重症肺栓塞是临床中比较凶险的疾病,病因复杂多样,其中以肺血栓栓塞最为常见,其栓子大多来源与下肢静脉,以肺循环和呼吸功能障碍为主的临床表现,死亡率很高,是许多地区和国家心血管死亡的第三大原因,漏诊率和误诊率均高,且预后较差。本文结合1例肺栓塞病例资料,分析了联合“心–肺–血管”超声对急性肺栓塞的早期诊断的重要性,提高该类疾病的早期识别及鉴别,对挽救患者生命及改善预后至关重要。Severe pulmonary embolism is a relatively dangerous disease in clinical practice, with complex and diverse causes. Among them, pulmonary thromboembolism is the most common, and its emboli mostly originate from lower limb veins. Clinical manifestations mainly include pulmonary circulation and respiratory dysfunction, with a high mortality rate. It is the third leading cause of cardiovascular death in many regions and countries, with high rates of missed diagnosis and misdiagnosis, and a poor prognosis. This article combines data from a case of pulmonary embolism to analyze the importance of combining “Cardio-Pulmonary-Vascular” ultrasound in the early diagnosis of acute pulmonary embolism. Improving the early identification and differentiation of this type of disease is crucial for saving patient lives and improving prognosis.
心力衰竭是各种心脏疾病的终末阶段,其病理过程贯穿发病的各个环节。SIRT3是SIRTUIN家族的重要一员,属于烟酰胺腺嘌呤二核苷酸(NAD+)依赖性脱乙酰酶的Sirtuin家族,亚细胞主要定位于线粒体,在心脏中高度表达。表观遗传学不牵涉DNA的序列变化,而基因组相关功能改变,比如组蛋乙酰化相关的SIRT3可通过各种通路及调节因子,对心肌纤维化、心肌肥厚、心肌凋亡等病理过程进行调节,对心力衰竭的发生、发展产生重要影响。本文主要综述SIRT3在心力衰竭各病理过程中的研究进展。Heart failure is the terminal stage of various heart diseases, and its pathological process runs through every link of the disease. SIRT3 is an important member of the Sirtuin family, belonging to the sirtuin family of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases, which is subcellular localized in mitochondria and is highly expressed in the heart. Epigenetics does not involve the sequence changes of DNA, but genome-related functional changes, such as egg acetylation- related SIRT3, can regulate myocardial fibrosis, myocardial hypertrophy, myocardial apoptosis and other pathological processes through various pathways and regulatory factors, and have an important impact on the occurrence and development of heart failure. This paper mainly reviews the progress of SIRT3 in each pathological process of heart failure.