右心声学造影被认为是卵圆孔未闭诊断的“金标准”，虽然有众多流程指导临床诊断，但在实践过程中依然有假阳性及假阴性的可能性。本文通过阐述1例卵圆孔未闭患者诊断过程中的诸多陷阱及应对策略，以期为临床提供参考。

Unlike other types of heart failure(HF),the efficacy of traditional medication and therapies are usually not reliable in patients with HF with preserved ejection fraction(HFpEF).It may be attributed to obviously heterogeneous etiologies and inconsistent pathophysiological pathways among such patients.GE's phenotyping is a novel etiology-oriented classification method.It not only facilitates grouping HFpEF patients with similar pathophysiological mechanisms,but also contributes to making appropriate diagnosis and treatment plans,and taking prognosis assessment and management measures for different types of HF patients.In the future,GE's phenotyping is expected to be an important reference for clinical study design for these patients.

Takotsubo综合征（TTS）以其左心室造影表现为收缩期窄颈、心尖球形膨出，类似于“章鱼壶”样改变而得名。TTS的心电图4个不同阶段的变化具有连续性：ST段抬高、T波倒置、T波倒置进行性加深以及QT间期逐渐延长。TTS心电图的标志特征对临床诊断及结局预测有一定敏感性和特异性。本文旨在简要回顾与TTS相关的重要心电图发现及其临床指导意义。

Abstract Background Post‐ischemic angiogenesis is critical for blood flow recovery and ischemic tissue repair. N6‐methyladenosine (m6A) plays essential roles in numerous biological processes. However, the impact and connected mechanism of m6A on post‐ischemic angiogenesis are not fully understood. Methods AlkB homolog 5 (ALKBH5) was screened out among several methyltransferases and demethylases involved in dynamic m6A regulation. Cardiac microvascular endothelial cells (CMECs) angiogenesis and WNT family member 5A (WNT5A) stability were analyzed upon ALKBH5 overexpression with adenovirus or knockdown with small interfering RNAs in vitro. The blood flow recovery, capillary, and small artery densities were evaluated in adeno‐associated virus (AAV)‐ALKBH5 overexpression or ALKBH5 knockout (KO) mice in a hind‐limb ischemia model. The same experiments were conducted to explore the translational value of transient silencing of ALKBH5 with adenovirus. Results ALKBH5 was significantly upregulated in hypoxic CMECs and led to a global decrease of m6A level. ALKBH5 overexpression further reduced m6A level in normoxic and hypoxic CMECs, impaired proliferation, migration, and tube formation only in hypoxic CMECs. Conversely, ALKBH5 knockdown preserved m6A levels and promoted angiogenic phenotypes in hypoxic but not in normoxic CMECs. Mechanistically, ALKBH5 regulated WNT5A expression through post‐transcriptional mRNA modulation in an m6A‐dependent manner, which decreased its stability and subsequently impeded angiogenesis in hypoxic CMECs. Furthermore, ALKBH5 overexpression hindered blood flow recovery and reduced CD31 and alpha‐smooth muscle actin expression in hind‐limb ischemia mice. As expected, ALKBH5‐KO mice exhibited improved blood flow recovery, increased capillary, and small artery densities after hind‐limb ischemia, and similar beneficial effects were observed in mice with transient adenoviral ALKBH5 gene silencing. Conclusion We demonstrate that ALKBH5 is a negative regulator of post‐ischemic angiogenesis via post‐transcriptional modulation and destabilization of WNT5A mRNA in an m6A‐dependent manner. Targeting ALKBH5 may be a potential therapeutic option for ischemic diseases, including peripheral artery disease.

科学界,错失诺贝尔奖的科学结论有很多,最让人印象深刻的可能是爱因斯坦的相对论和霍金黑洞理论.前者虽曾获过诺贝尔奖,但其当时的成绩与之后相比,似乎相差甚远.在心脏病学领域,用于诊疗的各种检查手段,包括心电图、X线、心导管、磁共振、CT都曾荣膺诺贝尔医学奖或物理学奖,唯独心脏超声与之擦肩而过. 第二次世界大战期间,有关超声波的军事研究间接促进了战后超声医学的发展.实际上,我们能追溯到的人类最早超声心动图检查记录,始于1953年10月29日.这一切的诞生,也出自临床尤其是心脏外科医生对心脏结构和功能评估的迫切需要[1].

患者,女性,72岁,主因"胸骨后疼痛10 h"于2020年7月16日收入院.入院前10h,患者无明显诱因开始出现胸骨后持续压榨性隐痛,伴恶心欲呕、心悸,无头晕、一过性黑矇,无呼吸困难、咳嗽咳痰,无大汗淋漓等症状.患者既往有高血压史4年,最高达180/110 mm Hg(1 mm Hg=0.133 kPa),服用"马来酸依那普利片10 mg,1次/d",自诉血压可控制;2年前植入永久起搏器,否认糖尿病病史,无烟酒等不良嗜好.

Post-transcriptional modifications play pivotal roles in various pathological processes and ischemic disorders. However, the role of N7-methylguanosine (m7G), particularly m7G in mRNA, on post-ischemic angiogenesis remains largely unknown. Here, we identified that methyltransferase like 1 (METTL1) was a critical candidate responsible for a global decrease of m7G within mRNA from the ischemic tissues. The in vivo gene transfer of METTL1 improved blood flow recovery and increased angiogenesis with enhanced mRNA m7G upon post-ischemic injury. Increased METTL1 expression using plasmid transfection in vitro promoted HUVECs proliferation, migration, and tube formation with a global increase of m7G in mRNA. Mechanistically, METTL1 promoted VEGFA mRNA translation in an m7G methylation-dependent manner. Our findings emphasize a critical link between mRNA m7G and ischemia and provide a novel insight of targeting METTL1 in the therapeutic angiogenesis for ischemic disorders, including peripheral arterial disease.

Background A series of studies showed that endocardial radiofrequency ablation (ERFA) could reduce the left ventricular outflow tract (LVOT) gradient in patients with septal hypertrophy. This study aimed to determine the safety and efficacy of a modified ERFA approach guided by transthoracic echocardiography (TTE) as an alternative to ablation performed under a three-dimensional (3D) electroanatomical system or intracardiac echocardiography (ICE). Methods Twenty-five patients with hypertrophic obstructive cardiomyopathy (HOCM) underwent ERFA of septal hypertrophy, guided by echocardiography. The LVOT gradient, left ventricular ejection fraction (LVEF), LV thickness, New York Heart Association (NYHA) class, and biochemical laboratory values were recorded before ablation and during follow-up. Results The patients’ peak and stress-induced LVOT gradients were significantly reduced after 12 months of follow-up (resting gradient: from 123.2±17.7 to 15.7±7.8 mmHg, P<0.05; provocative gradient: from 140.2±20.8 to 18.4±8.0 mmHg, P<0.05). Compared with baseline, the septal diameter was reduced slightly after 12 months, but the difference was not significant (24.8±3.5 vs. 24.2±3.4 mm, P>0.05). The reduction in LVOT gradient was associated with an improvement in NYHA functional classification (from 3.0±0.0 to 1.6±0.7, P<0.05), the 6-minute walking distance (413±129 m at baseline; 458±108 m immediately after ERFA; 471±139 m after 12 months, P<0.05), and pro B-type natriuretic peptide levels (from 924.00±139 to 137.45 ±75.73 pg/mL, P<0.05). After the procedure, the patients showed no worsening of LVEF compared with baseline (64%±5.3%), and no cases of bundle branch block nor complete heart block occurred. Conclusions ERFA guided by TTE provides a new treatment option for HOCM which can achieve symptomatic improvement as well as a significant and sustained reduction of the LVOT gradient. Moreover, by avoiding the use of the 3D electroanatomical system or ICE, this treatment has an acceptable cost.

最近一次教学查房中,让学生们讨论一个很有趣的话题:为什么心电图波形的命名是P-Q-R-S-T而不是A-B-C-D-E,或甲-乙-丙-丁-戊,甚至金-木-水-火-土呢? 这看起来似乎是一个很简单的问题. 同学们想当然地认为,字母P-Q-R-S-T分别是除极、复极电活动中某个过程单词的简写;就像我们做腔内电生理检查时,使用字母A代替心房(atrium)电活动,H代替希氏束(His)电活动,V代表心室(ventri-cle)电活动一样.

患者,女性,72岁,主因"胸骨后疼痛10 h"于2020年7月16日收入院.入院前10h,患者无明显诱因开始出现胸骨后持续压榨性隐痛,伴恶心欲呕、心悸,无头晕、一过性黑矇,无呼吸困难、咳嗽咳痰,无大汗淋漓等症状.患者既往有高血压史4年,最高达180/110 mm Hg(1 mm Hg=0.133 kPa),服用马来酸依那普利片10 mg,1次/d,自诉血压控制可;2年前植入永久起搏器,否认糖尿病病史,无烟酒等不良嗜好.

Objective:To investigate the image characteristics of woven coronary artery (WCA)on intravascular ultrasound(IVUS) and optical coherence tomography(OCT).Methods:Thirty-seven patients suspected of WCA on coronary angiography were enrolled from Teaching Hospital of Chengdu University of Traditional Chinese Medcine, Zhengzhou Cardiovascular Disease Hospital and Zhongshan Hospital of Fudan University from January 2013 to July 2020. The intraluminal imaging features of WCA were analyzed using IVUS and OCT.Results:Of the 37 patients admitted at the cardiology service, 9 patients had WCA. All the patients underwent coronary angiography, IVUS and OCT, of which 6 lesions were located on the right coronary artery, 2 lesions were located on the left anterior descending artery and 1 patient had WCA on the circumflex artery. The mean length of WCA lesions was 2.2 cm(ranged from 1.2 cm to 4.5 cm). The angiographic appearance of WCA was numerous small tortious channels origined form the main lumen. The channels appeared to be " doughnut" like pattern and they merged to normal artery again after the anomalous segment. Flow limitation was rare unless there was coronary atherosclerosis. OCT and IVUS showed multiple spiral channels in the anomalous segment, which were independent of each other and each channels had a relatively complete three-layers vascular structure.Conclusions:With typical image characteristics, IVUS and OCT are able to screen out WCA and guide the treatment decision making.

患者男性,67岁,因“反复双下肢水肿20+年,腹部、阴囊胀满4+年,胸闷气紧1d”人院.患者20+年前无明显原因出现双下肢水肿,四肢皮肤紫红色,无心慌、胸闷,无心前区疼痛等不适,至当地医院就诊,诊断为“心房颤动、心力衰竭”,予以对症治疗(具体诊治不详)后好转出院.后每至秋冬季节便出现双下肢反复水肿,均经治疗后好转.自述既往有高血压病史,院外长期口服“北京降压零号”治疗,血压控制可.

目的 探讨在内镜超声引导下,上消化道-胆囊吻合术及经口胆囊镜术在保留胆囊的情况下治疗胆囊结石和胆囊息肉等良性疾病的临床效果;比较不同吻合途径手术方法的治疗效果.方法 选择成都中医药大学附属医院在2016年8月至2018年12月期间,采用内镜超声引导下上消化道-胆囊吻合术及经口胆囊镜术治疗胆囊疾病的18例患者为研究对象,收集分析上消化道-胆囊吻合术的记录手术操作时长、吻合部位、手术成功率;观察患者术后状态,包括腹痛评分、发热以及有无并发症;经口胆囊镜术的手术操作时长、支架滞留时间、手术成功率以及有无并发症,瘘道愈合时间、是否扩张及是否成熟等指标.结果 经上腹部CT、MRI及内镜超声检查确诊,患者合并胆总管结石8例,所有患者均成功实施上消化道-胆囊吻合术,临床症状及实验室检查结果在术后48 h内恢复正常.患者经口胆囊镜术的手术成功率为100％,其中行胆囊镜取石术15例,行胆囊镜胆囊息肉切除术3例.术后无严重并发症,瘘道闭合延迟1例.瘘道愈合1个月复查腹部超声显示胆囊收缩率大于50％,随访结石复发1例.行胃-胆囊吻合术者4例,行十二指肠-胆囊吻合术者14例.十二指肠-胆囊吻合术平均手术时长大于胃-胆囊吻合术(P<0.05),平均腹痛评分小于胃-胆囊吻合术(P<0.05).不同吻合部位术后一过性白细胞增高和术后一过性发热发生率比较无统计学差异(P>0.05).结论 内镜超声引导下上消化道-胆囊吻合术及经口胆囊镜术在保留胆囊的情况下治疗胆囊结石和胆囊息肉等疾病的临床效果较好,能同时处理胆总管结石,且十二指肠-胆囊吻合术的临床效果优于胃-胆囊吻合术.

患者男性,86岁,因“反复心前区疼痛20余天”于2018年2月27日入住成都中医药大学附属医院(我院)心血管内科.入院前20余天,患者出现活动后心前区疼痛,疼痛性质呈压榨样,放射至左背部,每次发作持续约半小时,经含服“麝香保心丸”或休息后症状缓解,入院考虑冠状动脉粥样硬化性心脏病(冠心病)?入院后心电图结果提示:窦性心律,心率81次/min;顺钟转;完全性右束支传导阻滞;Ⅱ、V4～6导联ST段压低.超声心动图提示:二尖瓣、主动脉瓣轻度反流,左心室舒张功能稍低.胸片提示:心界不大,双肺未见明显异常.血常规、生化等检查未见明显异常.排除手术禁忌后行冠状动脉造影检查结果示:左主干血管内膜光滑.左前降支开口可见40％节段性偏心性狭窄,中远端可见最重80％弥漫性偏心性狭窄(图1A),左回旋支远段可见最重70％弥漫性偏心性狭窄,右冠状动脉开口至中段可见最重70％弥漫性偏心性狭窄,远段可见最重70％弥漫性偏心性狭窄.评估患者SYNTAX评分为22分.家属及患者本人拒绝行冠状动脉旁路移植术,要求行经皮冠状动脉介入治疗(percutaneous coronary intervention,PCI).

患者,女性,44岁,因“气紧8d”入院.入院前8天,患者无明显诱因出现气紧,无畏寒、发热,无咳嗽、咳痰,无胸闷、胸痛,无恶心、呕吐、心悸、黑矇等不适.活动后症状加重,休息可减轻,患者于当地医院,考虑“急性上呼吸道感染”,予“氨咖黄敏口服液”等治疗,症状缓解不明显.2d前气紧症状加重,就诊于成都中医药大学附属医院(我院),超声心动图检查提示“大量心包积液”,收入院.患者发病以来,饮食睡眠可,二便正常,体质量无明显变化.入院查体生命体征平稳,双肺呼吸音清,未闻及干湿啰音.心脏相对浊音界向双侧扩大,心音遥远、低钝,心率74次/min,律齐,各瓣膜未闻及杂音.腹部查体未见明显异常.

患者,80岁,女性,因"反复心慌、胸闷、胸痛7+ 年,复发加重伴发热、全身乏力3d"入院.7年前患者活动后出现心慌、胸闷、心前区闷痛,放射至背部,持续时间约几分钟,休息时缓解,情绪激动时加重,无咳嗽、咳痰,无腹痛、腹泻,无黑矇、晕厥等不适,遂至当地医院就诊,诊断为"冠状动脉性心脏病(冠心病)?",并予以"阿司匹林抗血小板聚集,他汀类药物降脂稳定斑块"等冠心病二级预防治疗,经治疗后好转出院.后上述症状仍反复发作.5+ 年前,患者心前区闷痛加重,放射至背部,持续时间约10min,休息及反复含服"硝酸甘油"未见明显缓解,再次至当地医院就诊,行超声心动图提示"左心房增大,左心室功能测值正常";行冠状动脉造影,提示"前降支内膜不规则";经对症支持治疗后好转出院,出院后长期服用"阿司匹林"等药物治疗.患者反复因"心绞痛"症状在当地医院就诊.入院前3天,患者因感冒后出现心慌、胸闷,持续时间较前延长,服用硝酸甘油效果不佳,并伴有发热、全身乏力,自测体温38℃,为求进一步治疗,遂转至成都中医药大学附属医院(我院)就诊.

患者男,79岁,因"反复胸痛5年余,加重伴双下肢水肿20余天"入院.入院心电图提示胸前导联V2~V6导联T波倒置,体格检查示颈静脉怒张,肝颈静脉回流征(一).双肺呼吸音粗,双下肺可闻及少量湿啰音,心界向左侧扩大,心率85次/min,律齐,主动脉瓣第二听诊区可闻及粗糙的3/6级收缩期喷射样杂音,腹部查体无殊,双下肢轻度凹陷性水肿.院内查血常规、肝功能、肾功能、电解质、凝血功能未见明显异常.超声心动图示室间隔基底段30 mm,左室后壁9 mm,SAM 征阳性(图1A);左室流出道血流加速, Vmax=6.10 m/s,PGmean=93.6 mmHg(1 mmHg=0.133 kPa)(图1B).冠状动脉造影未见确切狭窄,心导管测量左室-主动脉压力阶差为108 mmHg,诊断为肥厚型梗阻性心肌病,拟行室间隔化学消融术,但因其B型钠尿肽(BNP)居高不下(多次复查均>7 000 ng/L).为防止消融术后大面积心肌细胞坏死加重心力衰竭,遂行室间隔射频消融术.

患者,女,48岁,既往体健,因“突发胸闷、呼吸困难4h”于201 5年6月入成都中医药大学附属医院(我院)胸痛中心;急诊科快速床旁检验示心肌酶及心肌损伤标志物阴性,D-二聚体＞10(参考值＜0.5)mg/L;动脉血气分析示pH 7.084,二氧化碳分压(partial pressureof carbon dioxide,PCO2)41.5 mm Hg(1 mm Hg=0.133 kPa),氧分压(partial pressure of oxygen,PO2)63.5 mm Hg,碱剩余-17.2 mmol/L.心电图示窦性心律,V2～V5导联T波深倒置(图1).因患者辅助检查不符合急性冠状动脉综合征表现,且家属拒绝行侵入性检查,故收入心内科重症监护室(cardiac care unit,CCU).入院后查体示血压90/55 mm Hg,床旁超声心动图示肺动脉增宽(28 mm),右心房(57 mm)及右心室增大(30 mm),三尖瓣中量反流,估测肺动脉收缩压约61 mm Hg(图2);肺动脉增强CT示双下肺动脉、右肺下叶内侧基底段动脉充盈缺损(图3).

患者,女,48岁,既往体健,因“突发胸闷、呼吸困难4h”于2015年6月入成都中医药大学附属医院(我院)胸痛中心;急诊科快速床旁检验示心肌酶及心肌损伤标志物阴性,D--聚体＞10(参考值＜0.5)mg/L;动脉血气分析示pH 7.084,二氧化碳分压(PCO2)41.5 mm Hg(1 mm Hg=0.133 kPa),氧分压(PO2)63.5 mm Hg,碱剩余-17.2 mmol/L.心电图示窦性心律,Ⅴ2～Ⅴ5导联T波深倒置(图1).因患者辅助检查不符合急性冠状动脉综合征表现,且家属拒绝行侵入性检查,故收入心内科冠心病重症监护室(cardiac care unit,CCU).

患者女,60岁,因"反复腰骶部疼痛20 d,加重伴双下肢放射痛1周"入我院骨科.50 d前因风湿性心脏病于当地医院行"二尖瓣置换术+三尖瓣成形术",术后常规口服华法林抗凝,凝血酶原时间(INR)控制在2.5左右.入院后心电图提示心房颤动,心室率99次/min,时伴室内差异性传导.超声心动图示距主动脉瓣约3.5 cm处升主动脉前壁回声中断约1.5 cm;升主动脉通过破口与前纵隔内一大小约12.4 cm×8.7 cm×7.3 cm的瘤样结构相通,瘤壁菲薄,其内可见明显自发显影;受瘤体压迫,升主动脉明显变细(图1~3).胸主动脉CT A示前纵隔假性动脉瘤,大小约11.0 cm×8.9 cm×9.9 cm,瘤体与主动脉间破口大小约1.0 cm×0.9 cm× 0.5 cm(图4).建议患者尽早外科手术治疗,患方表示拒绝.1个月后患者因呼吸困难再次就诊,查体见患者胸骨较前明显膨出,复查CTA示瘤体及破口较前明显扩大,瘤体内大量附壁血栓形成(图5~6);遂收入胸外科行手术治疗.术中见心包内致密粘连,上段胸骨骨质侵蚀破坏,假性动脉瘤突入胸骨缺损间隙,瘤体内大量附壁血栓形成.患者胸骨切开过程中瘤体破溃,伴右心室前壁部分撕裂出血,予人工血管补片修补升主动脉,心包片修补右心室前壁,经食管超声验证人工血管通畅、瓣膜功能正常后返回监护病房.术后予抗感染、纠正心力衰竭等对症处理后好转出院.随访至今,人工机械瓣及人工血管无异常,呼吸困难等症状缓解.