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。     

冠状动脉痉挛致广泛性ST段压低并T波高尖一例

患者男性，60岁，因“间断胸闷2个月，再发1 h”入院。心电图示广泛导联ST段压低并T波高尖。冠状动脉造影显示右冠状动脉优势型，左前降支中远端弥漫性变细，回旋支，右冠状动脉未见明显狭窄。术中给予硝酸甘油注射后，左前降支狭窄较前恢复，提示广泛导联ST段压低并T波高尖为冠状动脉痉挛所致。     

冠状动脉痉挛的临床特征

为了研究冠状动脉痉挛与ST段偏移的关系,冠状动脉痉挛与固定的狭窄位置的关系以及冠状动脉痉挛发作时的血流动力学改变,对153例伴有冠状动脉痉挛的心绞痛病人的临床特征进行研究。对170例次冠状动脉痉挛发作病人,同时进行冠状动脉造影及使用射线可透过的碳纤维电极和导线的12导联心电图分析研究结果,58例次伴有ST段上     

变异型心绞痛患者动态心电图ST段抬高与冠状动脉病变的关系

目的观察变异型心绞痛患者12导联24h动态心电图ST段改变与冠状动脉造影提示冠状动脉狭窄的相关性。方法对25例动态心电图显示ST段抬高的变异型心绞痛患者进行冠状动脉造影检查,将两者结果进行对比分析。结果 25例动态心电图发现与症状相关的ST段抬高的患者中,17例患者68%冠状动脉造影证实存在>50%冠状动脉狭窄动态心电图判断的痉挛血管、LAD20例、LCX2例,RCA4例,其中1例LAD及RCA同时发生。其中动态心电图提示LAD痉挛的20例患者,8例未见冠状动脉存在>50%以上狭窄。对于7例双支或多支病变者,仅有1例动态心电图诊断与CAG结果完全符合。结论动态心电图ST段改变对变异性心绞痛诊断有重要价值,此类患者常合并有冠状动脉病变,以LAD最多见。     

冠状动脉轻中度狭窄病变合并痉挛的介入治疗12例分析

目的:观察冠状动脉内支架对物治疗效果不佳的变异型心绞痛患者的临床效果.方法:35例明确诊断为变异型心绞痛患者,均口服钙离子拮抗剂,硝酸脂类调脂类药物,并行冠状动脉造影术及血管内超声(IVUS).其中12例药物治疗效果不佳的患者行冠状动脉内支架术.术后随访1～3年,6～9个月时复查冠状动脉造影.结果:冠状动脉造影显示35例患者中3例未见明显狭窄,32例有32%～75%的固定狭窄.12例物治疗效果不佳的患者根据发病时心电图,结合冠状动脉造影及IVUS判断9例痉挛在右冠状动脉,痉挛部位2例在近段,5例在中段,1例在远段,近段合并远段1例,固定狭窄40%～75%;3例痉挛在左前降支,痉挛部位在近段,2例在中段,固定狭窄50%～75%.犯罪病变多为边缘不光滑,呈偏心稳定的纤维性斑块,伴血管正性重构.12例患者相应冠状动脉成功置入(3.0～405)mm×(16～36)mm药物涂层支架,完全覆盖病变.术后随访1～3年,1例患者仍有胸痛发作;2例患者偶有胸痛,但程度及持续时间较术前明显减轻;9例患者无明显症状.6～9个月时复查冠状动脉造影显示11例患者支架段有轻度内膜增生,未见再狭窄;1例患者支架内50%～60%再狭窄,但仅偶有胸痛症状;其他部位无明显变化.结论:正规合理的物治疗对多数变异型心绞痛患者有效,但对少数药物治疗效果不佳的变异型心绞痛患者,可考虑行冠状动脉内支架术,近期效果良好.     

动态心电图一过性ST段抬高对变异性心绞痛冠脉病变的诊断价值

目的:通过动态心电图观察一过性ST段抬高对变异性心绞痛冠脉病变的诊断价值。方法;对28例动态心电图有一过性ST段抬高患者行冠状动脉造影检查。结果:28例变异性心绞通患者中,冠脉造影检查示冠状动脉伴有意义狭窄者共26例,其中狭窄>75％者达19例(占68％);>75％狭窄者:ST段抬高在>0.2 mV,≤0.2 mV者中分别占85％(17/20),25％(2/8),二者差异显著(P<0.05);在ST段抬高最长持续叶间<3分钟者,≥3分钟者中分别占36％(4/11),88％(15/17),二者差异显著(P<0.05)。结论:变异性心绞痛更易于在有病变的冠状动脉上发生,当冠脉痉挛发生时,ST抬高的时间、高度与冠脉狭窄的程度呈正相关。     

中老年ST段抬高型心绞痛患者动态心电图与冠状动脉造影分析

为了解中老年ST段抬高型心绞痛患者的动态心电图特点及冠状动脉 (简称冠脉 )病变情况 ,对 18例动态心电图显示ST段抬高型心绞痛患者进行冠脉造影。结果 :变异型心绞痛发作时ST段呈多种形态上抬 ,且不断演变。 18例患者均有有意义冠脉狭窄 ,冠脉狭窄程度与ST段上抬幅度并非一一对应关系。结论 :冠脉狭窄的基础上发生痉挛可能是中老年ST段抬高型心绞痛患者的发生基础 ,心绞痛发作时ST段形态不断演变值得进一步研究。     

12导动态心电图诊断变异型心绞痛1例

以ST段压低的阵发性心肌缺血在Holter上报道较多．但用12导动态心电图诊断短暂的一过性冠状动脉痉挛致ST段抬高的变异性心绞痛报道较少。现将我院1例用美国PI公司128兆12导动态心电图诊断短暂冠状动脉痉挛致变异型心绞痛1例报道如下。     

变异型心绞痛的临床特征和诊治分析

目的总结变异型心绞痛的临床特征和诊断治疗状况。方法回顾性分析我院连续住院172例变异型心绞痛患者的临床特征、诊断方法和治疗措施。结果患者平均年龄50.7±9.9岁(男:女=8.6),75%的患者有吸烟史。确诊所需时间中位数为2.5个月,确诊时间≥6个月占43%。22.1%患者伴发心律失常,以缓慢性心律失常为主。155例行冠状动脉造影检查,冠状动脉无显著狭窄74例(47.7%),单支、双支和三支病变分别为47例(30.3%)、24例(15.5%)和10例(6.5%)。138例有心绞痛发作时心电图并行冠状动脉造影,冠脉痉挛发生在造影显示完全正常的冠脉占49.3%,发生在具有显著狭窄病变(≥50%)的冠脉占39.9%,右冠脉易发生痉挛。56例(32.6%)行介入或冠状动脉搭桥治疗,158例(91.9%)联合硝酸酯类和钙拮抗剂治疗。结论变异型心绞痛仍是易忽视的疾病,约50%患者冠状动脉正常,右冠状动脉痉挛更常见,治疗以药物为主。     

静脉注射三硝酸甘油对变异性心绞痛的有益作用

1959年,Prinzmetal描述了变异性心绞痛,其特征为心电图上ST段显著抬高,室性心律失常发生率很高。已证明这些病人有冠状动脉痉挛,并可能是大多数病人这类发作的原因。病人进行冠状动脉造影时,并发室性心律失常包括心室纤颤比一般病人发     

Significance of exercise induced ST elevation in patient without a history of previous myocardial infarct

Between 1980 and 1995, we observed twenty-five patients (22 males, 3 females) at the mean age of 50.6 +/- 13 years, without previous myocardial infarction who presented exercise induced ST elevation on a bicycle stress test. METHODS: Significant ST elevation was defined as a > or = 1 mm change present in > or = 1 lead measured 0.08 sec after the J point and in 3 consecutive beats. All patients have undergone coronary angiography in the days following the exercise test. RESULTS: Most of patients (56%) presented a history of typical angina that was either purely exertional (8 pts) or also occurred at rest (6 pts). Others (36%) had non typical angina or no angina (8%); 78% of pts were smokers. Sixteen patients (group I) had ST elevation during exercise (exercise duration: 7.6 +/- 4 min; peak heart rate: 135.5 +/- 29 batt/min; ST = 3.5 +/- 1.5 mm) and nine (group II) during the recovery phase (exercise duration 16.3 +/- 1.6 min; p < 0.05; peak heart rate 168 +/- 22 batt/min; p < 0.05; ST: 5.8 +/- 3 mm; p < 0.05). In group I, 1 patient had no vessel disease, 12 had one vessel disease, 3 had multivessel disease with 6 cases of hypersevere coronary stenose (> 90%). In group II, 4 patients had normal coronary arteries, there was one vessel coronary artery disease in 4 patients and multivessel in one subject, without hypersevere coronary stenosis. Correlation between anatomic location of stenosis and electrocardiographic ST elevation was excellent, particularly in case of single vessel disease (100%). All patients underwent one or more new exercise tests after therapeutic intervention (surgery n = 3; angioplasty n = 7; medical treatment n = 15), only 2 patients had persistent exercise induced ST elevation. During follow-up (5 +/- 3 years), 3 patients died (2 cardiac deaths) and 3 had recurrent angina controlled by new treatment. CONCLUSION: Exercise-induced ST elevation is a rare phenomenon in patients without prior myocardial infarction. When occurring purely during exercise, coronary lesions are frequent and often servere, in the other hand ST elevation of the recovery phase is frequently associate with normal arteries or less severe lesions. In most cases, revascularisation or medical therapy can abolish clinical and electrocardiographic abnormalities.     

冠状动脉旁路移植术后再发心绞痛的介入治疗分析

目的分析冠状动脉（冠脉）旁路移植术（CABG）后再发心绞痛的原因及进行介入治疗的有效性和安全性。方法再发缺血症状的CABG术后老年患者78例，进行冠脉和桥血管造影，并同时对53例进行介入治疗。结果78例均进行冠脉和桥血管造影，其中8例桥血管通畅，原冠脉病变无或有轻微发展；17例桥血管严重狭窄或全部闭塞，同时，原冠脉3支弥漫严重病变；53例原冠脉血管病变有明显进展或桥血管出现严重病变或闭塞。78例共移植桥血管226支（其中大隐静脉桥血管153支，乳内动脉桥69支，桡动脉桥4支）。大隐静脉桥血管153支中，110支发生病变（71．9％，其中长段弥漫性病变或完全闭塞77支，吻合口狭窄14支，体部狭窄19支）。乳内动脉桥共69支，27支发生病变，占39．1％（其中全程弥漫性病变和完全闭塞12支，吻合口狭窄15支）。桡动脉桥共4支，通畅3支，吻合口狭窄1支。226支桥血管发生病变共有138支（包括大隐静脉桥血管110支，乳内动脉桥27支，桡动脉桥1支），桥血管吻合口狭窄30支，体部病变19支，弥漫病变或完全闭塞89支。在吻合口狭窄的桥血管中，术后0～3个月发生21支（70.0％），术后3～12个月发生9支（30．0％），术后1年以上无吻合口狭窄。在体部病变的桥血管中术后0～3个月未发生病变，术后3～12个月发生10支（52．6％），术后1年以上发生9支（47．7％）。桥血管弥漫病变或完全闭塞术后0～3个月发生28支（31．5％），术后3～12个月发生14支（15．7％），术后1年以上发生47支（52．8％）。53例患者进行原发血管和（或）桥血管介入治疗，50例介入治疗成功（94、3％）。所有病变介入治疗后均即刻获得良好结果，30d随访，未出现严重心脏事件。结论CABG术后再发心绞痛介入治疗成功率、有效性、安全性均较高，介入治疗可作为CABG术后再发缺血的主要治疗手段之一。     

Induction of Prinzmetal's angina by stopping exercise. Apropos of 3 cases

Three cases of anginal pain with ST elevation occurring at the end of exercise are reported. In 2 cases, there was a symptom-free interval between exercise, which was well tolerated, and the clinical and electrical changes. The coronary circulation was angiographically normal, although one of the patients had have previous transmural myocardial infarction. Spontaneous coronary spasm was observed during coronary angiography in this patient. The third case was characterised by exclusively spontaneous angina. ST elevation was observed very early in the recovery phase after stress testing. This patient had severe triple vessel disease. Angiospastic manifestations were noted in the immediate postoperative period after myocardial revascularisation surgery. A review of the litterature shows two types of behaviour. In the rare cases of ST elevation after maximal stress testing (7 cases apart from those reported here) the coronary vessels were normal. On the other hand, when ST elevation occurred during exercise and/or followed ST depression, coronary artery disease was demonstrated: significant 52 cases (81%), less than 70%: 12 cases (19%). Overall, these results indicate that when ST elevation is observed in the recovery phase after stress testing, the coronary arteries are angiographically normal (specificity: 0,9).     

Coronary angioplasty for unstable angina: immediate and late results in 200 consecutive patients with identification of risk factors for unfavorable early and late outcome

Two hundred patients (mean age 56 years, range 36 to 74) with unstable angina (chest pain at rest, associated with ST-T changes) underwent coronary angioplasty. In 65 patients with multivessel disease, only the "culprit" lesion was dilated. The initial success rate was 89.5% (179 of 200 patients). At least one major procedure-related complication occurred in 21 patients (10.5%): (death in 1, myocardial infarction in 16 and urgent surgery in 18). All patients were followed up for 2 years. Five patients died late; 8 had a late nonfatal myocardial infarction and 52 had recurrence of angina pectoris. The restenosis rate was 32% (51 of 158) in the patients with initial successful angioplasty who had repeat angiography. At the 2 year follow-up, after attempted coronary angioplasty in all 200 patients, the total incidence rate of death was 3% (one procedure related; five late deaths), of nonfatal myocardial infarction 12% (16 procedure related and 8 late after angioplasty), and 13% (26 patients) were still symptomatic although they had improved in functional class. Multivariate analysis showed that variables indicating an increased risk 1) for major procedure-related complications were: ST segment elevation, persistent negative T wave and stenosis greater than or equal to 65% (odds ratio 3.7, 3.7 and 3.3, respectively); 2) for angiographic restenosis were: presence of collateral vessels, ST segment depression, multivessel disease, left anterior descending coronary artery stenosis and history of recent onset of symptoms (odds ratio: 2.2, 2.0, 1.9, 1.9 and 0.54, respectively); and 3) for late coronary events (recurrence of angina, late myocardial infarction or late death) were: multivessel disease, total occluded vessel and ST segment elevation (odds ratio 3.7, 2.8 and 0.44, respectively). Thus, coronary angioplasty for unstable angina can be performed with a high initial success rate, but at an increased risk of major complications. The prognosis is favorable after initial successful coronary angioplasty.     

Unstable angina with recurrent episodes of transient elevation of the ST segment: role of transluminal percutaneous angioplasty

Transluminal angioplasty was performed as an urgent treatment in 9 patients with unstable angina, refractory to medical therapy and ST elevation during pain. All had a coronary stenosis greater than 50% (89 +/- 12%; range 60-99%). The left anterior descending coronary artery was affected in 6 patients, the right coronary artery in 1 patient, the circumflex in 1 patient and 1 patient had two stenosis on both the left anterior descending and the first diagonal branch. A reduction of the luminal stenosis greater than 20% was obtained in all (residual stenosis 30 +/- 11%; range 11-40%). During a follow-up of 6-20 months, two patients only showed recurrence of chest pain. A maximal ergometric test was negative in all patients after 1, 3 and 6 months. A second arteriography, performed in 7 patients after 3-6 months, demonstrated a mean stenosis of 35% (range 30-40%). Transluminal coronary angioplasty is a feasible and effective therapeutic approach in patients with unstable angina and ST elevation, when a significant coronary stenosis is present.     

Myocardial ischemia due to coronary artery spasm during dobutamine stress echocardiography

Dobutamine stress echocardiography (DSE) is a useful and safe provocation test for myocardial ischemia. Until now, the test has been focused only on the organic lesion in the coronary artery, and positive DSE has indicated the presence of significant fixed coronary artery stenosis. The aim of the present study is to examine whether myocardial ischemia due to coronary spasm is induced by dobutamine. We performed DSE on 51 patients with coronary spastic angina but without significant fixed coronary artery stenosis. All patients had anginal attacks at rest with ST elevation on the electrocardiogram (variant angina). Coronary spasm was induced by intracoronary injection of acetylcholine, and no fixed coronary artery stenosis was documented on angiograms in all patients. DSE was performed with intravenous dobutamine infusion with an incremental doses of 5, 10, 20, 30, and 40 microg/kg/min every 5 minutes. Of the 51 patients, 7 patients showed asynergy with ST elevation. All 7 patients (13.7%) had chest pain during asynergy, and both chest pain and electrocardiographic changes were preceded by asynergy. These findings indicate that dobutamine can provoke coronary spasm in some patients with coronary spastic angina. When DSE is performed to evaluate coronary artery disease, not only fixed coronary stenosis, but also coronary spasm should be considered as a genesis of asynergy.     

Pathogenesis of unstable angina with 0- or 1-vessel disease. Important role of coronary artery spasm.

In order to examine the possible role of coronary artery spasm in the pathogenesis of unstable angina, provocative testing for coronary spasm was performed in 43 patients with unstable angina who had 0- or 1-vessel disease. Coronary spasm was induced in 20 (65%) of 31 patients by hyperventilation testing (ST increases in 18, ST decreases in 2). Anginal attacks with either ST-segment elevation or ST-segment depression in patients without a significant organic stenosis were induced in 23 (55%) of 42 patients during treadmill exercise testing. Coronary artery spasm, showing severe (> or = 90%) vasoconstriction with angina and/or ischemic electrocardiographic ST-segment deviation, was also documented angiographically in 42 (98%) of 43 patients following intracoronary injection of acetylcholine. We conclude that dynamic coronary obstruction plays an important role in the genesis of attacks in patients with unstable angina who had 0- or 1-vessel organic coronary artery disease.     

Coronary hemodynamic responses during spontaneous angina in patients with and patients without coronary artery spasm

The mechanisms of spontaneous angina were evaluated during cardiac catheterization in 13 patients who had angina occurring without provocation at rest. Left ventricular and systemic hemodynamics, coronary venous flows (thermodilution technique), electrocardiogram and coronary angiograms were recorded before and during spontaneous angina. Angiography during spontaneous angina showed that 5 patients had coronary spasm (group I) and 8 patients did not (group II). In group II there was a preponderance of multivessel coronary artery disease. Left ventricular end-diastolic pressure increased in all patients in both groups during spontaneous angina. In group I, 4 patients had transient ST elevation and 1 patient had peaked T waves during angina. Transient ST depression occurred during spontaneous angina in all group II patients. Group I patients had decreased coronary sinus flow (4 of 5 patients) or decreased regional flow (5 of 5) during spontaneous angina. Coronary resistance and ratio of double product to coronary blood flow increased in all patients. In group II, coronary hemodynamic responses during spontaneous angina varied. Coronary venous flows, coronary resistance and ratio of double product to coronary blood flow showed no uniform pattern. Thus, patients with severe coronary artery disease can have spontaneous angina without angiographic findings of coronary spasm. After analysis of angiograms and coronary hemodynamics in these patients, no apparent uniform mechanism for spontaneous angina was found.