急性心肌梗死时三度房室传导阻滞的发生特点

目的分析ST段抬高型急性心肌梗死(STEMI)患者出现三度房室传导阻滞(AVB)的特点以及三度AVB与房室结血供的相关性。方法入选保定市第二中心医院2012年1月至2017年12月期间接受急诊冠状动脉(简称冠脉)造影和急诊经皮冠状动脉介入术的581例STEMI患者,并将581例分为研究组(合并三度AVB,n=27),对照组(未合并三度AVB,n=554),观察罪犯血管分布,以及房室结血供来源情况。将罪犯血管为右冠脉是否出现三度AVB,分为有三度AVB组和无三度AVB组两个亚组,观察三度AVB与右冠脉远端的左室后侧支发出的房室结动脉有无相关性。结果 STEMI患者中三度AVB的发生率为4.6%,研究组中,冠脉造影显示右冠脉优势型96.3%(26例)、均衡性(1例);对照组中,左右冠脉优势型分别为4.3%(24例)、92.8%(514例),均衡型为2.9%(16例)。三度AVB全部发生于单支冠脉急性闭塞时。其中24例为右冠脉(RCA),2例为左前降支动脉(LAD),1例为左回旋支动脉。当一支或两支血管为慢性闭塞病变,另一支为急性闭塞时均未出现三度AVB。急性RCA闭塞时,是否累及房室结动脉(AVNA)与三度AVB的发生没有关系。结论 STEMI时三度AVB均发生于单支血管完全闭塞的患者,多数发生于RCA急性闭塞时,但与RCA发出的AVNA无关。     

急性前壁心肌梗死合并完全性房室传导阻滞的冠状动脉造影特点

目的:分析急性前壁心肌梗死合并完全性房室传导阻滞的冠状动脉造影特点.方法:2004-03-2009-03上海交通大学附属第一人民医院心内科共收治急性前壁心肌梗死合并新发完全性房室传导阻滞患者19例,其中14例行冠状动脉造影术,多体位投照观察病变特点,明确梗死相关动脉.并根据主要冠状动脉直径狭窄≥50%的支数,分为左主干病变,单支病变,2支病变,3支病变.结果:14例患者冠状动脉造影均提示冠状动脉严重病变.单支病变1例,2支病变3例,3支病变8例,左主干加3支病变2例.梗死相关动脉12例为左冠状动脉,闭塞部位1例在左主干;9例在左前降支近段,其中4例提供侧支至右冠状动脉远段,2例提供侧支至左回旋支远段;1例在左前降支中段,右冠状动脉变异,开口于闭塞远段;1例在左回旋支近段,提供侧支至右冠状动脉.2例梗死相关动脉为右冠状动脉,闭塞部位1例在近段,为优势型;1例在中段,远段提供侧支至左前降支之第一间隔支.结论:急性前壁心肌梗死合并新发完全性房室传导阻滞患者冠状动脉病变严重,多为多支多处重度狭窄,梗死相关动脉供血范围较广,分别或同时累及第一间隔支动脉、房室结动脉,间接提示临床预后较差.     

运动试验诱发房室传导阻滞二例

1例男性,36岁,活动劳累时反复心悸、胸痛一月余。运动试验诱发胸痛伴V1导联ST段上抬4～5 mm,恢复早期出现Ⅱ度房室传导阻滞(AVB),发生机制可能为冠状动脉病变导致房室结供血不足,影响房室传导功能而导致AVB;1例女性,52岁,活动时心悸、胸闷二月余,加重伴乏力十天。运动试验诱发Ⅲ度AVB,发生机制可能因先天性的房室传导障碍或传导系统及房室结心肌组织退行性改变。运动时频率增快的窦性激动在通过房室结下传过程中可连续落入房室结不应期,不能下传心室而产生房室传导的延缓或中断。     

急性心肌梗死合并Ⅲ°房室传导阻滞恢复正常房室结传导的影响因素分析

目的:探讨急性心肌梗死(AMI)合并Ⅲ°房室传导阻滞(Ⅲ°AVB)患者恢复正常的房室结传导的影响因素。方法:选择AMI合并Ⅲ°AVB患者82例,根据Ⅲ°AVB是否恢复正常房室结传导分为恢复组51例,未恢复组31例(其中安装永久人工心脏起搏器3例,死亡28例)。观察两组Killip分级、心源性休克等因素的差异。结果:AMI合并Ⅲ°AVB患者中,房室结传导恢复组与未恢复组在年龄、性别比例、吸烟史、高血压病史、糖尿病史、缺血预适应、到达急诊室时间、入院心率水平、入院收缩压、血红蛋白水平及实施早期再灌注治疗方面,差异无显著性(P0.05)。与恢复组比较,未恢复组Killip≥II级(39.2%比80.6%)、心源性休克(21.6%比45.2%)、前壁梗死比例(7.8%比32.3%)、肌酐水平[(107.25±6.69)μmol/L比(132.43±11.52)μmol/L]及死亡率(0%比90.3%)显著升高,而下壁梗死比例(92.2%比67.7%)显著降低,P0.05或0.01。多因素Logstic回归分析显示,Killip分级为影响AMI合并Ⅲ°AVB患者房室结功能恢复正常的独立预测因素(OR=0.190,P=0.002)。结论:Killip分级为影响急性心肌梗死合并Ⅲ°房室传导阻滞患者房室结功能恢复的独立预测因素。     

急性下壁心肌梗死并发房室传导阻滞的治疗方法与转归

本文综合近几年来的国内外文献，阐述了急性下壁心肌梗死并发房室传导阻滞的治疗方法与转归，认为积极、及时的冠脉再灌注治疗，尤其是右冠PTCA及支架治疗恢复房室结动脉供血，是房室传导阻滞转复为正常窦性心律的关键。     

小儿膜周部室间隔缺损介入治疗发生高度房室传导阻滞的特点及其处理（附9例报道）

目的探讨经导管介入治疗小儿膜周部室间隔缺损（VSD）发生高度房室传导阻滞（AVB）的特点及其处理。方法选择我科年龄小于12岁VSD患者,经导管介入治疗发生高度AVB的患儿,共计9（男4,女5）例,连续观察所有患儿封堵术前以及发生高度AVB后ECG的变化及其处理。结果①术中发生高度AVB5例,分别在AVB后10min～46h恢复正常窦性心律。其中3例为持续Ⅲ度AVB,经处理后2例转为持续Ⅱ度Ⅱ型,1例仍为持续Ⅲ度AVB;间歇性Ⅱ度Ⅱ型和Ⅲ度AVB各1例。②4例在术后12h～10d出现AVB,3例在AVB后1～12d恢复;1例未恢复,给予永久起搏器治疗。其中3例为间歇性高度或Ⅲ度AVB,1例为持续性Ⅲ度AVB。③术后AVB恢复的3例,在高度AVB时,ECG均表现为完全性右束支传导阻滞+左前分支传导阻滞。AVB后3～5d,ECG电轴左偏进一步加重,以后电轴左偏逐渐减轻,左前分支阻滞逐渐消失,至恢复时ECG仅遗留右束支传导阻滞。结论小儿膜周部VSD介入治疗有发生高度AVB的危险。对于高危患者,应尽早治疗。     

房室结慢径改良发生Ⅲ度房室传导阻滞的探讨

目的：探讨房室结慢径改良发生Ⅲ度房室传导阻滞（AVB）的特异性心电改变及预防，方法：232例房室结折返性心动过速（AVNRT）患者分三组：一组：81例，任何一次放电过程中无特异性心电改变；二组：82例，有一次或一次以上的放电过程中特异性心电改变701次，且放电时间小于3s，三组：69例，有一次或一次以上的放电过程中特异性心电改变97次，但放电时间大于3s，结果：232例患者均消融成功，其中发生一次性Ⅲ度AVB11例，永久性Ⅲ度AVB7例，结论：射频消融术改良房室结慢径时可发生Ⅲ度AVB，但只要我们术中发现特异性心电改变立即停止放电并选择适当的消融方法。可将Ⅲ度AVB降低到最低限度。     

室间隔缺损介入封堵术中及术后房室传导阻滞的转归与防治

目的探讨经导管介入封堵治疗室间隔缺损(VSD)术中及术后房室传导阻滞(AVB)的发生、发展、转归与防治。方法2005年3月至12月,共行VSD介入封堵术157例,术中及术后发生Ⅱ度及以上AVB8例。其中术中发生Ⅲ度AVB2例,术后予静脉注射糖皮质激素治疗;术后发生Ⅱ度AVB3例,Ⅲ度AVB3例,发生时间为术后4h至术后第8天,其中2例伴阿-斯综合征,1例给予临时起搏治疗,其余给予静脉注射糖皮质激素、利尿、脱水等治疗。结果2例术中发生Ⅲ度AVB的患者术后未再出现AVB;3例术后发生Ⅲ度AVB的患者分别于术后第7、8、18天恢复窦性心律,但有2例出院后再次出现Ⅲ度AVB,1例经转回我院积极治疗后恢复窦性心律,另外1例因院外治疗不及时,未能恢复;3例Ⅱ度AVB分别于术后第5、7、8天完全恢复,期间均出现Ⅱ度Ⅰ型和Ⅱ度Ⅱ型交替现象。结论AVB是VSD介入封堵术中及术后的常见并发症。对于AVB应积极治疗,若治疗不及时可能会转为永久性AVB。改进和提高导管技术及操作方法,可在一定程度上减少AVB的发生。     

房室结血供来源的新发现:临床与外科意义

心脏传导组织的解剖和其血供来源的研究已多年,该文作者应用一种特殊的解剖方法对20例人体心脏标本进行研究,发现40％标本的房室结由kugel's动脉供血,70％来自冠状动脉的右上降支动脉,为以往一直认为房室结动脉和左前降支的第一间隔支为唯一的房室结血供来源提供了新的发现。     

临时起搏在急性病毒性心肌炎合并Ⅲ度房室传导阻滞的应用分析

目的通过对15例合并Ⅲ度房室传导阻滞(ⅢoAVB)的急性病毒性心肌炎的临床特征辅助检查,临时起搏治疗和转归的分析,总结临时起搏的作用。方法分析15例合并Ⅲ度房室传导阻滞的急性病毒性心肌炎患者应用临时起搏后的治疗效果。结果15例患者接受临时起搏治疗后能恢复窦性心律,临时起搏留置时间2～13d。结论急性病毒性心肌炎合并Ⅲ度房室传导阻滞时应及时使用临时起搏并辅以其他治疗,可在较短时间内恢复窦性心律。     

Site of myocardial infarction. A determinant of the cardiovascular changes induced in the cat by coronary occlusion.

The influence of site of acute myocardial infarction on heart rate, blood pressure, cardiac output, total peripheral resistance (TPR), cardiac rhythm, and mortality was determined in 58 anesthetized cats by occlusion of either the left anterior descending (LAD), left circumflex or right coronary artery. LAD occlusion resulted in immediate decrease in cardiac output, heart rate, and blood pressure, an increase in TPR, and cardiac rhythm changes including premature ventricular beats, ventricular tachycardia, and occasionally ventricular fibrillation. The decrease in cardiac output and increase in TPR persisted in the cats surviving a ventricular arrhythmia. In contrast, right coronary occlusion resulted in a considerably smaller decrease in cardiac output. TPR did not increase, atrioventricular condition disturbances were common, and sinus bradycardia and hypotension persisted in the cats recovering from an arrhythmia. Left circumflex ligation resulted in cardiovascular changes intermediate between those produced by occlusion of the LAD or the right coronary artery. Mortality was similar in each of the three groups. We studied the coronary artery anatomy in 12 cats. In 10, the blood supply to the sinus node was from the right coronary artery and in 2, from the left circumflex coronary artery. The atrioventricular node artery arose from the right in 9 cats, and from the left circumflex in 3. The right coronary artery was dominant in 9 cats and the left in 3. In conclusion, the site of experimental coronary occlusion in cats is a major determinant of the hemodynamic and cardiac rhythm changes occurring after acute myocardial infarction. The cardiovascular responses evoked by ligation are related in part to the anatomical distribution of the occluded artery.     

Early atrial fibrillation during evolving myocardial infarction: a consequence of impaired left atrial perfusion

Seven of 214 patients (3%) with acute myocardial infarction (120 inferior and 94 anterior) developed atrial fibrillation within 3 hr of the onset of chest pain. All seven patients had an inferior infarction and in all seven the left circumflex artery was occluded proximal to the origin of its left atrial circumflex branch. In five patients this occlusion was acute and was the cause of inferior infarction and in the remaining two patients the occlusion was old and the inferior infarction was due to an acute occlusion of the right coronary artery that also supplied extensive collaterals to the previously occluded left circumflex artery. All seven patients also had impaired perfusion to the atrioventricular nodal artery, as evidenced by total occlusion proximal to its origin or by stenosis proximal to its origin associated with second- or third-degree atrioventricular block. In contrast, early atrial fibrillation did not occur in any of the 18 patients with inferior myocardial infarction due to acute occlusion of the distal left circumflex artery or in any of the five patients with inferior infarction due to acute occlusion of the proximal left circumflex artery if perfusion to the atrioventricular nodal artery was not impaired. Early atrial fibrillation did not occur in any of the 90 patients with inferior infarction due to acute occlusion of the right coronary artery, including 12 patients with occlusion proximal to the sinus nodal artery, but without coexistent occlusion of the left circumflex artery.(ABSTRACT TRUNCATED AT 250 WORDS)     

A clinical angiographic study of the arterial blood supply to the sinus node

We studied the arterial blood supply to the sinus node area in 309 consecutive patients undergoing coronary arteriography. Seventy-nine had had a previous myocardial infarction. In two who developed temporary sinus node dysfunction, the sinus node artery arose from the distal portion of a severely stenotic left circumflex coronary artery, but in 307 of the 309 patients the sinus node arteries themselves were free of atheroma. The sinus node artery arose from the right coronary artery in 182 patients, from the proximal 3 cm in 179, near the origin of the acute marginal in one, and left of the crux in two. In 119 patients it arose from the left circumflex coronary artery, proximally in 87, and in 32 from anywhere throughout its length, running posteriorly as the posterior sinus node artery. Finally, eight patients had two sinus node arteries, one arising from the right coronary artery and one from the left circumflex.     

Induction of transient third degree atrioventricular block during radiofrequency catheter ablation in a patient with ventricular tachycardia and remote myocardial infarction

INTRODUCTION: Radiofrequency catheter ablation has been demonstrated to bean effective and safe therapy in patients with so-called idiopathicventricular tachycardia, whereas the benefit/risk profile forablation of ventricular tachycardia in patients with chronicmyocardial infarction and severely compromised left ventricularfunction still needs to be determined. The present report describesthe unintended induction of transient third-degree atrioventricularblock in a patient with remote myocardial infarction who underwentradiofrequency catheter ablation of ventricular tachycardia. METHODS AND RESULTS: Endocardial catheter mapping and radiofrequency ablation wereperformed in a 57-year-old patient with chronic recurrent ventriculartachycardia, who had previously suffered from anterior and posteriorwall myocardial infarction. Additionally, the patient presentedwith complete right bundle branch block during sinus rhythm.Radiofrequency energy applied to a critical site of the reentranttachycardia at the left ventricular basal septum during sinusrhythm induced third-degree atrioventricular block after 20s of current delivery, which lasted for 24 h. At this site,a presumable left bundle branch potential was recorded duringsinus rhythm. CONCLUSIONS: Radiofrequency current application for ablation of ventriculartachycardia may induce third-degree atrioventricular block inpatients with remote myocardial infarction. When current isdelivered to target sites at the left ventricular basal septum,radiofrequency energy should be applied during sinus rhythmto allow continuous monitoring of atrioventricular conduction.Special caution should be given to patients with right bundlebranch block during sinus rhythm.     

Early atrial arrhythmias in acute myocardial infarction. Role of the sinus node artery.

We studied atrial arrhythmias during the first 12 h of admission to the hospital in 266 consecutive patients with acute myocardial infarction who subsequently underwent coronary angiography. Ten patients developed atrial fibrillation, one atrial flutter, and one supraventricular tachycardia. Another five developed sinus dysrhythmias. All of the above patients had an acute inferior myocardial infarction, and in 10 of the 12 patients with supraventricular arrhythmias and in four of five with sinus dysrhythmias, the origin of the sinus node artery started just after an occluded right coronary or left circumflex artery or was involved in the occlusion. Thus, ischemia of the sinus node due to coronary occlusion proximal to the origin of the sinus node artery was a likely cause of these arrhythmias.     

Origin of all major coronary arteries from left sinus of Valsalva as a common coronary trunk: single coronary artery--a case report

Coronary anomalies are divergent and can occur in up to 1% to 2% of patients. The most common of these anomalies is separate ostia of the left anterior descending and left circumflex arteries, followed by origin of the circumflex coronary artery from the right coronary artery and the left coronary artery from the right sinus of Valsalva, either as a separate ostium or as a part of single coronary artery. Anomalous origin of right coronary artery from the left sinus of Valsalva with a separate ostium or from the left main coronary artery is very rare. These coronary anomalies may be incidentally diagnosed on routine angiography or may present with myocardial ischemia, infarction, or sudden death. A case is described in which all 3 coronary arteries were originating from the left sinus of Valsalva as a common trunk (single coronary artery), which trifurcated to left anterior descending, left circumflex, and right coronary artery.     

Myocardial bridging of the left anterior descending coronary artery and right coronary artery in a patient with mitral valve stenosis

Myocardial bridging is defined as the intramural course of a major epicardial coronary artery, and is mostly confined to the left ventricle and the left anterior descending coronary artery (LAD). Although it is considered to be a benign anomaly, it can lead to such complications as acute myocardial infarction, ventricular tachycardia, syncope, atrioventricular block and sudden cardiac death. Isolated myocardial bridging of the right coronary artery (RCA) and left circumflex artery have been reported in the literature In our case, myocardial bridging was observed in both the LAD and the RCA in a patient with mitral valve stenosis.     

Anatomical Reasons for the Discrepancies in Atrioventricular Block after Inferior Myocardial Infarction with and without Right Ventricular Involvement

The incidence of arrhythmias after acute myocardial infarction of the inferior wall varies with the affected segment and increases when there is right ventricular involvement. This paper provides a clear review of the blood supply to the conduction system and gives an anatomic explanation of that supply.We dissected 20 human hearts after anterograde and retrograde injection of latex. In every heart, we dissected the conduction system and its blood supply. Retrograde perfusion enabled proper injection of the atrial vessels that originate at the beginning of the coronary trunks.We describe the 4 main arteries that supply blood to the conduction system. The classic concept included the atrioventricular node artery and the 1st septal artery. To that we add Kugel''s artery and the right superior descending artery.The incidence of arrhythmias after acute myocardial infarction of the inferior wall is greater when the occlusion of the coronary trunk is at or near the origin. This is due to the existence of the right superior descending artery, which is given off by the right coronary trunk less than 1 cm from the origin. The arrhythmias caused by the occlusion of the circumflex artery are due to the existence of Kugel''s artery, which displays a peculiar anastomotic pattern.Key words: Atrioventricular node, cadaver, coronary vessels/anatomy & histology, heart atria, heart block/etiology, humans, heart conduction system, myocardial infarction, inferior/complicationsArrhythmias as a complication of acute myocardial infarction of the inferior wall vary in their occurrence, depending on the presence or absence of right ventricular involvement.^1–3 Many articles have made this observation, but, to the best of our knowledge, none has offered a clear morphologic explanation: that is, there have been few images of the heart''s conduction system, particularly of the blood supply to the conduction system in the atrioventricular (AV) node and of the alternative blood supply to that conduction system (which has been shown in drawings and diagrams, but not in photographs). This paper reviews our present knowledge of the blood supply to the conduction system and supplements it with new findings that help to explain why the incidence of postinfarction arrhythmias is greater when there is right ventricular involvement. Two atrial arteries have been described⁴ by the authors as sources of the blood supply to the conduction system: Kugel''s artery (arteria anastomotica auricularis magna) and the right superior descending artery. These vessels, which appear to constitute the chief explanation for the phenomenon mentioned above, are thoroughly discussed herein.     

Three cases of single coronary artery

Single coronary artery has been considered a minor coronary anomaly without clinical importance. With the wide spread of coronary angiography, however, the disease has been reported to develop complications at a high rate, such as angina, myocardial infarction and arrhythmia. We report three patients with single coronary artery with several complications. Case 1: A 56-year-old woman having a past history of diabetes mellitus and myocardial infarction was admitted because of the recently developed frequent attacks of effort angina. Treadmill test was positive and thallium-201 exercise myocardial scintigraphy revealed redistribution in the lateral wall. Ascending aortogram suggested that the right coronary artery (RCA) arose from the left sinus of Valsalva. An injection into the right sinus of Valsalva revealed no coronary ostium. Selective left coronary angiogram resulted in the diagnosis of single coronary artery (Smith's type 2) with 90% stenosis in the left circumflex artery (LCX). Left ventriculogram showed hypokinesis in the anterolateral wall. PTCA performed on this patient revealed clinical and nucleomedical improvement. Case 2: A 48-year-old man experienced chest pain and syncope. Electrocardiogram revealed ST-elevations in II, I and a VF, sinus bradycardia and atrioventricular junctional rhythm. Angiography resulted in the diagnosis of single coronary artery (Smith's type 2) with 75% stenosis in the RCA. Ergonovine test was positive. Case 3: A 69-year-old man complained of chest pain. Electrocardiogram showed complete right bundle branch block, sinus bradycardia and atrioventricular junctional rhythm. Cardiac catheterization revealed that this was also a case of single coronary artery (Smith's type 2) with no significant stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

急性心肌梗死早期血钾浓度与冠状动脉造影相关罪犯血管及室性心律失常的关系

目的 探讨急性心肌梗死患者早期血钾浓度与冠状动脉造影相关罪犯血管及室性心律失常的关系.方法 选择136例符合“急性心肌梗死诊断标准”,且发病时间＜12 h的患者.入院后立即采静脉血3ml,测血钾浓度,做18导联心电图.患者均同意做急诊介入治疗,给予冠状动脉造影,确定急性心肌梗死的罪犯血管.观察急性心肌梗死患者早期血钾浓度与冠状动脉造影确定罪犯血管及室性心律失常的关系,并进行统计学分析.结果 急性心肌梗死罪犯血管为左前降支的血钾浓度最低,左回旋支血钾浓度最高,右冠状动脉的血钾浓度位于左前降支及左回旋支之间.左前降支病变与左回旋支病变血钾浓度对比差异有统计学意义（P＜0.01）.右冠状动脉病变与左回旋支病变血钾浓度对比差异有统计学意义（P＜0.05）.急性心肌梗死低血钾组与正常血钾组室性心律失常发生率对比差异有统计学意义（P＜0.01）.结论 急性心肌梗死患者,罪犯血管是左前降支的发病早期最容易合并低血钾,预后普遍较差.急性心肌梗死早期合并低血钾易发生室性心律失常.