X线、MSCT和MRI对主动脉夹层的临床运用对比研究

目的对比分析X线、MSCT及MRI在主动脉夹层（AD）中影像学特征,并评价其临床运用价值。方法 30例经手术或行DSA造影证实的AD患者,对其X线、MSCT及MRI检查影像资料进行分析,总结归纳其影像特点。结果 X线仅见AD的间接征象,而MSCT和MRI均能不同程度地显示真假两腔、内膜破口、内膜片及附壁血栓。结论 X线对AD只能提示诊断,而MSCT和MRI可作特异性诊断,并且MRI在显示AD的破口位置、无钙化的内膜片及附壁血栓时均优于MSCT,但对内膜及主动脉壁钙化和急危重者的检查MSCT优于MRI。     

硫代硫酸钠治疗慢性肾脏病患者血管钙化临床应用进展

近年来,慢性肾脏病(CKD)作为世界范围内主要的公共卫生问题受到越来越多的关注.慢性肾脏病矿物质和骨异常(CKD-MBD)是由于CKD的矿物质及骨代谢异常综合征所致,严重地影响了 CKD患者的生存率和生活质量.血管钙化是CKD-MBD的临床表现之一,其包括:动脉内膜钙化、中膜钙化、心脏瓣膜钙化和钙化防御.目前临床上还未...     

Reduced H+ channel activity disrupts pH homeostasis and calcification in coccolithophores at low ocean pH

Coccolithophores are major producers of ocean biogenic calcite, but this process is predicted to be negatively affected by future ocean acidification scenarios. Since coccolithophores calcify intracellularly, the mechanisms through which changes in seawater carbonate chemistry affect calcification remain unclear. Here we show that voltage-gated H⁺ channels in the plasma membrane of Coccolithus braarudii serve to regulate pH and maintain calcification under normal conditions but have greatly reduced activity in cells acclimated to low pH. This disrupts intracellular pH homeostasis and impairs the ability of C. braarudii to remove H⁺ generated by the calcification process, leading to specific coccolith malformations. These coccolith malformations can be reproduced by pharmacological inhibition of H⁺ channels. Heavily calcified coccolithophore species such as C. braarudii, which make the major contribution to carbonate export to the deep ocean, have a large intracellular H⁺ load and are likely to be most vulnerable to future decreases in ocean pH.

Anthropogenic CO₂ emissions and the subsequent dissolution of CO₂ in seawater have resulted in substantial changes in ocean carbonate chemistry (1). The resultant decrease in seawater pH, termed ocean acidification, is predicted to be particularly detrimental for calcifying organisms (2). Mean global surface ocean pH is currently around 8.2 but is predicted to fall as low as 7.7 by 2100 (3) and is likely to continue to fall further in the following centuries. Present-day marine organisms can experience significant fluctuations in seawater pH, particularly in coastal and upwelling regions (4, 5). Ocean acidification is therefore predicted to have an important influence not only on mean surface ocean pH but also on the extremes of pH experienced by marine organisms (6, 7).Coccolithophores (Haptophyta) are a group of globally distributed unicellular phytoplankton that are characterized by their covering of intricately formed calcite scales (coccoliths). Coccolithophores account for a significant proportion of ocean productivity and are the main producers of biogenic calcite, making major contributions to global biogeochemical cycles, including the long-term export of both inorganic and organic carbon from the ocean photic zone to deep waters (8, 9). Unlike the vast majority of calcifying organisms, coccolithophore calcification occurs in an intracellular compartment, the Golgi-derived coccolith vesicle (CV), effectively isolating the calcification process from direct changes in seawater carbonate chemistry. Nevertheless, extensive laboratory observations indicate that ocean acidification may negatively impact coccolithophore calcification, albeit with significant variability of responses between species and strains (10–14). The negative impact on calcification rates occurs at calcite saturation states (Ω_calcite) >1, indicating that it results primarily from impaired cellular production rather than dissolution (10, 15). However, prediction of how natural coccolithophore populations may respond to future changes in ocean pH are hampered by lack of mechanistic understanding of pH impacts at the cellular level (10).As calcification occurs intracellularly using external HCO₃⁻ as the primary dissolved inorganic carbon (DIC) source (16–18), coccolith formation is not directly dependent on external CO₃²⁻ concentrations. However, the uptake of HCO₃⁻ as a substrate for calcification results in the equimolar production of CaCO₃ and H⁺ in the CV (18). In order to maintain saturation conditions for calcite formation, H⁺ produced by the calcification process must be rapidly removed from the CV, placing extraordinary demands for cellular pH regulation to prevent cellular acidosis (18).Lower calcification rates under ocean acidification conditions appear to be primarily due to decreased pH rather than other aspects of carbonate chemistry (10, 19, 20). Coccolithophores exhibit highly unusual membrane physiology, including the presence of voltage-gated H⁺ channels in the plasma membrane (21) and a high sensitivity of cytosolic pH (pH_cyt) to changes in external pH (pH_o) (21, 22). Voltage-gated H⁺ channels are associated with rapid H⁺ efflux in a number of specialized animal cell types (23) and contribute to effective pH regulation in coccolithophores (21). As H⁺ channel function is dependent on the electrochemical gradient of H⁺ across the plasma membrane, this mechanism could be impaired under lower seawater pH. However, it remains unknown whether H⁺ channels play a direct role in removal of calcification-derived H⁺ or contribute to the sensitivity of coccolithophores to ocean acidification.Coccolithophores exhibit significant diversity in their extent of calcification (SI Appendix, Fig. S1). The ratio of particulate inorganic carbon to particulate organic carbon (PIC/POC) of a coccolithophore culture is a measure of the relative rates of inorganic carbon fixation by calcification and organic carbon fixation by photosynthesis, respectively, and is commonly used as a simple metric to define the degree of calcification. The abundant bloom-forming species Emiliania huxleyi is moderately calcified (PIC/POC of around 1) and has been the focus of the vast majority of the studies into the effects of environmental change in coccolithophores (13). Coastal species belonging to the Pleurochrysidaceae and Hymenomonadaceae are lightly calcified, commonly exhibiting a PIC/POC of less than 0.5 (24–27). Species such as Coccolithus braarudii, Calcidiscus leptoporus, and Helicosphaera carteri exhibit much higher PIC/POC ratios and contribute the majority of carbonate export to the deep ocean in many areas (28–30). The physiological response of heavily calcified coccolithophores to ocean acidification is therefore of considerable biogeochemical significance. Growth and calcification rates in C. leptoporus and C. braarudii are sensitive to pH values predicted to prevail on a future decadal timescale (10, 15, 31, 32). However, a mechanistic understanding of the different sensitivity of coccolithophore species to changing ocean carbonate chemistry is lacking.The net H⁺ load in a cell is determined by the combination of metabolic processes that consume or produce H⁺. H⁺ fluxes in coccolithophores will be primarily determined by the balance of H⁺ consumed by photosynthesis and H⁺ generated by calcification, with uptake of different carbon sources a particularly important consideration (Fig. 1A). CO₂ uptake for photosynthesis results in no net production or consumption of H⁺, whereas uptake of HCO₃⁻ requires the equimolar consumption of H⁺ in order to generate CO₂. Growth at elevated CO₂ causes a switch from HCO₃⁻ uptake to predominately CO₂ uptake in E. huxleyi (33, 34). The associated net decrease in H⁺ consumption will therefore increase the H⁺ load in coccolithophores grown at elevated CO₂, which may exacerbate the potential for cytosolic acidosis caused by lower seawater pH.Open in a separate windowFig. 1.Physiology and H⁺ fluxes of C. braarudii cells grown at different seawater pH. (A) Schematic indicating H⁺ fluxes associated with photosynthesis and calcification in a coccolithophore cell. While many metabolic processes may contribute to the cellular H⁺ budget, these two processes are likely to be the major contributors. In a cell taking up HCO₃⁻, the overall H⁺ budget is determined by the relative rates of H⁺ consumed during photosynthesis and H⁺ generated during calcification. In a cell taking up CO₂, the H⁺ budget is determined primarily by calcification, as 2 H⁺ are produced for each molecule of CaCO₃ produced and H⁺ are no longer consumed during photosynthesis. In both scenarios, excess H⁺ may be removed from the cell by H⁺ transporters in the plasma membrane, such as voltage-gated H⁺ channels (H_v). Coccolithophores take up both HCO₃⁻ and CO₂ across the plasma membrane, with increasing proportions of DIC taken up as CO₂ as seawater CO₂ increases (34). (B) Growth rate of C. braarudii cells acclimated to different seawater pH. n = 3 replicates per treatment; line represents polynomial fit to mean. (C) Cellular production of POC through photosynthesis and PIC through calcification. The optima for both processes are close to the control conditions (pH 8.15). (D) As a consequence of the unequal changes in cellular POC and PIC production across the applied pH values, cellular PIC/POC ratios are minimal at pH 7.55 (∼1.0) and maximal at pH 8.45 (∼1.8). (E) Calculated net H⁺ budgets under the different pH regimes, based on rates of photosynthesis and calcification shown in C (see Materials and Methods). The concentration of CO₂ in seawater is also shown (dashed line). Estimates are shown for cells using taking up only HCO₃⁻ or only CO₂. As C. braarudii cells will likely take up a mixture of both DIC species, with a shift toward greater CO₂ usage at elevated CO₂, the shaded area represents the potential range of H⁺ production. Regardless of DIC species used C. braarudii produces excess H⁺ at all applied pH values, but H⁺ production is much lower at pH 7.55 due to the decrease in calcification.In this study we set out to better understand the cellular mechanisms underlying the sensitivity of coccolithophore calcification to lower pH. We subjected the heavily calcified species C. braarudii, which is commonly found in temperate upwelling regions (35, 36), to conditions that reflect the range of pH values it may experience in current and future oceans. We show that acclimation to low pH leads to loss of H⁺ channel function and disruption of cellular pH regulation in C. braarudii. These effects are coincident with very specific defects in coccolith morphology that can be reproduced by direct inhibition of H⁺ channels. We conclude that H⁺ efflux through H⁺ channels is essential for maintaining both calcification rate and coccolith morphology. By providing a mechanistic insight into pH regulation during the calcification process, our results indicate that disruption of coccolithophore calcification in a future acidified ocean is likely to be most severe in heavily calcified species.     

Total arch replacement using frozen elephant trunk technique with Frozenix for distal aortic arch aneurysms

Open in a separate window OBJECTIVESTotal arch replacement (TAR) using an endovascular approach has been initially introduced as the frozen elephant trunk technique (FET). In our institute, TAR using the FET with Frozenix has been used as the first-line treatment for distal aortic arch aneurysms since 2014. This study aimed to evaluate the early and long-term outcomes and demonstrate the efficacy of this procedure.METHODSBetween 2014 and 2021, 121 consecutive patients were treated with TAR using the FET with Frozenix for distal aortic arch aneurysms. Early and long-term outcomes were retrospectively analysed.RESULTSThe 30-day mortality rate was 2.5% (3/121). Of postoperative complications, paraplegia due to spinal cord injury occurred in 2 (1.7%) patients, stroke in 12 (9.9%) and acute renal failure in 10 (8.3%). At follow-up, 23 secondary aortic interventions were required and 8 (6.6%) patients underwent intended secondary thoracic endovascular aortic repair for residual descending aortic aneurysm. Late and aortic-related deaths occurred in 16 (13.2%) and 4 (3.3%) patients, respectively. The overall long-term survival rates at 1, 3 and 5 years were 87.6%, 83.1% and 65.4%, respectively, while the rates of freedom from aortic-related death at 1, 3 and 5 years were 95.7%, 95.7% and 84.8%, respectively.CONCLUSIONSTAR using the FET with Frozenix for distal aortic arch aneurysms has acceptable early mortality and morbidity. Spinal cord injury and paraplegia occur less frequently than previously reported. The technique has satisfactory long-term survival and freedom from aortic-related death.     

Prior intake of new oral anticoagulants adversely affects outcome following surgery for acute type A aortic dissection

Open in a separate window OBJECTIVESOral anticoagulation prior to emergency surgery is associated with an increased risk of perioperative bleeding, especially when this therapy cannot be discontinued or reversed in time. The goal of this study was to analyse the impact of different oral anticoagulants on the outcome of patients who underwent emergency surgery for acute type A aortic dissection (ATAAD).METHODSThis was a single-centre retrospective study of patients treated with oral anticoagulation at the time of surgery for ATAAD. Outcomes of patients on new oral anticoagulant (NOAC) therapy were compared to respective outcomes of patients on Coumadin. Additionally, a survival analysis was performed comparing these 2 groups with patients who were operated on with no prior anticoagulation.RESULTSBetween January 2013 and April 2020, a total of 437 patients (63.8 ± 11.8 years, 68.4% male) received emergency surgery for ATAAD; 35 (8%) were taking oral anticoagulation at the time of hospital admission: 20 received phenprocoumon; 14, rivaroxaban; and 1, dabigatran. Compared to Coumadin, NOAC was associated with a greater need for blood-product transfusions and haemodynamic compromise. Operative mortality was 53% in the NOAC group and 30% in the Coumadin group. A 5-year survival analysis showed no significant difference between the NOAC and the Coumadin group (P = 0.059). Compared to 402 patients treated during the study period without anticoagulation, patients taking NOAC had significantly worse survival (P = 0.001), whereas that effect was not observed in patients undergoing surgery who were taking Coumadin (P = 0.99).CONCLUSIONSEmergency surgery for ATAAD in patients taking NOAC is associated with high morbidity and mortality. NOAC are a major risk factor for uncontrollable bleeding and haemodynamic compromise. New treatment strategies must be defined to improve surgical outcomes in these high-risk patients.     

Single-stage repair for ascending aortic aneurysm,artery stenosis and occlusion of neck vessels caused by Takayasu arteritis

Takayasu arteritis results in a variety of vascular symptoms, and there are some cases in which progressive vascular lesions require surgical intervention. We present a case with ascending aortic aneurysm, right common carotid artery stenosis, left common carotid artery occlusion and left subclavian artery stenosis caused by Takayasu arteritis that was successfully treated with total arch replacement and ascending aorta to right internal carotid artery bypass.     

血管平滑肌细胞表型的成骨转换与血管钙化

血管钙化是血管壁中钙盐沉积的过程,导致血管硬化和失去弹性。它通常发生在中老年人,尤其是患有动脉粥样硬化、高血压、糖尿病和慢性肾脏疾病等疾病患者。血管钙化是一个主动的过程,其中平滑肌细胞的成骨转换是重要事件之一。这些细胞在钙化过程中释放钙离子,导致钙盐的沉积,形成钙化斑块。血管钙化受多种因素调节,包括高磷、高钙水平及氧化应激、机械应力等。此外,中医药研究在减轻血管钙化方面显示出潜力,例如灵芝孢子粉和其衍生物,三七、黄芩素、根皮素、雷公藤甲素等。这些研究为进一步理解和干预血管钙化提供了重要的证据,并揭示了一些潜在的抑制因子,可以作为未来治疗血管钙化的研究方向。     

IABP救治心脏手术后低心排血量的疗效观察

目的：评价主动脉内球囊反捕（ＩＡＢＰ）在心脏手术后不许治低心排血量（低心排）的效果。方法：２８例术后应用中等剂量心脏活性药物支持不能改善的低心排患,均立即使用ＫＡＡＴⅡＰｌｕｓ ＩＡＢＰ（４０ｍｌ）。监 桡动脉和主动脉压力波形,持续监测左心功能,记录尿量,观察末梢循环状况。结果：全组患ＩＡＢＰ辅助时间为（４８±３２）ｈ,早期生存率为７５．０％。所有患在应用ＩＡＢＰ后,桡动脉压力（基础收缩压）     

主动脉瓣膜重度狭窄行经导管主动脉瓣膜置入术的围手术期管理

目的探索主动脉瓣膜重度狭窄行经导管主动脉瓣膜置入治疗患者的围手术期管理.方法选择1例主动脉瓣膜重度狭窄行经导管主动脉瓣膜置入治疗的患者,组成多学科协作手术团队,术前充分评估,术中严密监测,术后安全监护(CCU)及康复,定期随访.结果本例手术成功,无处置及护理不当并发症;随访12个月,患者活动后胸闷症状明显缓解,活动耐力逐步提升,生存质量提高.结论利用团队优势,做好围手术期管理,可以顺利完成手术,促进患者康复.