恶性快速性室性心律失常致心脏骤停的临床观察

目的探讨恶性快速性室性心律失常致心脏骤停的原因与高危心电表现。方法分析45例在入院时或入院后至少发生1次心脏骤停患者的原因及其发作时与发作前后的常规12导联心电图或持续心电监视心电图形。结果45例恶性快速性心律失常致心脏骤停最常见的基本原因为冠心病急性或陈旧性心肌梗死,次为特发性及继发性巨大异常J波、扩张型心肌病;低钾血症是最常见的诱因;最常见的恶性快速性室性心律失常类型是心室颤动。其高危心电图表现:①复杂性室性早搏;②异常J波;③继发性长Q-T间期综合征;④Brugada综合征;⑤广泛前壁心肌梗死伴墓碑样ST段抬高。上述各种原因心脏骤停者有各自不同的临床及心电学特征。结论恶性快速性室性心律失常所致心脏骤停存在多种原因及高危心电图表现。     

心肌梗死病人发生心肌缺血、损伤和坏死的心电图表现与诊断价值

目的探讨心肌梗死病人发生心肌缺血、损伤和坏死的心电图表现与诊断价值。方法回顾性分析2013年11月—2016年11月收治的91例心肌梗死病人的临床资料,均实施心电图检查。观察病人的检查结果以及心电图表现情况、合并室性心律失常情况,并进行分析。结果 91例病人中均具有胸痛症状以及典型的临床症状,梗死部位主要位于前间壁和下壁以及前壁。经心电图检查,多在发病24 h内即表现出典型的心电图特征,相应导联ST段弓背向上抬高,并出现病理性Q波。91例中,共有54例出现ST段抬高表现,其中:(1)45例为ST段抬高、T波倒置、出现病理性Q波;(2)9例为ST段抬高,胸前导联R递增不良;其余37例出现非ST段抬高表现:(1)28例为ST段下移伴T波倒置或低平;(2)9例为ST段正常,伴T波倒置或低平。具有ST段抬高心电图表现病人的室性心律失常并发率为27.78%,显著高于具有非ST段抬高心电图表现的病人(5.41%),经比较差异均有统计学意义(P0.05)。结论心肌梗死发生之后,经心电图检查,可发现随着时间的推移先后出现心肌缺血、损伤和坏死三种类型的心电图表现。具有ST段抬高心电图表现的病人具有更高的室性心律失常并发可能,临床应积极予以综合性的分析判断。     

典型Brugada综合征伴明显下壁导联心电图动态变化一例

患者男性,40岁.以"发作性意识丧失2年"入院,常规心电图示Brugada综合征Ⅱ型改变(V2导联呈"马鞍型"ST段抬高)并伴下壁导联S波增宽,升支与T波升支相连,ST段难以辨认.动态心电图显示心电图呈动态变化,尤其当心率减慢时,V2导联呈下斜型ST段抬高(Brugada综合征Ⅰ 型改变),下壁导联S波变得更宽,与T波...     

低血钾诱发Brugada综合征室颤发作1例

患者男、76岁,因＂反复晕厥两天＂入院。在当地医院记录心电图提示：V1～V2导联J点抬高伴ST段抬高T波倒置,V3、V4导联ST段水平抬高伴T波直立（图1A）。入院后患者仍反复出现晕厥,心电监护提示室颤反复发作（图2）。经多次电复律后能     

急诊PCI患者aVR导联T波方向的预后意义

目的 探讨急性前壁ST段抬高心肌梗死行急诊经皮冠脉介入治疗(PCI)患者,入院心电图中aVR导联T波方向与预后的关系.方法 排除不符合病例后,共91名急性前壁ST段抬高性心肌梗死行急诊PCI患者入选.基于入院时的心电图,患者被分为T波正向组(n=20,组1)和T波负向组(n=71,组2),所用的患者的临床特点、急诊PCI结果及院内临床事件被记录.结果 T波正向的患者比T波负向患者的年龄更大,住院期间的死亡率更高(15％ vs.1.4％ p=0.03).结论 急性前壁ST段抬高性心肌梗死行急诊介入治疗的患者,aVR导联T波正向与院内升高的死亡率相关.     

J波综合征一家系

先证者男性,45岁。间断胸痛4月,晕厥1次入院。心电图V2～V4导联可见J波,J波后ST段抬高0.05～0.1mV,T波直立。平板运动试验、心脏超声、冠状动脉造影无异常。其祖父、父亲、二叔早发猝死史。其弟、其弟之子心电图亦有J波伴ST段抬高。考虑可能系一少见的有明显家族遗传倾向的恶性心律失常疾病。     

长QT综合征心电图和临床诊断

长QT综合征(LQTS)是指心电图上表现为QT间期延长、ST—T波异常、易产生恶性室性心律失常如尖端扭转型室速(Tdp)的一组综合征，临床上常有反复发作晕厥或猝死的病史以及家族史。     

Brugada综合征合并先天性长QT综合征一例

目的报告1例反复发作晕厥伴胸前导联J—ST—T显著抬高患者的临床过程。方法1例15岁男孩反复于夜间卧床休息时发生晕厥，对该患者及其父母进行病史询问、体格检查、心电图及超声心动图检查，并行普罗帕酮激发试验。对患者进行冠状动脉，左、右心室造影和心内电生理检查。结果患者及其父母无器质性心脏病依据，无阳性猝死家族史。患者直立倾斜试验阴性，冠状动脉和左、右心室造影正常，心内电生理检查未发现异常，未诱发室性心律失常。患者基础心电图胸前导联J-ST—T显著抬高，晕厥后窦性心动过速时J—ST—T降低伴QTc延长。静脉注射普罗帕酮70mg后胸前导联J—ST与T波第二峰进一步抬高。患者母亲基础心电图ST—T类似于LQT3，但QTc正常。患者父母在静脉注射普罗帕酮70mg后胸前导联ST—T均进一步抬高。结论该患者心电图不同于已报道的Brugada综合征合并LQT3，可能为新的SCN5A基因突变导致的一种新的表型。     

心电图Brugada征与处理对策

Brugada综合征于1992年由西班牙Brugada兄弟首先报道。该综合征多见于东南亚地区无心脏结构异常的年轻男性，其发病与心脏钠通道基因SCN5A突变有关。患者有心室颤动发作，可致猝死。心电图表现为右束支传导阻滞和V1～V3导联ST段穹窿形或马鞍形抬高，T波倒置。有学者将以上心电图改变称为Brugada征。     

高龄急性心肌梗死患者直接经皮冠状动脉介入术后并发室间隔穿孔行介入封堵治疗一例

正1病例资料患者,女,80岁。2015年5月20日因"胸痛4 h"入院。患者5月20日9时突发心前区胸痛,压榨性,向左上肢放射,伴大汗,无黑矇、晕厥、喘气。症状持续不缓解,外院诊断"急性ST段抬高型广泛前壁心肌梗死",给予"阿司匹林、氯吡格雷"各300 mg口服后转我院急诊科。复查心电图提示"广泛前壁导联ST段抬高,较外院心电图无回落"(图1),心脏超声示"左房扩大,左室节段性室壁运动异常,二、三尖瓣轻度反流,左室收缩功能减低(LVEF 42%)"。再次给予口服"氯吡格雷"300 mg,紧急送介入中心行直接经皮冠状动     

The cardiac component of cardiac cachexia

Background Recent evidence suggests the importance of noncardiac mechanisms in the genesis of the syndrome of cardiac cachexia. This raises the question of the relative role of the heart itself in this syndrome. This study sought to assess the cardiac dimensions, mass, and function and changes in these parameters over time in patients with chronic heart failure with and without cachexia. Methods Doppler echocardiography was performed in 28 patients with nonedematous weight loss (>7.5% over a period of >6 months) compared with 56 matched patients without weight loss in a ratio of 1:2 (age 71 ± 13 vs 67 ± 8 years, P = .07; New York Heart Association class 2.9 ± 0.7 vs 2.6 ± 0.6, P = .08). In 18 cachectic and 35 noncachectic patients with previous echocardiographic recordings, we analyzed the changes in left ventricular (LV) dimensions and mass over time. Results Cardiac dimensions including LV diastolic (69 ± 9 mm vs 67 ± 13 mm) and systolic cavity diameter (58 ± 11 mm vs 55 ± 15 mm), LV mass (480 ± 180 g vs 495 ± 190 g), and LV systolic and diastolic function including fractional shortening (16% ± 10% vs 18% ± 10%), isovolumic relaxation time (29 ± 22 ms vs 36 ± 27 ms), and E/A ratio (2.7 ± 1.6 vs 3.3 ± 2.9) did not differ between cachectic and noncachectic patients (all P > .1). By analyzing changes in LV mass over time, we found an increase (>20%) in 2 (11%) cachectic and 14 (40%) noncachectic patients and a decrease in LV mass (>20%) in 9 (50%) cachectic and 8 (23%) noncachectic patients (χ² test, P < .05). Conclusions Although no specific cardiac abnormality could be detected echocardiographically in cachectic patients compared with patients with noncachectic chronic heart failure in a cross-sectional study, over time a significant loss of LV mass (>20%) occurs more frequently in patients with cardiac cachexia. (Am Heart J 2002;144:45-50.)     

Analysis of cardiac symptoms preceding cardiac arrest

Prodromal symptoms and cardiac history were examined in 227 patients with coronary artery disease who were successfully resuscitated after out-of-hospital cardiac arrest. Cardiac arrest was sudden—with either no symptoms or symptoms for less than 1 hour—in 71% of the patients. Nonsudden death—death occurring after more than 1 hour of symptoms—occurred in 29% of the patients. A history of cardiovascular disease was present in 85% of patients with sudden cardiac arrest and in 83% with nonsudden arrest. Cardiac arrest occurred without symptoms in 38% of the patients with sudden cardiac arrest and was the first expression of coronary artery disease in 4% of the entire study group. This study indicates that cardiac arrest usually occurs with symptoms and almost always in the setting of a history of cardiovascular disease.     

心脏骤停和心脏性猝死

心脏性猝死(SCD)是目前社会关注的热点问题.2005年WHO的数据表明,在全球死于心脑血管疾病的约1700万人群中,40%～50%是SCD.SCD虽然有多种定义,但目前一般认为是在1 h内出现的由于心血管原因导致的非预期死亡事件或无目击者的死亡事件.心脏骤停(SCA)不等同于SCD,SCA如果救治失败会引起真正的SCD.     

Sodium-induced cardiac aldosterone synthesis causes cardiac hypertrophy

High sodium intake causes cardiac hypertrophy independently of increases in blood pressure. Aldosterone is synthesized in extraadrenal tissues such as blood vessels, brain, and heart. Effects of 8 weeks of high sodium intake on cardiac aldosterone synthesis, as well as cardiac structure, mass, and aldosterone production, levels of mRNA coding for aldosterone synthase (CYP11B2) and the angiotensin II AT1 receptor, were studied in normotensive Wistar-Kyoto (WKY) rats. Isolated rat hearts were perfused for 2 hr, and the perfusate was analyzed by high-performance liquid chromatography and mass spectrometry. Aldosterone synthase activity was estimated from the conversion of [14C]deoxycorticosterone to [14C]aldosterone. Levels of mRNA for CYP11B2 and AT1 receptor were determined by competitive polymerase chain reactions. A high sodium intake for 8 weeks produced left ventricular hypertrophy without elevation of blood pressure. Plasma aldosterone concentrations and plasma renin concentrations were decreased by high sodium intake. Aldosterone production, activity of aldosterone synthase, and expression of mRNA for CYP11B2 and AT1 receptor were increased in hearts of rats with high sodium intake. These results suggest that high sodium intake increases cardiac aldosterone synthesis, which may contribute to cardiac hypertrophy independently of the circulating renin-angiotensin-aldosterone system.     

Occult cardiac lymphoma presenting with cardiac tamponade

Subxiphoid pericardiostomy is the procedure of choice for treatment of a pericardial effusion with tamponade. We report a case in which this procedure not only failed to reveal the presence of an occult malignancy, but also resulted in a recurrent symptomatic effusion.     

Acute cardiac tamponade due to cardiac actinomycosis

Cardiac actinomycosis occurs in less than 2 percent of the patients with infections due to Actinomyces israelii. We describe the findings in a patient with acute cardiac tamponade who survived through pericardial drainage and aggressive medical therapy. Although uncommon, this disorder is important to recognize because it is curable with current medical and surgical therapy.     

External cardiac pacing during in-hospital cardiac arrest

External noninvasive cardiac pacing offers a rapid and simple method of pacing the heart during an emergency. It has been suggested that early use of cardiac pacing for bradycardia or asystole may improve survival in patients who have cardiac arrest. To investigate this possibility 58 consecutive episodes of cardiac arrest occurring on the medical wards or emergency room. Twenty-six episodes underwent external noninvasive pacing for bradycardia or asystole refractory to standard drugs. Only 2 patients survived, and survival could be directly attributed to pacing in only 1 of them. Of the 32 episodes not undergoing pacing, 23 had transient asystole or bradycardia, 13 of which rapidly responded to medications. The 17 cases (53%) not undergoing pacing survived. In conclusion, when bradycardia or asystole during cardiac arrest fails to respond to standard pharmacologic measures, it is an indicator of severe myocardial damage, and attempts at cardiac pacing rarely improve survival.     

Coronary angioscopy during cardiac catheterization and cardiac surgery

Summary Coronary angioscopy (CA) was performed in 30 patients (pts) during cardiac catheterization (Group 1) and in 11 pts during coronary bypass surgery (Group 2) using ultrathin fiberoptic angioscopes (Ø1.2–1.8 mm). For percutaneous CA (Group 1) the angioscope was introduced through a 9F guiding catheter from the femoral artery. The viewing field was cleared by flushing Ringer's solution and short-time occlusion of the coronary ostium by the guiding catheter. In Group 2 CA was performed retrogradely from the distal arteriotomy and through the bypass vein during flushing with cardioplegic solution. In Group 1 in 17/30 pts the coronary artery could be successfully examined by CA. In 13 pts the obstruction was eccentric and irregular shaped. In 2/5 pts, in whom CA was performed successfully pre and post balloon dilatation, CA after PTCA revealed an intimal rupture without clinical or angiographical signs of the intimal dissection. In Group 2 in 9/11 pts good visualization of stenoses could be achieved. At the obstruction site CA revealed thrombi in 3 pts and ulcer in 1 pts. In contrast to angiography, which estimates the lumen diameter of a segmental lesion, CA gives information about the luminal shape and the underlying substance of the obstruction (e.g. atheroma, thrombus, ulceration). The main problems in percutaneous CA are the insufficient intraluminal guidance, the insufficient depth of view of the angioscopes, and the limited examination time.     

心脏介入性治疗并发心脏压塞的处理策略

目的 探讨心脏介入治疗并发心脏压塞的处理策略。方法 12例心脏压塞患者，男性5例，女性7例，年龄28～52岁。其中经皮二尖瓣球囊扩张术8例，冠状动脉腔内成形术1例，先天性动脉导管未闭封堵术2例，右心室起搏1例。根据心脏穿孔的不同原因、可能的部位及心脏压塞情况，分别采用心包穿刺引流、心包穿刺引流与开胸修补或开胸置管引流等方法治疗。结果 3例单纯心包穿刺引流均痊愈；8例紧急心包穿刺引流后开胸修补有7例痊愈，1例主动脉根部破裂者因心源性休克时间过长，死于呼吸衰竭；1例冠状动脉腔内成形术者左回旋支穿孔，紧急心包穿刺引流后心包切开、胸腔置管引流痊愈。结论 根据心脏介入性治疗导致心脏压塞的不同原因、可能部位及心脏压塞进展情况，采取相应措施，可有效治疗此类并发症。