Dendale P, Franken P R, van der Wall E E, de Roos A
Department of Cardiology, AZVUB, Brussels, Belgium.
Coron Artery Dis. 1997 May;8(5):259-64. doi: 10.1097/00019501-199705000-00002.
Abnormalities in wall thickening and their reaction to stimulation can be studied by magnetic resonance imaging.
To analyse the relationship between these abnormalities and changes in myocardial perfusion and fatty acid metabolism.
Fifteen patients with a myocardial infarction underwent low-dose dobutamine magnetic resonance imaging to assess their wall thickening and contractile reserve, and technetium-99m sestamibi (MIBI) and beta-methyl-iodophenyl-pentadecanoic acid (BMIPP) single-photon emission tomography to assess their myocardial perfusion and fatty acid uptake. For nine segments per patient, the wall thickening was scored as normal, hypokinetic or akinetic, and the myocardial perfusion as normal (> 65%), mildly to moderately reduced (35-65%) or severely reduced (< 35%). Abnormalities in fatty acid uptake were compared with the myocardial perfusion and defined as matched (difference < or = 10%) or mismatched (difference > 10%) reduction.
Thirty-four segments had abnormal wall thickening (13 hypokinetic and 21 akinetic). The wall thickening at rest was significantly related to the uptake of MIBI (P < 0.001), but not to abnormalities in the uptake of BMIPP. All of the akinetic segments had an abnormal uptake of MIBI (15 severely and six mildly to moderately reduced), whereas 7 of 13 hypokinetic segments had a normal and five a midly to moderately reduced uptake. A significant relationship between abnormalities of fatty acid metabolism and the contractile reserve was also found (P < 0.002): 14 of 16 segments with and only six of 18 without contractile reserve had a mismatched reduction in uptakes of MIBI and BMIPP.
This study confirms the relationship between the wall thickening at rest and the residual perfusion after infarction. On the other hand, the contractile reserve, which is an accepted indicator of the viability of the infarct region, is associated strongly with abnormalities of fatty acid metabolism.
可通过磁共振成像研究心肌壁增厚异常及其对刺激的反应。
分析这些异常与心肌灌注及脂肪酸代谢变化之间的关系。
15例心肌梗死患者接受低剂量多巴酚丁胺磁共振成像以评估其心肌壁增厚及收缩储备,并用锝-99m甲氧基异丁基异腈(MIBI)和β-甲基-对碘苯基十五烷酸(BMIPP)单光子发射断层扫描来评估其心肌灌注及脂肪酸摄取。对每位患者的9个节段,将心肌壁增厚分为正常、运动减弱或运动消失,心肌灌注分为正常(>65%)、轻度至中度降低(35%-65%)或重度降低(<35%)。将脂肪酸摄取异常与心肌灌注进行比较,并定义为匹配(差异≤10%)或不匹配(差异>10%)降低。
34个节段存在心肌壁增厚异常(13个运动减弱,21个运动消失)。静息时的心肌壁增厚与MIBI摄取显著相关(P<0.001),但与BMIPP摄取异常无关。所有运动消失的节段MIBI摄取均异常(15个重度降低,6个轻度至中度降低),而13个运动减弱节段中有7个MIBI摄取正常,5个轻度至中度降低。还发现脂肪酸代谢异常与收缩储备之间存在显著关系(P<0.002):16个有收缩储备的节段中有14个以及18个无收缩储备的节段中有6个MIBI和BMIPP摄取呈不匹配降低。
本研究证实了静息时心肌壁增厚与梗死后残余灌注之间的关系。另一方面,收缩储备作为梗死区域存活能力的公认指标,与脂肪酸代谢异常密切相关。