Wada Hideichi, Sakata Noriyuki, Tashiro Tadashi
Cardiovascular Surgery, Faculty of Medicine, Fukuoka University, Fukuoka, 814-0180, Japan.
General Medical Research Center, Faculty of Medicine, Fukuoka University, 45-1, 7-chome Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.
Heart Vessels. 2016 Nov;31(11):1855-1861. doi: 10.1007/s00380-016-0813-2. Epub 2016 Feb 18.
An intimal tear is responsible for the development of aortic dissection (AD). Plaque rupture is thought to progress to a penetrating atherosclerotic ulcer (PAU). However, the influences of mechanical stress and atherosclerosis on the intimal tear of AD and plaque rupture of PAU have not been fully understood. We enrolled 27 patients with AD [67.6 ± 11.2 years, female/male (F/M) 12/15] and 10 patients with PAU (71.0 ± 8.64 years, F/M 2/8) who underwent aortic reconstructive surgery in our hospital between 2007 and 2011. We analyzed the clinical data and morphological features of these patients and discuss the role of mechanical stress in the initial event. On clinical examination, hypertension was frequently observed in the patients of both the AD (77.8 %) and PAU groups (90.0 %), while hypercholesterolemia was significantly more prevalent in the PAU group (90.0 %) than in the AD (22.2 %) group. Most lesions of AD (96.3 %) were found in the ascending aorta up to the aortic arch, while those of PAU (90.0 %) were found in the descending and abdominal aortas. On pathological examination, the entrance tear was found in 21 (77.8 %) of the 27 patients with AD, and histologically comprised nonatherosclerotic intima and media. In contrast, the entrance tear was considered as plaque ulcer in 8 (80.0 %) of the 10 patients with PAU. The patients with PAU showed a significantly higher prevalence of soft plaque, complicated lesions, and medial fibrosis than those with AD, whereas patients with AD showed no complicated lesions and had a significantly higher prevalence of cystic medial necrosis than those with PAU. The present study suggests that less atherosclerosis and impairment of media could proceed to intimal tear formation in AD and that the disruption of the fibrous cap could cause the plaque ulcer of PAU.
内膜撕裂是主动脉夹层(AD)形成的原因。斑块破裂被认为会发展为穿透性动脉粥样硬化溃疡(PAU)。然而,机械应力和动脉粥样硬化对AD内膜撕裂和PAU斑块破裂的影响尚未完全明确。我们纳入了2007年至2011年间在我院接受主动脉重建手术的27例AD患者[67.6±11.2岁,女性/男性(F/M)12/15]和10例PAU患者(71.0±8.64岁,F/M 2/8)。我们分析了这些患者的临床资料和形态学特征,并探讨了机械应力在初始事件中的作用。临床检查发现,AD组(77.8%)和PAU组(90.0%)患者中高血压较为常见,而PAU组(90.0%)的高胆固醇血症患病率显著高于AD组(22.2%)。AD的大多数病变(96.3%)位于升主动脉直至主动脉弓,而PAU的病变(90.0%)位于降主动脉和腹主动脉。病理检查发现,27例AD患者中有21例(77.8%)存在入口撕裂,组织学上由非动脉粥样硬化的内膜和中膜组成。相比之下,10例PAU患者中有8例(80.0%)的入口撕裂被认为是斑块溃疡。PAU患者的软斑块、复杂病变和中膜纤维化患病率显著高于AD患者,而AD患者无复杂病变,囊性中膜坏死患病率显著高于PAU患者。本研究表明,AD中较少的动脉粥样硬化和中膜损伤可导致内膜撕裂形成,而纤维帽的破坏可导致PAU的斑块溃疡。