U wave inversion during attacks of variant angina.

Sequential 12 lead electrocardiograms were recorded during angina pectoris induced by ergonovine maleate in 38 patients with variant angina. Transient U wave inversion was observed in 17 patients with ST segment elevation in anterior chest leads, but in only three of 21 patients with ST segment elevation in the inferior leads associated with right coronary artery spasm. In the 17, all of whom had spasm of the left anterior descending coronary artery, the sensitivity of ST segment elevation in V5 was only 41%, and that of U wave inversion 71%. U wave inversion without ST segment elevation occurred during attacks in 35% of patients. During the recovery phase, the sensitivity of U wave inversion was 82% in V4 and 65% in V5, though ST segment elevation was absent in both V4 and V5. Thus, inverted U waves without ST segment elevation often appear in marginal ischaemic zones or during the time of recovery from temporary ischaemia. Detection of inverted U waves should aid in the diagnosis of variant angina when only lead V5 is used as a monitor and when electrocardiograms are recorded only during the recovery phase.     

Value of the negative U wave during exercise test in the diagnosis of coronary insufficiency

In order to determine the value of inversion of the U wave during exercise for the diagnosis of coronary insufficiency, the stress tests of 227 patients were reviewed and confronted with the results of coronary angiography which showed 93 subjects with angiographically normal arteries and 134 subjects with left anterior descending disease; 37 patients had single vessel disease (Group I), 38 had double vessel disease (Group II) and 59 had triple vessel disease (Group III). When compared to the two classical criteria, anginal pain and less than or equal to 1 mm ST depression, inversion of the U wave was more specific: 82.8 +/- 7.6 p. 100 vs 77.4 p. 100 for anginal pain, and 66.7 +/- 9.6 p. 100 for ST depression. The sensitivity of this new sign for the detection of coronary insufficiency was 26.9 +/- 7.5 p. 100 vs 80.6 +/- 6.7 p. 100 for ST depression and 56.7 +/- 8.4 p. 100 for anginal pain. The positive predictive value of U wave inversion on effort was 70.9 +/- 12 p. 100 compared to 77.7 +/- 6.9 p. 100 for ischaemic ST depression and 78.3 +/- 8.2 p. 100 for induced anginal pain. Conversely, in angiographically normal coronary arteries, the absence of U wave inversion had a negative predictive value of 44.8 +/- 7.4 p. 100 compared to 70.5 +/- 9.5 p. 100 for the absence of ischaemic ST changes and 55.4 +/- 8.5 for the absence of anginal pain. These results confirm previously published data.(ABSTRACT TRUNCATED AT 250 WORDS)     

Vasospastic ischemic mechanism of frequent asymptomatic transient ST-T changes during continuous electrocardiographic monitoring in selected unstable angina patients

Asymptomatic episodes of ST segment and/or T wave changes are often reported during Holter monitoring in patients with angina pectoris. However, the interpretation of such changes is debated relative to silent myocardial ischemia. We studied 11 patients admitted to the CCU because of frequent episodes of unstable anginal attacks who had undergone repeated periods of Holter monitoring, characterized by predominantly occurring asymptomatic episodes of ST segment and/or T wave changes associated with less frequent typical anginal attacks. In a total of 89 days of Holter monitoring, the patients evidenced 520 episodes of transient ECG changes including 180 of ST elevation, 73 of ST depression, and 267 of T wave alterations. Only 12% of episodes were symptomatic. Coronary injection during asymptomatic ST-T changes was performed in eight patients. In six it was possible to document spontaneous coronary spasm. In seven patients ergonovine administration induced anginal pain, ST-T changes, and coronary spasm. In all patients the anginal attacks completely disappeared with medical treatment and the asymptomatic episodes were abolished in six and reduced in four. Our findings support the hypothesis that in certain selected unstable anginal patients, transient asymptomatic ECG changes are caused by acute myocardial ischemia.     

Clinical characteristics of sudden cardiac death in patients with vasospastic angina

Of 383 patients with vasospastic angina who were followed for a period of 3.2 +/- 0.1 years, 9 (2%) died suddenly from cardiac causes. Calcium antagonists had been given to 98% of our patients. Only one patient who died suddenly had a fixed coronary stenosis of 75% or greater. Eight of the 9 patients showed ST segment elevation during anginal attack at rest, and 3 patients showed ST segment elevation at both anterior and inferior leads. Sudden death occurred in 6 of 41 patients (12.5%) who were documented to have multivessel coronary spasm, but in only 3 of 342 patients (1%) who had single vessel spasm (p less than 0.01). Serious arrhythmia occurred during anginal episode in 3 of 9 patients who died suddenly (53%) and in 52 of 374 who did not (14%). These results suggest that the frequency of sudden cardiac death was rather low in Japanese patients with vasospastic angina. The risk of sudden death was increased in patients with multivessel spasm and serious arrhythmia during anginal attacks but not these with fixed coronary stenosis.     

Coronary angiography in patients with U wave inversion during coronary artery spasm

During ergonovine-induced vasospastic angina, U wave inversion without significant ST segment deviation on the precordial electrocardiograms was documented in four patients. Coronary angiography revealed incomplete spastic obstruction of the left anterior descending artery without delayed filling and runoff in three patients. In the remaining patient, the proximal left anterior descending artery was totally occluded and there were well-developed collaterals from the non-spastic artery. Thus, ergonovine-induced U wave inversion was related to the presence of coronary vasospasm, and angiography demonstrated less severe myocardial ischemia in such patients than in cases with ST segment elevation or depression, which is usually associated with subtotal or total obstruction of a major coronary artery without adequate collaterals. In their clinical courses, two patients had episodes of angina with ST segment elevations or depressions. It was suggested that vasospastic angina with U wave inversion alone is one aspect of a continuous spectrum of vasospastic myocardial ischemia.     

Vasospastic Ischaemia Induced by the Hyperventilation Test in Patients with a Negative Response to Ergometrine

ABSTRACT. We present the case histories of two patients with angina pectoris who developed coronary artery spasm in response to provocation with prolonged hyperventilation (verified by ST segment elevation in both and coronary angiography in one) despite a negative ECG response to intravenous injection of 0.4 mg ergometrine. This new observation, which is in conflict with recent publications stating that ergot provocation is more sensitive than hyperventilation, suggests that in some patients diagnostic provocation with hyperventilation may be an alternative to the widely used ergot provocation.     

Pure arrhythmic form of the pre-infarction syndrome or spasm responsible for myocardial necrosis

A 74 years old man was admitted as an emergency for syncopal attacks due to recurrent ventricular fibrillation (VF). These attacks were observed at the height of myocardial ischaemia as shown by ST elevation in Leads II, III and RV without associated anginal pain. Inferior myocardial infarction occurred during recurrent VF on the 4th day; the outcome was favourable. Coronary angiography was performed on the 10th day and showed double vessel disease; ergometrine (0.2 mg) induced anginal pain and ST elevation in Leads II, III and AVF. A good clinical result was obtained by calcium antagonists with an 18 months follow-up. Coronary spasm, documented in this case by the ergometrine provocation test, is now recognised as a cause of resting angina, effort angina and also some cases of myocardial infarction. This report suggests that coronary spasm may also induce apparently isolated severe ventricular arrhythmias without associated chest pain, which raises the question as to whether arrhythmias induced by spasm could play a primary role in aggravating myocardial ischaemia, leading to myocardial infarction.     

Increased plasma fibrinopeptide A levels during attacks induced by hyperventilation in patients with coronary vasospastic angina

Plasma fibrinopeptide A levels, beta-thromboglobulin levels and platelet factor 4 levels were estimated by enzyme-linked immunosorbent assay before and after hyperventilation in 12 patients with coronary vasospastic angina and in 12 control subjects matched for age and gender. In all 12 study patients, anginal attacks accompanied by electrocardiographic (ECG) changes (ST elevation in 11 patients and ST depression in 1 patient) were induced by hyperventilation. Coronary angiography was performed on 11 of the 12 patients, and coronary artery spasm with the same ECG changes was induced by intracoronary injection of acetylcholine in all 11. The plasma fibrinopeptide A levels increased significantly from 2.0 +/- 0.4 to 10.0 +/- 2.4 ng/ml during the attack (p less than 0.001) in the study patients, but remained unchanged before and after hyperventilation in the control subjects. The plasma levels of beta-thromboglobulin and platelet factor 4 remained unchanged after hyperventilation in both groups. Our data indicate that coronary artery spasm may induce thrombin generation and trigger thrombus formation in the coronary artery.     

变异型心绞痛的心电图特征

变异型心绞痛常见于冠脉正常或无严重冠脉狭窄的患者，本文主要探讨变异型心绞痛患者的心电图变化。变异型心绞痛常出现典型的心电图变化，近50％的患者出现高耸对称的 T 波，如果痉挛持续则出现进行性抬高的 ST 段，持续数分钟后逐步回落。与 ST 段抬高相关的心电图改变还包括 R 波增高和 S 波减小，部分病例出现 TQ 段斜率上升、ST 段抬高和 T波深倒置的电交替。除此以外，变异型心绞痛发作时易发生室性心律失常。     

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.     

The provocation of coronary arterial spasm in patients with recent transmural myocardial infarction

Provocative tests for coronary spasm were performed in a groupof 131 patients (124 men and 7 women) with recent (<6 weeks)transmural myocardial infarction. Coronary arteriography wasperformed 27±9 days after the onset of the infarction.The provocative test was performed using a single IV bolus of0.4 mg of ergometrine. Aortic pressure, ECG and arteriogramsof the two coronary vessels were repeated 3 and 5 min later.Provoked spasm was observed in 27 (21%) of the patients. In13 (48%) the coronary spasm occurred in a vessel presumed tobe responsible for the myocardial infarction, while it was observedin coronary artery unrelated to the area of the infarct in 14(52% of the cases with spasm). Thus, this study demonstratesa high degree of reactivity of the coronary tree of patientswith recent transmural myocardial infarction suggesting thelikelihood of a role for spasm in the infarction process andoffering some explanation for subsequent recurrent ischemicevents.     

Relationship between C-reactive protein and the electrocardiographic pattern on admission in patients with acute coronary syndrome

BACKGROUND: In patients with acute coronary syndrome (ACS), the prevalence of a primary inflammatory pathogenic component of coronary instability, as detectable by elevated C-reactive protein (CRP), varies considerably. The aim of the present study was to assess the prevalence of inflammation in patients with ACS according to the different electrocardiographic (ECG) patterns on admission. METHODS: Hundred and thirty-six consecutive patients with the diagnosis of acute myocardial infarction were divided in three groups according to the ECG pattern on admission. Group 1 included 59 patients with ST segment elevation, group 2 included 50 patients with ST depression and/or T wave inversion and group 3 included 27 patients with no ECG changes. CRP was measured on admission in all patients. For the prevalence of inflammation analysis, we used a cutoff value of 3 mg/l. RESULTS: CRP was above cutpoint significantly more often in patients with ST depression and/or T wave inversion (44.1% in group 1, 70% in group 2 and 40.7% in group 3; p=0.009). Patients with similar ECG pattern and CRP levels above the cutpoint presented a poorer outcome (coronary death, myocardial infarction and recurrence of instability) at one-year follow-up: 54 versus 27% for group 1, 74 versus 27% for group 2 and 45 versus 31% for group 3. CONCLUSIONS: Patients with ST depression and/or T wave inversion on admission exhibit a higher prevalence of elevated CRP than those with ST elevation or no ECG changes, suggesting an important heterogeneity of the role of inflammatory triggers of the clinical syndromes of coronary instability.     

Comparison of electrocardiography and thallium-201 myocardial scintigraphy for the detection of ergonovine-induced coronary artery spasm: angiographic correlation

This study was performed to determine the sensitivity of thallium imaging vs ECG monitoring for detecting coronary artery spasm noninvasively following intravenous ergonovine administration as compared to simultaneous coronary angiography. Thirty-two patients with insignificant coronary artery disease and chest pain underwent 12-lead ECG monitoring, thallium imaging, and coronary arteriography following the administration of 0.05, 0.1, 0.2, and 0.3 mg of ergonovine given 5 minutes apart or until chest pain occurred. One minute following the last dose of ergonovine, 2.5 mCi of thallium-201 was injected intravenously, and a final ECG was recorded and repeat coronary arteriography performed. Within 10 minutes following the injection of thallium, imaging was performed in the 40-degree and 70-degree left anterior oblique and anterior projections. The ECG, thallium study, and coronary arteriogram were read blindly and results were compared. The ECG, angiogram, and thallium study were read as positive if the following occurred, respectively: greater than or equal to 1 mm ST segment elevation, depression, or T wave reversal; greater than 50% vessel narrowing,; and reversible perfusion defect. Five patients were excluded from analysis because of either catheter-induced spasm, suboptimal thallium studies, or protocol violations. Of the 27 patients included for analysis, six had chest pain, five had a positive angiogram, five had a positive thallium study, and one had a positive ECG. The sensitivity of thallium vs ECG monitoring was 80% vs 25%, and the accuracy was 92% vs 80%. We conclude that thallium imaging greatly increases the noninvasive detection of ergonovine-induced coronary spasm as compared with the ECG with no loss of accuracy.     

Long-term study of recurrent vasospastic angina using coronary angiograms during ergonovine provocation tests.

Chronologic changes of coronary spasm were examined by repeated ergonovine provocation tests during angiography. A total of 322 patients who had variant angina without severe atherosclerosis demonstrated a positive response to the first test. Ninety of these patients had recurrent variant anginal symptoms after an angina-free period of 38 +/- 12 months (mean +/- SD). Of these 90 patients, 76 (84%) had symptoms or electrocardiographic (ECG) findings similar to those of the first test. The initial 9 of these 76 patients underwent a second provocation test and showed coronary responses analogous to those on the first test. Of the 90 patients, 14 (16%) had different symptoms or ECG findings from those elicited at the first episode. All 14 patients again had a positive response to a second ergonovine test and the following angiographic changes were observed in the three major vessels between the two tests. Of the 21 vessels that had spasm on the first test, eight vessels (19%) did not have spasm on the second test. Of the 21 vessels that did not demonstrate spasm on the first test, 10 (24%) demonstrated spasm on the second test. In the present study it is concluded that the majority of patients with recurrent angina seemed to have consistency in the location of coronary spasm, while in some patients the fluctuation of coronary spasm was confirmed by two ergonovine provocation tests.     

Coronary arteriography and left ventriculography during spontaneous and exercise-induced ST segment elevation in patients with variant angina

The present study is an angiographic demonstration of coronary artery spasm during both spontaneous and exercise-induced angina in three patients with variant angina. In each case, clinical, ECG, coronary angiographic, and left ventriculographic observations were made at rest, during spontaneous angina, and during exercise-induced angina. The character of chest pain was similar during spontaneous and exercise-induced episodes. ST segment elevation was present in the anterior ECG leads during both episodes. The left anterior descending coronary artery became partially or totally obstructed during both types of attacks. When coronary spasm was demonstrated during both types of attacks, left ventriculography disclosed akinetic or dyskinetic wall motion in the area supplied by the involved artery. In those patients with reproducible exercise-induced ST segment elevation and chest pain, thallium-201 scintigraphy showed areas of reversible anteroseptal hypoperfusion. Thus in selected patients exercise-induced attacks of angina were similar to spontaneous episodes.     

Delayed filling of the anterior interventricular artery. Apropos of 9 cases

Selective coronary angiography has shown that typical angina pectoris may occur in the absence of atheromatous coronary stenosis. Other causes of these attacks of pain have been found: coronary spasm, small vessel disease, abnormal dissociation of haemoglobin or metabolic disturbances of the myocardial cell. Of all the patients undergoing coronary angiography in 1984 at the Centre Cantini, 9 had no classical coronary lesions but delayed filling of the left anterior descending artery. This syndrome was described for the first time in 1972 by Tambe as the "slow flow velocity syndrome". The aim of this study was to analyse the clinical, ECG and haemodynamic profiles of those patients. Five of them also underwent stress Thallium myocardial scintigraphy. An ergometrine provocation test was performed afterwards under ECG control. Delayed filling was appreciated by comparison with the other vessels and also by measuring the filling time which was two or three times longer than in a control series of 9 patients with angina and normal coronary arteries. The difference was statistically significant. These findings were only observed in strictly normal coronary vessels; they were reproducible and unaffected by the administration of nitrate derivatives. In our series all 9 patients were men with an average age of 51.4 years. One patient was asymptomatic and had a history suggestive of myocardial infarction, and 4 others had typical angina of effort: all had abnormal exercise stress tests. The other 3 patients had spontaneous atypical chest pain, normal resting ECG and a negative exercise stress test (impossible in one case). The five stress Thallium scintigraphies showed myocardial perfusion defects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Repeated epicardial coronary artery endothelial injuries lead to a global spontaneous coronary artery spasm

OBJECTIVES: This study was conducted to develop a spontaneous coronary spasm model. MATERIALS AND METHODS: Balloon endothelial denudation was carried out in the epicardial left anterior descending coronary artery (LAD) every 2 weeks, for a total of four times, in 12 pigs. Changes in the denuded site diameter and LAD blood flow caused by acetylcholine or serotonin were assessed before each denudation and at week 8. Blood pressure, electrocardiogram (ECG) from the LAD area and LAD blood flow were monitored continuously in conscious and unrestrained pigs. RESULTS: Spontaneous ECG ST depression with a decrease in LAD blood flow appeared at around 2 weeks. In accordance with this, 0.5 microg/kg acetylcholine induced similar ECG and LAD blood flow changes without denuded site narrowing, suggesting microvascular spasm. Thereafter, ECG ST depression or elevation by serotonin via a denuded site spasm was found after 6 weeks and spontaneous ECG ST changes due to epicardial coronary artery spasm were observed. CONCLUSION: Epicardial coronary artery endothelial injury may induce spontaneous vasospasticity in the downstream coronary microvessels as well as in the denuded portion, suggesting functional abnormality through the entire coronary arterial tree.     

Myocardial bridge of the left anterior descending coronary artery and myocardial infarction: does coronary spasm play a part?]

The association of a myocardial bridge of the left anterior descending (LAD) coronary artery and myocardial infarction is rare. The mechanisms by which the myocardial bridge could predispose to myocardial infarction are tachycardia (reducing the duration of diastolic coronary filling), thrombosis at the site of the myocardial bridge, and coronary spasm which, however, has never been demonstrated in the context of infarction. The aim of this study was to detect coronary spasm by provocative ergometrine testing in 4 patients, all male, aged 21 to 49 years, average 39 years old, who had anterior myocardial infarction associated with myocardial bridging of the LAD artery without atheromatous coronary stenosis. The ergometrine tests were performed during (2 cases) or after coronary angiography (2 cases). The systolic narrowing due to the myocardial bridge ranged from 25 to 95% (average 70%). The ergometrine test was strongly positive in 1 patient and negative in the other 3. Repermeabilisation of a thrombus was suggested in these 3 patients by the recording of an accelerated idioventricular rythm in the acute phase of infarction (2 cases) or by the demonstration of abnormal platelet aggregation (1 case). This is the first report of coronary spasm in a patient with myocardial bridging associated with infarction. However, it is not possible to determine the respective roles of spasm and myocardial bridging in the genesis of the infarct. We suggest systemic provocative ergometrine testing in this situation to orientate the most appropriate treatment.     

Electrocardiographic changes with coronary artery spasm

The presence or absence of important ECG changes (e.g., ST elevation or depression ≥ 1 mm) was evaluated in 79 consecutive patients with coronary artery spasm. In eight of these patients ECG changes usually did not accompany episodes of rest angina. Evaluation before, during, and after cardiac catheterization included multiple ECGs and ambulatory monitoring during angina. Our observations suggest that the ECG may not always be a sensitive indicator of coronary spasm. Thus the diagnosis of transient myocardial ischemia secondary to coronary spasm should not necessarily be excluded because of a lack of ECG changes during rest angina.     

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).