心脏骤停与心脏性猝死

1概述心脏性猝死(SCD)通常定义为存在或不存在心脏疾病的人,临床表现出现的1h内发生由于心血管原因导致的非预期死亡[1]。心脏骤停(SCA)不等同SCD,SCA如果抢救及时会发展成流产的SCD,如果救治失败会引起真正的SCD。大多数SCD被认为是室速恶化为室颤(VT)以及心脏停搏。在60%~80%     

心力衰竭患者心源性猝死的预警和治疗策略

心源性猝死(SCD)是指心脏的临床状态突然变化而发生在1h内的死亡或瞬间死亡.SCD的分类包括心律失常死亡(SAD)和非心律失常事件死亡[1].心力衰竭患者的SCD发生率是普通人群的6～9倍,而SCD的预警和治疗则是临床医生所面临的棘手问题.在过去的20年里,尽管心力衰竭的治疗已有了较大进展,但心力衰竭患者的4年存活率却低于公众对照组的50%.现已确定在严重充血性心力衰竭患者中室性心律失常的发生率高达85%以上.埋藏式心脏复律除颤器(ICD)是终止致命性室性心动过速最有效的方法,而且在选择性高危患者中已证实ICD降低死亡率的费用-效果最佳.在公众人群中心力衰竭约占1%～2%,而且数量还在增加 .目前,确定心力衰竭合并有高度心律失常危险性的患者,及时置入ICD并采取其他抗心律失常措施是一个重大挑战[2].     

应进一步加强对心脏性猝死的一、二级预防

现代心脏性猝死(sudden cardiac death,SCD)的定义为(1)临床上有心脏骤停(sudden cardiac arrest,SCA)的证据;(2)从突发症状到死亡的时间在1 h之内;(3)不明原因的死亡,此前24 h内病人情况良好.     

心肺复苏2011中国专家共识

1 前言 心脏骤停（sudden cardiac arrest,SCA）是公共卫生和临床医学领域中最危急的情况之一,表现为心脏机械活动突然停止,患者对刺激无反应,无脉搏,无自主呼吸或濒死叹息样呼吸,如不能得到及时有效救治,常致患者即刻死亡,即心脏性猝死（sudden cardiac death,SCD）.我国SCD的发生率为每年41.84/10万（0.04%）,以13亿人口推算,我国每年发生SCD 54.4万例[1].     

冠状动脉性心脏病与心脏性猝死

1966年Kuller等提出了心脏性猝死(sudden cardiac death,SCD)的初步概念,1997年Braunwald提出并进一步完善了SCD的定义.目前,将由心脏原因导致的1 h之内发生的不可预料的自然死亡定义为SCD.在中国及西方国家,SCD是心血管疾病的主要死亡原因之一,是一个影响人类健康的重要问题.大约40%的猝死患者是在没有旁观者的情况下发生的,因此根据临床症状对猝死的病因进行准确判断非常困难.尽管近年来对SCD的病因、发病机制、危险因素及预防措施都已进行了大量的研究,但辨别高风险病人及预防SCD的措施依然不足.     

院内心脏性猝死177例临床回顾分析

目的　分析院内心脏性猝死 (SCD)的临床特点。方法　以 1999年 1月至 2 0 0 1年 12月 177例院内SCD的临床资料进行回顾性研究。结果　院内SCD事件中 0～ 14岁占 8 5 % ,6 0岁及以上占 6 3 9%。导致院内SCD的常见病因是冠心病 (47 5 % )、风心病 (11 3% )和先心病 (11 3% )。导致院内冠心病性猝死的常见病因是急性心肌梗死 (AMI) (5 3 6 % )和不稳定型心绞痛 (UAP) (30 9% )。 75 1%的院内SCD合并心力衰竭 (HF)。心脏骤停即时检测示室性心律失常占 6 7 8% ,心室颤动占 5 2 0 %。结论　院内SCD事件以老年人所占比例最大 ,最防治重点 ,同时也应注意到儿童占有较高比例 ;对于AMI、UAP及HF患者应警惕其SCD的高度危险性 ;尽早除颤是提高院内SCD事件抢救成功率的关键之一。     

心脏磁共振在肥厚型心肌病危险分层中的研究

目的探讨心脏磁共振(CMR)在肥厚型心肌病(HCM)危险分层中的价值。方法本研究为单中心回顾性研究, 连续选取2012年3月至2013年5月于阜外医院接受CMR检查并诊断为HCM的患者, 收集患者的临床及CMR资料, 通过电话随访和病案记录确认患者生存情况。主要终点为心原性猝死(SCD)或SCD等位事件, 次要终点为全因死亡及心脏移植复合终点, 根据是否发生主要终点事件分组。采用Cox回归探索不良事件的危险因素, 采用受试者工作特征(ROC)曲线评估延迟强化百分比(LGE%)对终点事件的预测效能和最佳临界值, 采用Kaplan-Meier法和log-rank检验分析组间生存差异。结果共纳入患者442例, 年龄(48.5±12.4)岁, 女性143例(32.4%)。随访(7.6±2.5)年, 共30例(6.8%)患者发生主要终点事件, 包括23例SCD和7例SCD等位事件;共36例(8.1%)患者发生次要终点事件, 包括33例死亡, 3例心脏移植。多因素Cox回归示, 晕厥(HR=4.531, 95%CI 2.033～10.099, P<0.001)、LGE%(HR=1.075, ...     

植入型心律转复除颤器在心脏性猝死防治中的应用

心脏性猝死（sudden cardiac death,SCD）是指患者在突发症状后的1h内,由于心脏骤停等原因引起的死亡。目前采用的症状发作后1h内死亡的严格时间定义使约90%以上的SCD归因于心律失常,其中恶性室性心律失常[室性心动过速（室速）,心室颤动（室颤）]约占85％。近年SCD逐渐成为导致人类死亡的一个重要疾病。在美国每年SCD的发病人数超过所有脑卒中、肺癌、乳腺癌和获得性免疫缺陷综合征（AIDS）患者死亡人数的总和，SCD事件的发生超过30万例次／年囡，占总死亡的13％。     

心脏性猝死危险预测因子的研究现状

心脏性猝死(sudden cardiac death,SCD)是由于心脏方面的原因所导致的自然死亡,往往于急性症状出现以后1 h内发生意识丧失和心脏骤停.猝死事件发生的时间和方式是无法预料的,患者既可以有也可以没有明确的基础心脏病史.SCD的病因可以是各种心脏病,也可以是其他疾病或因素.其中,常见的原因是冠脉病变、心肌病变和心电异常,冠心病所致者占80%以上,是引发SCD的主要器质性心脏病.本文主要对临床上较常引起SCD的疾病的危险分层的研究现状作一综述.     

肥厚型心肌病患者标准12导联体表心电图J点抬高与心脏骤停的关系

目的:探讨肥厚型心肌病(HCM)患者标准12导联体表心电图(ECG)J点抬高(J波)与心脏骤停(SCA)之间的关系。方法:入选北京7家三级甲等医院345例HCM患者,采集所有入选者静息标准12导联体表心电图。J波定义为在下壁(Ⅱ、Ⅲ和aVF)、侧壁(V4~V6导联)或高侧壁(Ⅰ和aVL)连续2个及以上导联出现J点较基线抬高≥0.1mV。SCA包括心脏性猝死(SCD)、有证据的心室颤动(VF)、由VF或快室性心动过速(VT,200次/min)导致的植入式心脏复律除颤器(ICD)放电。结果:在(47.9±46.6)个月的随访期间,共14例HCM患者发生SCA事件。在发生SCA的HCM患者中,J点抬高的检出率为43%(6/14),在无SCA的HCM患者中,J点抬高的检出率为10%(34/331),J波的存在显著增加HCM患者发生SCA风险(OR:5.67,95%CI:2.38~13.50,P0.001)。在SCA组和无SCA组之间,J点抬高的形态(包括顿挫和光滑延续)和ST段的形态(包括水平/下斜型压低和弓背向下抬高/快速抬高)在所有导联均无统计学差异。结论:HCM患者ECG存在J波与SCA的发生相关。     

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.     

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.     

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.