目前确定肺毛细血管楔压的方法易使肺动脉高压患者分类出现严重误差

左心室充盈压的精确测量对于区分第1类肺动脉高压(pulmonary arterial hypertension,PAH)和由于左心疾病导致的第2类肺高血压(pulmonary hyper-tension associated with left-side heart failure and pre-served ejection fraction,PH-HFpEF)是十分重要的。研究人员假设常规依赖数字化的平均肺毛细血管楔压(the digitized mean pulmonary capillary wedge pres-sure,PCWP-digital)可导致错误的诊断,而呼气末肺     

《中国肺动脉高压诊断与治疗指南(2021版)》解读——具有明显肺静脉或肺毛细血管受累的肺动脉高压

肺静脉闭塞病(PVOD)和肺毛细血管瘤病(PCH)是一类引起肺动脉高压的罕见疾病,目前统称为具有明显肺静脉或肺毛细血管受累的肺动脉高压,是动脉性肺动脉高压(PAH)中的一个亚类.这一类型肺动脉高压以肺小静脉或肺毛细血管受累为主要特点,临床表现、病理特征上具有高度相似性,目前认为这两种疾病是同一种疾病的两种表现.PVOD...     

遗传性出血性毛细血管扩张症相关性肺动脉高压六例的临床特征

目的 初步探讨遗传性出血性毛细血管扩张症相关性肺动脉高压的临床特征.方法 回顾性分析6例临床诊断为遗传性出血性毛细血管扩张症相关性肺动脉高压的临床表现.结果 6例患者年龄8～67岁,平均34岁,均有反复鼻出血病史,4例诊断为重度肺动脉高压,2例诊断为中度肺动脉高压.6例患者首次入院诊断均未明确肺动脉高压原因.除2例合并弥漫肝动静脉瘘患者外,其余4例经内科治疗后症状改善明显.结论 遗传性出血性毛细血管扩张症合并肺动脉高压易误诊,需对其相应的病症采用及时有效的治疗.

Abstract：

Objective To investigate the clinical manifestations of patients with pulmonary artery hypertension (PAH) associated with hereditary hemorrhagic telangiectasia (HHT). Methods This retrospective analysis summarized the clinical features of 6 patients with PAH associated with HHT hospitalized at department of cardiology in Cardiovascular Institute and Fuwai Hospital between January 2006 and May 2009. Results The mean age of the 6 patients (3 male) was 34 years (8 -67years). Recurrent epistaxis were present in all patients, there were 4 patients with severe PAH and 2 patients with moderate PAH. All of the six patients with PAH associated with HHT were misdiagnosed at the first hospital visit.Clinical symptoms were significantly improved in 4 patients and remained unchanged in 2 patients combined hepatic venous malformation post medical therapy. Conclusions Misdiagnosis for patients with PAH associated with HHT is a common phenomenon in daily clinical practice. Patients could benefit from the corresponding medical therapy after the establishment of the correct diagnosis.     

缺氧性肺动脉高压发病机制及靶向治疗研究

缺氧性肺动脉高压（hypoxia pulmonary hypertension,HPH）是慢性肺源性心脏病及慢性高原病等临床疾病发病的重要病理生理变化之一,是由于长期慢性缺氧导致的,其主要特征为低氧性肺动脉收缩增强,肺小动脉中层平滑肌异常增生,肺血管重构,最终导致右心室肥大及右心衰竭[1].WHO对肺高压的分型中,将“伴发肺脏疾病和/或低氧血症的肺高血压”归纳为第Ⅲ型,包括慢性阻塞性肺疾病（chronic obstructive pulmonary disease,COPD）间质性肺疾病（结缔组织疾病,硬皮病）,睡眠呼吸障碍,慢性高原病,肺泡低通气综合征及肺泡毛细血管发育不良[2].     

肺内源性急性呼吸窘迫综合征(ARDS)与肺外源性ARDS

急性呼吸窘迫综合征 (ARDS)是因肺内外多种病因导致的肺毛细血管损伤后以急性进行性缺氧性呼吸衰竭为主要表现的综合征。虽然导致ARDS的病因诸多 ,但从病因可以分为肺内源性 (如重症肺炎 )与肺外源性 (如坏死性胰腺炎 ) 2类。传统观念认为 ,各种病因导致的ARDS肺部损伤的病理生理学改变基本相同 ,即非心源性肺毛细血管通透性增高性肺水肿、肺实变及通气 /血流比值失衡 ,病理学以肺泡腔内大量蛋白质渗出及透明膜形成为主要改变[1] 。 1998年 ,Gattinoni等[2 ] 首先发现 ,因肺炎导致的ARDS与因腹部疾病导致的ARDS在病理改变及使用外…     

老年高血压左心室肥厚患者心肌毛细血管病理改变特点

目的 :了解老年高血压左心室肥厚 (LVH)患者心肌毛细血管病变的特点 ,并在LVH分级相同的条件下 ,观察高血压、冠心病、糖尿病心肌毛细血管病变的区别。方法 :从我院 195 4年～ 1996年间3195例连续尸检标本中选取年龄≥ 6 0岁的高血压病、冠心病、高血压合并冠心病、糖尿病 2 0 6例和对照组 30例共 2 36例心脏标本进行CD31免疫组化染色 ,显示心肌间质 5～ 8μm毛细血管 ,通过光镜和电脑图象分析 ,定量检测心肌毛细血管密度 (capillarydensity ,CD)及其内皮细胞面积 (areaofendothelialcells,AEC) ;根据左室游离壁厚度将LVH分为 0级～Ⅲ级 ;高血压组LVH 0～Ⅲ级 ,冠心病组、高血压合并冠心病组、糖尿病组LVH均为I级。各组间比较采用SAS系统处理。结果 :高血压组随LVH加重 ,CD与AEC逐渐减小 (P <0 0 5 ) ;冠心病组上述变化不明显 (P >0 0 5 )而高血压合并冠心病组有上述改变且程度更重 (P <0 0 1) ;糖尿病组MCD及AEC也明显减少 (P <0 0 5 )。结论 :高血压LVH组毛细血管减少 ,糖尿病组有相似改变而冠心病组变化不明显。高血压和糖尿病的这种微血管病变是导致心血管事件的重要病理基础 ,应引起进一步重视     

系统性硬化症患者:运动可诱发肺高血压

系统性硬化症(systemic sclerosis,SSc)患者发生运动性肺高血压(exercise-induced pulmonary hypertension,exPH)的病因仍然是一个复杂的难题,因为左心室舒张功能受损和肺血管疾病都可促进其发展。该研究旨在确定SSc患者exPH的发生率,探讨肺动脉收缩压(pulmonary artery systolic pressure,PASP)和通过组织多普勒检测的肺毛细血管楔压(pulmonary     

高血压合并糖尿病对大鼠心肌微血管密度影响的研究

目的分析高血压合并糖尿病对大鼠心肌内微动脉及毛细血管密度的影响。方法选择自发性高血压大鼠(SHR)及SD大鼠24只,将大鼠腹腔注射链脲佐菌素后诱导糖尿病模型,分为对照组、SHR组、糖尿病组、自发性高血压合并糖尿病组(SHDM组),每组6只,进行左心室心肌标本电镜和HE染色及六氨银特染光镜检查,α-平滑肌肌动蛋白、CD31免疫组织化学染色测定各组大鼠心室微动脉及毛细血管密度。结果与对照组比较,SHR组、糖尿病组和SHDM组大鼠心肌内毛细血管密度明显降低,差异有统计学意义(P<0.01),微动脉密度明显增高,差异有统计学意义(P<0.01),心肌毛细血管表面积所占比例明显降低,差异有统计学意义(P<0.05,P<0.01)。结论高血压、糖尿病均导致心肌微动脉密度增高,毛细血管密度降低;高血压合并糖尿病时,毛细血管密度降低更明显。     

肺动静脉畸形合并遗传性出血性毛细血管扩张症1例报告并文献复习

肺动静脉畸形(pulmonary arteriovenous malformations,PAVMs)是一种少见的肺血管畸形,是肺动脉和肺静脉之间异常沟通所形成的肺部疾病。此病可合并遗传性出血性毛细血管扩张症(hereditary hemorrhagic telangiectasia,HHT)。现将本院收治的1例PAVMs合并HHT报道如下,并结合文献     

肺高血压与细胞代谢

肺高血压(pulmonary hypertension,PH)是一种以血管僵硬和细胞代谢改变为特征的进行性疾病.PH患者的肺动脉进行性重塑,引起肺血管阻力进行性升高,最终导致右心衰竭甚至死亡.尽管对PH已有广泛的研究,但确切发病机制尚未完全阐明.近年来,研究发现肺血管细胞代谢改变与PH发病机制有关,在PH患者中存在肺血管细胞(如平滑肌细胞、内皮细胞)代谢异常.这些细胞代谢改变可引起肺血管细胞损伤和肺血管重塑.本文就肺血管细胞代谢改变在PH发生发展过程中的作用进行综述.     

高血压降压治疗目标的再认识

根据传统的高血压水平的定义,1993年WHO高血压治疗指南提出血压控制目标为<140/90mm Hg(1mm Hg=0.133kPa),但是并非所有患者都必须将血压降至同一水平,而应根据患者情况进行个体化治疗。Framingham进行的一项长达10～12年的心血管事件研究发现,第5年后,正常上限血压[收缩压(SBP     

Inhibition of intimal thickening of the carotid artery of rabbits and of outgrowth of explants of aorta by probucol.

The effect of administration of probucol in preventing intimal thickening of rabbit carotid artery after balloon catheter injury and the mechanism of action of the drug were studied. Groups of 6 male New Zealand-White rabbits were given normal diet (Group I), high cholesterol diet (Group II) or high cholesterol diet plus probucol (Group III) for 4 weeks. Balloon catheter injury was made in week 2 and animals were killed in week 4. No significant differences in the total cholesterol levels in Groups II and III were found in week 4. The medians of areas of the intimal layer in cross-sections of the carotid arteries of Groups I, II and III were 0.237, 0.475 and 0.309 mm2, respectively. Thus high-cholesterol diet increased the thickness of the intimal layer and probucol reduced its effect. There were no significant differences in the areas of the medial layers in these 3 groups. For the examination of the mechanism of the effect of probucol, rabbits were given chow containing 0.5% cholesterol with and without 0.5% probucol (7 rabbits each) and then the numbers of explants from their aortas showing outgrowth were compared. The plasma total cholesterol levels of these two groups were the same. The probucol concentrations in the plasma and aorta of the former group were 18.6 +/- 13.2 micrograms/ml and 7.3 +/- 5.4 micrograms/g wet tissue, respectively. The number of explants showing outgrowth on day 14 was suppressed by 34% in the probucol-treated group.(ABSTRACT TRUNCATED AT 250 WORDS)