乙酰胆碱试验诱发冠状动脉痉挛时的心电图改变

目的:探讨冠状动脉痉挛发生时的心电图变化规律。方法:64名因胸痛而接受冠状动脉造影的患者,排除具有缺血意义的病变后进行乙酰胆碱试验,术中进行包括胸前V1,3,5在内的9导联心电图记录,比较阳性组和阴性组心电图ST段、T波变化及各种心律失常情况。结果:乙酰胆碱试验阳性组(n=46)中ST段抬高者为19.60%,阴性组(n=18)无ST段抬高(P<0.05);ST段压低者分别为39.1%及11.1%(P<0.05);出现T波高尖者分别为82.6%和16.7%(P<0.001),阳性者ST段变化幅度与冠状动脉痉挛发生时的狭窄程度呈正相关(r=0.62,P=0.042),其中ST段抬高患者的冠状动脉痉挛时狭窄程度均在99% 以上;两组心律失常的发生率无显著差异(P>0.05)。结论:短暂性冠状动脉痉挛不一定伴有ST段抬高,ST段变化与冠状动脉痉挛程度有关,而T波高尖町能比缺血性ST段改变更敏感。试验中的心律失常可能与乙酰胆碱的药理作用有关而与冠状动脉痉挛无关。     

非典型性冠状动脉痉挛患者的临床特点及近期预后

目的总结非典型性冠状动脉痉挛患者的临床特点。方法选择临床具有静息性胸痛或胸闷,且冠状动脉造影无显著狭窄的64例患者进行乙酰胆碱冠状动脉痉挛激发试验,将乙酰胆碱试验阳性即冠状动脉痉挛患者根据胸痛或胸闷发作时心电图上是否有ST段抬高分为典型变异型心绞痛组（典型组）和非典型变异型心绞痛性冠状动脉痉挛组（非典型组）,比较两组的临床症状特点（危险因素、心电图和核素心肌灌注显像负荷试验结果以及冠状动脉造影和乙酰胆碱试验的影像学）。结果共有46例（72％,46／64）患者诱发冠状动脉痉挛,其中典型组和非典型组分别为12及34例。典型组的平均年龄偏低（P〈0．05）,血脂代谢紊乱在非典型组更常见,运动心电图试验两组多为阴性,核素灌注心肌显像负荷试验两组均表现有反向再分布,冠状动脉造影典型组多为轻度局限性狭窄或节段性内膜不光滑,肌桥发生率更高,乙酰胆碱试验多诱发节段性痉挛。而非典型组为弥漫性血管细小、内膜不光滑、僵硬,血管迂曲伴远端血流缓慢,乙酰胆碱试验多诱发弥漫性血管痉挛,并可见多支血管同时痉挛。结论非典型性冠状动脉痉挛较典型变异型心绞痛更常见,且具有一定的特征性,应引起临床医生高度重视。     

乙酰胆碱诱发冠状动脉痉挛试验中缓慢型心律失常的原因探讨

目的探讨乙酰胆碱诱发冠状动脉痉挛试验中缓慢型心律失常的发生原因。方法64例因静息性胸痛而接受冠状动脉造影的患者,排除具有缺血意义的病变后进行乙酰胆碱试验,术中连续记录心电图变化,比较痉挛组和非痉挛组缓慢型心律失常情况,并选择冠状动脉痉挛合并缓慢型心律失常的25例患者分别在冠状动脉内注射硝酸甘油及静脉注射阿托品后重复乙酰胆碱试验,观察冠状动脉痉挛和心律失常的变化情况。结果乙酰胆碱试验痉挛组(46例)和非痉挛组(18例)缓慢型心律失常的发生率无差异(P>0.05),痉挛组中14例经过冠状动脉内注射硝酸甘油后重复乙酰胆碱试验均未能诱发痉挛,但12例仍出现缓慢型心律失常,另11例静脉注射阿托品后重复乙酰胆碱试验均未诱发冠状动脉痉挛,仅1例出现缓慢型心律失常。结论乙酰胆碱试验中的缓慢型心律失常可能与乙酰胆碱的药理作用有关而与冠状动脉痉挛无关。     

冠状动脉痉挛患者~(201)Tl心肌灌注显像反向再分布与血管内皮功能紊乱的关系

目的:探讨冠状动脉痉挛患者在201Tl(铊)心肌灌注显像负荷试验中的反向再分布现象与血管内皮功能的关系。方法:选择接受201Tl心肌灌注显像负荷试验的患者为研究对象,根据最后临床诊断将患者分为冠状动脉痉挛组(n=30)、冠心病组(n=30)和对照组(n=30),分别在201Tl心肌灌注显像心肌负荷试验前、负荷试验后即刻(负荷显像)及负荷后3h(再分布显像)时采集外周静脉血测定并比较各组间及不同时点内皮素-1、一氧化氮水平以及内皮素-1/一氧化氮比值的动态变化,组间比较采用方差分析进行统计学处理。结果:负荷试验前,冠状动脉痉挛组内皮素-1水平[(163.53±8.58)pg/ml]高于对照组[(116.15±6.65)pg/ml,P0.01]及冠心病组[(137.73±8.32)pg/ml,P0.01],一氧化氮水平[(60.32±8.20)μmol/L]低于对照组[(70.10±6.90)μmol/L,P0.05]亦略低于冠心病组[(62.64±7.45)μmol/L,P=0.238],内皮素-1/一氧化氮比值(2.75±0.39)显著高于对照组(1.67±0.18,P0.01)及冠心病组(2.22±0.31,P0.05)。负荷试验后即刻,冠状动脉痉挛组较对照组内皮素-1水平降低[(151±9.15)pg/ml,P0.01]、一氧化氮水平升高[(63.78±8.30)μmol/L,P0.01]、内皮素-1/一氧化氮比值降低(1.40±0.12,P0.01);负荷后3h,冠状动脉痉挛组内皮素-1恢复至负荷前水平,一氧化氮降低且低于负荷前水平,内皮素-1/一氧化氮比值升高且高于负荷前水平,从而有利于血管收缩;对照组在负荷后即刻内皮素-1/一氧化氮比值较负荷前水平轻度降低,3h后回到负荷前水平;而冠心病组在负荷试验中的内皮素-1/一氧化氮比值差异无统计学意义。结论:冠状动脉痉挛患者的反向再分布可能与内皮细胞功能紊乱所引起的病变血管在静息状态下痉挛及负荷时扩张、从而导致心肌血流灌注改变有关。     

心肌桥合并冠状动脉痉挛患者的临床特点

目的 探讨心肌桥合并冠状动脉痉挛患者的临床特征及其与血管内皮细胞功能的关系.方法 接受冠状动脉痉挛激发试验的118例患者,根据冠状动脉造影显示是否合并心肌桥分为肌桥组(n=26)和非肌桥组(n=92),比较两组乙酰胆碱试验、运动心电图、核素灌注心肌显像负荷试验的结果及血浆内皮素1和一氧化氮水平.结果 肌桥组乙酰胆碱试验阳性21例(81%),非肌桥组乙酰胆碱试验阳性52例(57%,P＜0.05);心电图运动试验阳性者两组分别为19例(73%)和7例(8%,P＜0.001),核素灌注心肌显像负荷试验显示缺血性改变者两组分别为20例(77%)和9例(10%,P＜0.001),反相再分布分别为23例(88%)和68例(74%,P＞0.05),两组患者的临床症状发作特点亦显著不同,肌桥合并痉挛患者的内皮素水平明显增高[(132.1±6.5)ng/L比(108.5±8.2)ng/L,P＜0.01],而一氧化氮水平明显降低[(84.7±17.5)ng/L比(99.8±18.2)ng/L,P＜0.05].结论 心肌桥患者易发生冠状动脉痉挛,可能与血管内皮细胞功能紊乱有关,该类患者多具有特征性的临床表现和心脏负荷试验结果.     

替罗非班对急性心肌梗死急诊冠状动脉介入治疗冠状动脉血流和微循环的影响

目的分析应用替罗非班对ST段抬高性心肌梗死患者急诊行冠状动脉介入治疗冠状动脉血流和微循环的影响。方法ST段抬高性心肌梗死行直接冠状动脉介入治疗患者58例,随机分为替罗非班组(n=30)和对照组(n=28)。比较两组患者临床基础情况、冠状动脉介入治疗前梗死相关血管开通率、手术前后心肌梗死溶栓治疗血流情况、心电图ST段回落、术后内皮细胞凋亡数及凝血状态、住院期间出血事件、主要心脏不良事件发生率和出院前左心室射血分数等。结果替罗非班组使术前TIMI血流分级达到1级血流比例明显高于对照组(P<0.05),2级及3级血流两组之间差异无显著性(P>0.05),同时在对照组血流完全闭塞率高于替罗非班组(P<0.01),术中无复流现象、再灌注心律失常、内皮细胞凋亡数及凝血因子在替罗非班组均显著低于对照组(P<0.05),再通后90min心电图相关导联ST段回落值替罗非班组明显大于对照组(P<0.05),出院前左心室射血分数、两组患者主要心脏不良事件发生率和住院期间主要出血事件发生率差异无统计学意义(P>0.05)。结论替罗非班对急性ST段抬高性心肌梗死急诊行介入治疗可改善术前梗死相关血管TIMI血流情况,使介入手术顺利更好进行,争取更多时间避免较多的心肌细胞永久性坏死,改善心肌微循环障碍,减少无复流现象。     

丹芪通络胶囊在改善急性ST段抬高型心肌梗死患者冠状动脉微循环障碍中的临床作用

目的探讨丹芪通络胶囊在改善急性ST段抬高型心肌梗死患者冠状动脉微循环障碍中的临床作用。方法以急性ST段抬高型心肌梗死患者40例为研究对象,随机分为观察组和对照组,对照组实施常规治疗,观察组在此基础上加用丹芪通络胶囊,比较两组患者的心功能及血浆内皮素、血管紧张素II、白介素1水平。结果治疗后观察组LVEDV、LVESV明显小于对照组,LVEF、SV明显高于对照组(P0.05),血浆内皮素、血管紧张素II、白介素I水平均明显低于对照组(P0.05)。结论为急性ST段抬高型心肌梗死患者行丹芪通络胶囊治疗,可有效改善患者心功能,减轻冠状动脉微循环障碍,值得推广。     

冠状动脉内乙酰胆碱激发试验的临床应用

目的 探讨选择性冠状动脉内乙酰胆碱激光试验的方法及其诊断冠状动脉痉挛的敏感性和特异性。方法 用选择性冠状动脉造影方法分别向左、右冠状动脉内注入乙酰胆碱生理盐水，注药剂量依次为右冠状动脉20μg和50μg，左冠状动脉20μg、50μg和100μg。测量注入最大剂量乙酰胆碱后冠状内径，以血管完全或接近完全闭塞（狭窄≥99％）为痉挛激发试验阳性。对41例患者实施了乙酰胆碱激发试验，Ⅰ组为20例胸痛伴ST段抬高或下降的患者，Ⅱ组为21例冠状动脉造影正常，无心电图ST段改变的患者。结果 Ⅰ组中18例诱发出冠状动脉痉挛，Ⅱ组中18例血管内径不同程度缩小，3例血管内径增大，无一例诱发出冠状动脉痉挛。结论 乙酰胆碱激发试验安全、简便，诊断冠状动脉痉挛性心绞痛的特异性为100％，敏感性为90％。     

血清骨保护素和脑利钠肽水平与非ST段抬高型急性冠状动脉综合征患者冠状动脉病变程度的相关性

目的 探讨血清骨保护素和脑利钠肽水平与非ST段抬高急性冠状动脉综合征患者冠状动脉病变程度之间的关系.方法 192例受试者分为三组:稳定型心绞痛患者58例,不稳定型心绞痛/非ST段抬高心肌梗死患者99例,对照者35例,入院时检测血清骨保护素和脑利钠肽水平,并进行冠状动脉造影.根据造影结果对冠状动脉病变进行Gensini评分,分析两种标志物与冠状动脉狭窄数及冠状动脉病变Gensini评分的相关性.结果所有冠心病患者骨保护素水平高于对照组(P<0.01),稳定型心绞痛组骨保护素水平低于不稳定型心绞痛/非ST段抬高心肌梗死组(P<0.01);稳定型心绞痛组脑利钠肽水平略高于对照组(P>0.05),不稳定型心绞痛/非ST段抬高心肌梗死组脑利钠肽水平明显高于稳定型心绞痛组(P<0.01);多支血管病变患者脑利钠肽水平显著高于单支血管病变患者(P<0.01),脑利钠肽与冠状动脉病变Gensini评分轻微相关(r=0.45,P<0.01),骨保护素与冠状动脉病变Gensini评分显著相关 (r=0.64,P<0.001),多元回归分析发现骨保护素和脑利钠肽与冠心病独立相关(P<0.01).结论血清骨保护素与不稳定型心绞痛/非ST段抬高心肌梗死患者冠状动脉狭窄程度及病变进展有关,提示骨保护素可能参与了冠状动脉疾病的进程.不稳定型心绞痛/非ST段抬高心肌梗死患者脑利钠肽水平也增高,表明脑利钠肽水平与缺血范围以及严重程度有较大的关联.     

aVR导联ST段改变对急性非ST段抬高型心肌梗死相关血管的判定及临床意义

目的探讨体表心电图a VR导联ST段改变对急性非ST段抬高型心肌梗死病人梗死相关血管(IRA)的判定及临床意义。方法回顾性分析230例临床确诊为急性非ST段抬高型心肌梗死病人的临床资料、心电图及冠状动脉造影结果。依据心电图a VR导联ST段变化将病例分为A组(ST抬高组)、B组(ST下移组)和C组(ST无偏移组)。结果冠状动脉造影结果:ST抬高组左主干病变、左前降支病变的发生率明显高于ST下移组和ST无偏移组,差异有统计学意义(P0.05);ST下移组左回旋支病变及右冠状动脉病变的发生率明显高于ST抬高组和ST无偏移组,差异有统计学意义(P0.05);ST抬高组和ST下移组双支病变及三支病变的发生率明显高于ST无偏移组,差异均有统计学意义(P0.05)。a VR导联ST段抬高组、下移组主要不良心血管事件发生率均明显高于ST无偏移组(P0.05)。结论急性非ST段抬高型心肌梗死病人如果伴有a VR导联ST段抬高或下移可能提示梗死相关血管为左主干病变、左前降支病变、左回旋支病变、右冠状动脉病变或严重的多支病变,且住院期间不良心血管事件发生率增高。a VR导联ST段改变对急性非ST段抬高型心肌梗死病人梗死相关血管的判定及临床预后均具有重要的临床指导意义。     

首次急性ST段抬高与非ST段抬高心肌梗死患者临床及冠状动脉病变特点比较

目的回顾性分析比较首次发生急性ST段抬高心肌梗死与非ST段抬高心肌梗死的临床及冠状动脉病变的特点。方法选择首次急性ST段抬高心肌梗死患者50例(ST段抬高组)和急性非ST段抬高心肌梗死患者50例(非ST段抬高组),均行冠状动脉造影检查,对其发病特点、临床表现、并发症、心功能以及冠状动脉病变进行回顾性分析。结果 ST段抬高组起病急,主要以剧烈胸痛为主,就诊时间较早,非ST段抬高组首发症状多样。ST段抬高组总并发症、室性心律失常、窦性心动过缓及传导阻滞发生率明显高于非ST段抬高组(P<0.01),左心室射血分数明显低于非ST段抬高组(P<0.05)。与ST段抬高组比较,非ST段抬高组冠状动脉病变血管支数较多,3支病变、侧支循环比例较高(P<0.05,P<0.01)。结论急性ST段抬高心肌梗死起病急,并发症多,影响心功能,应积极尽快实施血运重建,以开通梗死相关血管,但急性非ST段抬高心肌梗死冠状动脉病变往往较重。急性心肌梗死的近期预后与起病急缓、透壁性心肌坏死范围等有关。     

Clinical characteristics of coronary artery spasm: electrocardiographic, hemodynamic and arteriographic assessment

We studied the clinical characteristics of 153 patients with angina pectoris associated with coronary artery spasm (CAS). The study was designed to investigate the relationship of CAS to ST segment deviation and to the site of fixed stenosis, and hemodynamic alteration during a spastic event. Analysis of coronary arteriograms and multilead electrocardiograms obtained simultaneously from 170 events of CAS by the use of radioluscent carbon-fiber electrodes resulted in 58 events with ST elevation which were related to total occlusion of major coronary arteries due to CAS; another 54 events with ST depression, in which the affected coronary arteries demonstrated severe but incomplete occlusion, or total occlusion but were visualized via collateral vessels; and remaining 58 events without ST deviation showing mild occlusion. The results indicate a close correlation between magnitude of CAS and ST segment deviation. CAS occurred at the site of pre-existing fixed stenosis including minor plaque defect in 133 patients and at apparently normal site in 20 patients. In the former group, only four patients had triple vessel disease, while 95 had nonsignificant fixed lesion. In the latter group, 10 patients had minor lesion distant from the site of CAS. Thus, CAS is closely related to fixed stenosis, which may have but a limited role as a cause of CAS. Hemodynamic measurements during spastic events were obtained from 49 patients including 41 events with spasm of the left anterior descending artery (LAD) and 21 events with spasm of the right coronary artery (RCA). The onset of an increase in left ventricular (LV) filling pressure and a reduction in LV dP/dt preceded ST segment deviation in all events. The first hemodynamic variable manifested in the spastic event was the reduction of LV contraction dP/dt in the majority of patients. The increase of LV filling pressure was greater in LAD spasm than RCA spasm (11 +/- 6 mmHg vs 7 +/- 4 mmHg, P less than 0.0125) and in events with ST elevation than with ST depression (11 +/- 5 mmHg vs 6 +/- 5 mmHg, p less than 0.001). Right ventricular functional impairment was mild in most patients during CAS. The study indicates that mechanical impairment precedes electrical impairment during CAS and that LAD spasm with ST elevation represents the most severe LV dysfunction.     

Provocation of microvessel spasm by low-dose acetylcholine in patients with suspected coronary artery disease--two case reports

Endothelial dysfunction plays an important role in the pathogenesis of cardiac syndrome X, and intracoronary low-dose acetylcholine infusion is a widely used diagnostic modality for studying the coronary artery endothelial function. The authors herein report 2 cases of cardiac syndrome X with coronary artery endothelial dysfunction and microvessel spasm. The findings of non-invasive testing were positive for ischemia. Coronary angiograms appeared entirely normal in both cases. However, the intracoronary infusion of low-dose (1.5-15 microg/minute) acetylcholine demonstrated an impairment of the coronary blood flow response and consequently provoked an ST-segment elevation in an electrocardiogram. The coronary angiograms showed no spasm in the epicardial arteries. These patients are thus suggested to have cardiac syndrome X with microvessel spasms associated with coronary artery endothelial dysfunction.     

Correlation of the location of coronary arterial spasm with the lead distribution of ST segment elevation during variant angina

The lead distribution of ST segment elevation produced by severe “spasm” of major coronary arteries was correlated with the specific artery involved in a group of 110 cases of variant angina with single vessel coronary arterial spasm made up from eight cases personally observed and 102 cases abstracted from published literature.The most sensitive and specific lead for ST elevation during anterior descending (LAD) coronary arterial spasm was V₃; V₂ was almost as good. For spasm of either the right (RCA) or circumflex coronary artery (CMFX), Leads 3 and aV_F showed ST elevation most frequently; electrocardiographically it was difficult to distinguish between spasm of these two vessels. ST elevation in Leads V₅ and V₆ was not specific, occurring in some cases of spasm of each of the three major coronary arteries. ST elevation in Lead V₁ occurred in either RCA or LAD spas, but never in CMFX spasm. ST elevation in Lead 1 was never seen with isolated RCA spasm.No single lead can detect all cases of transient ST elevation. Simultaneous monitoring of Leads 3 and V₃ would have detected 98.2% of 333 cases of ST elevation reviewed, and addition of Lead aV_L would have detected most of the remainder. These findings should be considered in lead selection for monitoring to detect ST elevation, and in using the ECG to identify spastic coronary arteries.     

Transient appearance of collaterals during vasospastic occlusion in patients without obstructive coronary atherosclerosis

Coronary angiography of both right and left coronary arteries, using the Sones technique, was performed during the attack of total spastic obstruction in 11 patients with clinically documented history of variant angina. None of the patients had more than 70% stenosis of organic atherosclerosis in any coronary artery and none had a history of myocardial infarction. Total spastic obstruction occurred spontaneously in 3 of 11 patients, and was provoked by ergonovine maleate in eight patients. Six patients had total spastic obstruction in the left anterior descending coronary artery, four patients had total obstruction in the right coronary artery, and one patient had total obstruction in the left anterior descending and right coronary arteries. In 7 of 11 patients, the coronary artery distal to the total spastic obstruction received collaterals from the nonspastic artery. The collaterals disappeared promptly when the spastic coronary artery was patent. These patients had ST segment elevation in the ECG during the attacks. In the remaining four patients, the spastic artery did not receive any collaterals from the nonspastic artery, associated with ST segment elevation during the attacks. These findings suggest that the brief, repetitive total occlusion of the coronary artery may stimulate the enlargement of collaterals. These collaterals may not always function to prevent the ischemia of the myocardium on the ECG.     

Hyperventilation-induced simultaneous multivessel coronary spasm in patients with variant angina: an echocardiographic and arteriographic study

Left ventricular wall motion abnormalities during an attack of coronary spasm induced by hyperventilation were examined with use of two-dimensional echocardiography in 27 patients with variant angina. Transient abnormal wall motion (asynergy) confined to one coronary artery region was found in 18 of the 27 patients and transient abnormal motion extending over more than one coronary artery region in the remaining 9 patients. Spasm of more than one major coronary artery was demonstrated separately by coronary arteriography during an attack induced by injection of acetylcholine or ergonovine in seven of the nine patients who manifested asynergy in more than one coronary artery region. In one patient, spasm was demonstrated in one major coronary artery, and the other coronary arteries were severely stenosed or occluded organically. In the remaining patient, acetylcholine was not injected into both arteries; however, the attack was sometimes associated with ST segment elevation in the anterior leads and at other times in the inferior leads. Therefore, simultaneous multivessel coronary spasm seems to have occurred in eight of the nine patients who exhibited asynergy in more than one coronary artery region. The 8 patients with simultaneous multivessel coronary spasm had a higher degree and longer duration of ST segment elevation and a higher incidence of arrhythmias during the attack induced by hyperventilation than did the 19 patients with single vessel coronary spasm, and all of them had no significant organic stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Arteriographic features of angina pectoris associated with ST segment depression during coronary arterial spasm

To examine the angiographic features of vasospastic angina associated with ST segment depression, we attempted to analyze the coronary arteriograms of 12 patients who exhibited ST segment depression during the ergonovine provocative test. Right and left coronary arteriograms were obtained successively within a short period when the ergonovine administration revealed ST segment depression. Eight out of 12 patients showed non-total spastic obstructions in one of the major coronary arteries. Among them, a collateral augmentation was found only in one patient. Two cases exhibited the well-developed collateral channels during non-anginal periods and in one case a collateral blood supply was reduced by the spasm occurred in the donating artery. In another one, the collateral circulation did not change during anginal period. Three out of 4 patients who showed total spastic obstructions demonstrated transiently augmented collateral circulation which was supplied by the non-spastic artery. These findings may indicate that ST segment depression during coronary artery spasm could attribute to a subendocardial ischemia caused by an incomplete occlusion of large coronary artery and transient reduction or augmentation of collateral blood flow.     

Provocation of coronary spasm by dopamine in patients with active variant angina pectoris

The effects of dopamine on arteries are different depending on the dose, route of administration, and receptor population. Its administration can cause vasodilation by stimulation of dopaminergic receptors, vasoconstriction by stimulation of alpha-adrenergic and serotonergic receptors, and even spasm of cerebral arteries when given intracisternally in dogs. The ability of dopamine to provoke coronary spasm was assessed in 18 patients with active vasospastic angina in whom this amine was infused at rates of 5, 10, and 15 micrograms/kg/min for periods of 5 min each. The 12-lead electrocardiogram and blood pressure (cuff) were monitored throughout the whole test. In nine patients dopamine caused angina and ischemic electrocardiographic changes suggestive of coronary spasm: ST segment elevation in six patients and ST segment depression in the absence of important coronary stenoses in the remaining three. Infusion of dopamine was repeated during coronary angiography in three patients with positive test results: this provoked occlusive coronary spasm with ST segment elevation in two patients and nonocclusive spasm with ST segment depression in the remainder. In conclusion, infusion of dopamine provokes coronary spasm in a sizeable proportion of patients with active vasospastic angina. Its administration may be detrimental in patients susceptible to coronary spasm, such as those with acute myocardial infarction.