] The novelty of these findings is that by using a short chain fatty acid, we have elucidated a continued oxidation of fatty acids that would otherwise not be detected with labeled LCFA. The indication that butyrate contributions increased during ischemia in this study may be the result of inhibition of LCFA oxidation through CPT1, as suggested by previous work on the regulation of LCFA oxidation through malonyl CoA sensitivity in mitochondria from ischemic dog hearts.…”
Section: Discussionmentioning
confidence: 99%
“…Reduced long chain fatty acid (LCFA) oxidation in ischemic but viable human hearts has also been reported. 2,3 However, oxidation of fuels within the mitochondria of the hypoperfused myocardium has not been examined with substrates that bypass the highly regulated transfer of LCFA into the mitochondrial matrix. The current protocol tests the oxidative capability of mitochondria in the in vivo heart during restricted blood flow.…”
mentioning
confidence: 99%