Kovarnik Tomas, Chen Zhi, Wahle Andreas, Zhang Ling, Skalicka Hana, Kral Ales, Lopez John J, Horak Jan, Sonka Milan, Linhart Ales
2nd Department of Internal Medicine, Department of Cardiovascular Medicine, First Faculty of Medicine, Charles University in Prague and General University Hospital in Prague, Praha, Czech Republic.
Department of Intravascular Imaging, Iowa Institute for Biomedical Imaging, The University of Iowa, Iowa City, United States.
Rev Esp Cardiol (Engl Ed). 2017 Jan;70(1):25-33. doi: 10.1016/j.rec.2016.04.058. Epub 2016 Sep 5.
Pathologic intimal thickening (PIT) has been considered a benign plaque phenotype. We report plaque phenotypic changes in a baseline/follow-up intravascular ultrasound-based virtual histology study.
A total of 61 patients with stable coronary artery disease were analyzed from the HEAVEN trial (89 patients randomized between routine statin therapy vs atorvastatin 80mg and ezetimibe 10mg) with serial intravascular ultrasound imaging of nonculprit vessels. We compared changes in 693 baseline and follow-up 5-mm long segments in a novel risk score, Liverpool Active Plaque Score (LAPS), plaque parameters, and plaque composition.
The PIT showed the highest increase of risk score and, with fibrous plaque, also the LAPS. Necrotic core (NC) abutting to the lumen increased in PIT (22 ± 51.7; P = .0001) and in fibrous plaque (17.9 ± 42.6; P = .004) but decreased in thin cap fibroatheroma (TCFA) (⿿15.14 ± 52.2; P = .001). The PIT was the most likely of all nonthin cap fibroatheroma plaque types to transform into TCFA at follow-up (11% of all TCFA found during follow-up and 35.9% of newly-developed TCFA), but showed (together with fibrous plaque) the lowest stability during lipid-lowering therapy (24.7% of PIT remained PIT and 24.5% of fibrous plaque remained fibrous plaque).
Over the 1-year follow-up, PIT was the most dynamic of the plaque phenotypes and was associated with an increase of risk score and LAPS (together with fibrous plaque), NC percentage (together with fibrous plaque) and NC abutting to the lumen, despite a small reduction of plaque volume during lipid-lowering therapy. The PIT was the main source for new TCFA segments.
病理性内膜增厚（PIT）一直被认为是一种良性斑块表型。我们在一项基于血管内超声虚拟组织学的基线/随访研究中报告了斑块表型变化。
从HEAVEN试验中分析了61例稳定型冠心病患者（89例患者随机接受常规他汀类药物治疗与阿托伐他汀80mg和依折麦布10mg治疗），对非罪犯血管进行了连续血管内超声成像。我们比较了693个基线和随访的5毫米长节段在一种新的风险评分（利物浦活性斑块评分，LAPS）、斑块参数和斑块成分方面的变化。
PIT显示风险评分增加最多，与纤维斑块一样，LAPS也增加。在PIT（22±51.7；P = 0.0001）和纤维斑块（17.9±42.6；P = 0.004）中，紧邻管腔的坏死核心（NC）增加，但在薄帽纤维粥样斑块（TCFA）中减少（−15.14±52.2；P = 0.001）。PIT是所有非薄帽纤维粥样斑块类型中在随访时最有可能转变为TCFA的（随访期间发现的所有TCFA中的11%以及新出现的TCFA中的35.9%），但在降脂治疗期间显示出（与纤维斑块一起）最低的稳定性（24.7%的PIT仍为PIT，24.5%的纤维斑块仍为纤维斑块）。
在1年的随访中，PIT是最具动态变化的斑块表型，与风险评分和LAPS增加（与纤维斑块一起）、NC百分比（与纤维斑块一起）以及紧邻管腔的NC相关，尽管在降脂治疗期间斑块体积略有减小。PIT是新的TCFA节段的主要来源。
