PDF(Pubmed)
Abstract：
UNASSIGNED: The sinus node (SN) is the main pacemaker site of the heart, located in the upper right atrium at the junction of the superior vena cava and right atrium. The precise morphology of the SN in the human heart remains relatively unclear especially the SN microscopical anatomy in the hearts of aged and obese individuals. In this study, the histology of the SN with surrounding right atrial (RA) muscle was analyzed from young non-obese, aged non-obese, aged obese and young obese individuals. The impacts of aging and obesity on fibrosis, apoptosis and cellular hypertrophy were investigated in the SN and RA. Moreover, the impact of obesity on P wave morphology in ECG was also analyzed to determine the speed and conduction of the impulse generated by the SN.
UNASSIGNED: Human SN/RA specimens were dissected from 23 post-mortem hearts (preserved in 4% formaldehyde solution), under Polish local ethical rules. The SN/RA tissue blocks were embedded in paraffin and histologically stained with Masson\'s Trichrome. High and low-magnification images were taken, and analysis was done for appropriate statistical tests on Prism (GraphPad, USA). 12-lead ECGs from 14 patients under Polish local ethical rules were obtained. The P wave morphologies from lead II, lead III and lead aVF were analyzed.
UNASSIGNED: Compared to the surrounding RA, the SN in all four groups has significantly more connective tissue (P ≤ 0.05) (young non-obese individuals, aged non-obese individuals, aged obese individuals and young obese individuals) and significantly smaller nodal cells (P ≤ 0.05) (young non-obese individuals, aged non-obese individuals, aged obese individuals, young obese individuals). In aging, overall, there was a significant increase in fibrosis, apoptosis, and cellular hypertrophy in the SN (P ≤ 0.05) and RA (P ≤ 0.05). Obesity did not further exacerbate fibrosis but caused a further increase in cellular hypertrophy (SN P ≤ 0.05, RA P ≤ 0.05), especially in young obese individuals. However, there was more infiltrating fat within the SN and RA bundles in obesity. Compared to the young non-obese individuals, the young obese individuals showed decreased P wave amplitude and P wave slope in aVF lead.
UNASSIGNED: Aging and obesity are two risk factors for extensive fibrosis and cellular hypertrophy in SN and RA. Obesity exacerbates the morphological alterations, especially hypertrophy of nodal and atrial myocytes. These morphological alterations might lead to functional alterations and eventually cause cardiovascular diseases, such as SN dysfunction, atrial fibrillation, bradycardia, and heart failure.
UNASSIGNED: Human SN/RA specimens were dissected from 23 post-mortem hearts (preserved in 4% formaldehyde solution), under Polish local ethical rules. The SN/RA tissue blocks were embedded in paraffin and histologically stained with Masson\'s Trichrome. High and low-magnification images were taken, and analysis was done for appropriate statistical tests on Prism (GraphPad, USA). 12-lead ECGs from 14 patients under Polish local ethical rules were obtained. The P wave morphologies from lead II, lead III and lead aVF were analyzed.
UNASSIGNED: Compared to the surrounding RA, the SN in all four groups has significantly more connective tissue (P ≤ 0.05) (young non-obese individuals, aged non-obese individuals, aged obese individuals and young obese individuals) and significantly smaller nodal cells (P ≤ 0.05) (young non-obese individuals, aged non-obese individuals, aged obese individuals, young obese individuals). In aging, overall, there was a significant increase in fibrosis, apoptosis, and cellular hypertrophy in the SN (P ≤ 0.05) and RA (P ≤ 0.05). Obesity did not further exacerbate fibrosis but caused a further increase in cellular hypertrophy (SN P ≤ 0.05, RA P ≤ 0.05), especially in young obese individuals. However, there was more infiltrating fat within the SN and RA bundles in obesity. Compared to the young non-obese individuals, the young obese individuals showed decreased P wave amplitude and P wave slope in aVF lead.
UNASSIGNED: Aging and obesity are two risk factors for extensive fibrosis and cellular hypertrophy in SN and RA. Obesity exacerbates the morphological alterations, especially hypertrophy of nodal and atrial myocytes. These morphological alterations might lead to functional alterations and eventually cause cardiovascular diseases, such as SN dysfunction, atrial fibrillation, bradycardia, and heart failure.
摘要：
■窦房结（SN）是心脏的主要起搏器部位，位于上腔静脉和右心房交界处的右心房上部。人体心脏中SN的精确形态仍然相对不清楚，尤其是老年人和肥胖个体心脏中SN的显微解剖结构。在这项研究中,从年轻的非肥胖患者中分析了SN与周围右心房（RA）肌肉的组织学，老年非肥胖，老年肥胖和年轻肥胖个体。衰老和肥胖对纤维化的影响，在SN和RA中研究了细胞凋亡和细胞肥大。此外，还分析了肥胖对心电图P波形态的影响，以确定SN产生的脉冲的速度和传导。
■从23个死后的心脏（保存在4％甲醛溶液中）中解剖人SN/RA标本，根据波兰当地的道德规则。将SN/RA组织块包埋在石蜡中，并用Masson三色染色进行组织学染色。拍摄了高倍率和低倍率图像，并对棱镜(GraphPad，美国）。根据波兰当地道德规则，从14名患者中获得了12导联心电图。来自II铅的P波形态，分析了三联铅和aVF铅。
■与周围的RA相比，四组中的SN具有显著更多的结缔组织(P≤0.05)(年轻非肥胖个体，老年非肥胖个体，老年肥胖个体和年轻肥胖个体)和显著较小的淋巴结细胞(P≤0.05)(年轻非肥胖个体，老年非肥胖个体，老年肥胖个体，年轻的肥胖个体)。在衰老中，总的来说,纤维化显著增加，凋亡，SN（P≤0.05）和RA（P≤0.05）的细胞肥大。肥胖并未进一步加剧纤维化，但导致细胞肥大进一步增加（SNP≤0.05，RAP≤0.05），尤其是年轻的肥胖个体。然而,肥胖患者的SN和RA束内有更多的浸润性脂肪。与年轻的非肥胖个体相比，年轻肥胖个体在aVF导线中显示P波振幅和P波斜率降低。
■衰老和肥胖是SN和RA广泛纤维化和细胞肥大的两个危险因素。肥胖加剧了形态学改变，尤其是结节和心房肌细胞肥大。这些形态学改变可能导致功能改变并最终导致心血管疾病，如SN功能障碍，心房颤动,心动过缓,和心力衰竭。
■从23个死后的心脏（保存在4％甲醛溶液中）中解剖人SN/RA标本，根据波兰当地的道德规则。将SN/RA组织块包埋在石蜡中，并用Masson三色染色进行组织学染色。拍摄了高倍率和低倍率图像，并对棱镜(GraphPad，美国）。根据波兰当地道德规则，从14名患者中获得了12导联心电图。来自II铅的P波形态，分析了三联铅和aVF铅。
■与周围的RA相比，四组中的SN具有显著更多的结缔组织(P≤0.05)(年轻非肥胖个体，老年非肥胖个体，老年肥胖个体和年轻肥胖个体)和显著较小的淋巴结细胞(P≤0.05)(年轻非肥胖个体，老年非肥胖个体，老年肥胖个体，年轻的肥胖个体)。在衰老中，总的来说,纤维化显著增加，凋亡，SN（P≤0.05）和RA（P≤0.05）的细胞肥大。肥胖并未进一步加剧纤维化，但导致细胞肥大进一步增加（SNP≤0.05，RAP≤0.05），尤其是年轻的肥胖个体。然而,肥胖患者的SN和RA束内有更多的浸润性脂肪。与年轻的非肥胖个体相比，年轻肥胖个体在aVF导线中显示P波振幅和P波斜率降低。
■衰老和肥胖是SN和RA广泛纤维化和细胞肥大的两个危险因素。肥胖加剧了形态学改变，尤其是结节和心房肌细胞肥大。这些形态学改变可能导致功能改变并最终导致心血管疾病，如SN功能障碍，心房颤动,心动过缓,和心力衰竭。
