Variant angina induced by biliary colic.

A 65 year old woman with gall stones presented with crushing chest pain after an attack of biliary colic. The electrocardiogram showed ST segment elevation in leads I, aVL, and V1-V3 while leads II, III, and aVF showed ST segment depression. Cardiac enzyme activity remained within the normal range. During the next three weeks attacks of epigastric and right hypochondrial pain preceded by crushing chest pain with identical electrocardiogram changes occurred with decreasing frequency. Coronary arteriography showed 60% obstruction of the left anterior descending coronary artery and good left ventricular function. During the next three years the patient complained both of mild abdominal pain, probably biliary colic, and mild effort related angina pectoris without a relation between the two symptoms. It is suggested that the attack of variant angina was triggered by biliary colic through sympathoadrenal discharge causing vasospasm.     

Clinical presentation and prognosis of left main coronary artery disease in the 1980s

Clinical presentation and course were studied in 127 consecutive patients with angiographically proven left main coronary artery disease. Mean age was 62 (37-79) years. Thirteen patients (10%) had no history of chest pain, seven (5%) had atypical chest pain, and the remaining 107 (85%) typical angina pectoris. Eighty-two patients (65%) had unstable angina, 73 had suffered a myocardial infarction (MI) in the past, and 50 (68%) had post MI angina pectoris. The electrocardiogram was analysed in 102/125 patients during an episode of chest pain and also when they were without chest pain. Outside an episode of chest pain the ST segment was normal in 42 patients (32%), the T wave was normal in 50 patients (38%) and both the ST and T were normal in 33 patients (25%). During chest pain all patients had an abnormal ECG, the most frequent pattern being ST segment depression in leads V3, V4 and V5 (with maximal depression in V4), and ST segment elevation in leads V1 and aVR. The average number of leads with ST-T abnormalities was 6.4. A symptom-limited exercise test on a treadmill with 12-lead ECG monitoring was performed in 89 patients. The exercise test was abnormal in 88 patients (99%), most of whom (74 patients) were already in the first or second stage of the Bruce protocol. The most frequently observed abnormality was ST segment depression of 2 mm or more in leads V4, V5, and V6, and ST segment elevation in leads V1 and aVR. The systolic blood pressure during exercise fell or remained at the same level in 38 patients (43%).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Anginal attack following a sodium bicarbonate and hydrocortisone injection

A case of a 73-year-old man with variant angina who developed chest pain and shock following an injection of sodium bicarbonate and hydrocortisone is reported. The electrocardiogram (ECG) during the chest pain attack revealed ST elevation in leads II, III and aVF. It returned to a normal pattern 10 min later. Coronary angiography, performed 2 hours after the anginal attack, showed no significant coronary arterial stenosis. One month later, an injection of ergonovine (16 micrograms) into the right and left coronary arteries induced spasms in segments 4 and 13, with ischemic ECG changes. Possible causes of the anginal attack are a coronary arterial spasm induced by the allergic reaction to hydrocortisone and/or serum alkalosis due to the sodium bicarbonate injection triggered by hyperventilation.     

Class I antiarrhythmic drug and coronary vasospasm-induced T wave alternans and ventricular tachyarrhythmia in a patient with Brugada syndrome and vasospastic angina

A 50-year-old man presented with a history of transient chest pain and palpitations. The 12-lead ECG at rest showed normal sinus rhythm. A slight ST segment elevation was observed in leads V1 to V3. During hospitalization, atrial fibrillation developed, and oral pilsicainide was administered. Thirty minutes after the drug was given, the ECG showed marked ST segment elevation in leads V1 to V3, and T wave alternans became visible in leads V2 and V3. Self-terminating ventricular tachycardia was initiated following frequent ventricular premature complexes, which showed a left bundle branch block pattern. The coronary angiogram was normal, but in the provocation test of vasospastic angina, acetylcholine administration into the left coronary artery resulted in complete occlusion of the left anterior descending and circumflex arteries. Marked ST segment elevation developed in leads I, aVL, and V3 to V6 concomitant with visible QT/T alternans in leads V4 and V5, and ventricular tachyarrhythmia was initiated. Brugada syndrome and vasospastic angina coexisted in this patient, and T wave alternans can be used as a predictor of ventricular tachyarrhythmias in such patients.     

An adrenaline-induced vasospasm as the form of presentation of variant angina

A 41-year-old-man without previous ischemic heart disease, developed a severe anaphylactic reaction. After administration of epinephrine (0.5 mg) the patient complained of chest pain. The electrocardiogram showed an elevation of ST segment in inferior leads. Myocardial necrosis was ruled out. Coronary arteriography disclosed normal coronary arteries. Eight months later, the patient developed severe chest pain during physical activity. ST elevation was again seen in inferior leads. ECG changes disappeared, when sublingual nitroglycerin was administered. A diagnosis of vasospastic angina was made. Exercise test was negative, during treatment with calcium-blocking agents. The patient subsequently remain free of symptoms taking medication. The physiological mechanisms of vasospastic angina and precipitating factors are discussed.     

Intracoronary administration of nicorandil for the treatment of spontaneous microvascular spasm with ST segment elevation.

A 64-year-old man with a history of previous coronary intervention of the left anterior descending artery was admitted to hospital because of recurrent chest pain at rest. Coronary angiography revealed no significant coronary artery stenosis. During preparation for the second shot of the right coronary artery, chest pain occurred unexpectedly, represented by ST segment elevation in leads II, III and aV(F). Immediate right coronary angiography revealed no significant coronary artery stenosis, but markedly delayed contrast medium washout. Intracoronary administration of nicorandil attenuated this phenomenon, and the patient was diagnosed as having angina pectoris caused by microvascular spasm with ST segment elevation.     

Refractory Case of Coronary Artery Spasm with Interesting Findings: A Case Report

This is a case of refractory vasospastic angina with unusual electrocardiographic findings and rare coronary angiographic documentation of diffuse spasm of the left coronary system with a baseline of near normal coronary arteries. A 66-year-old man presented with severe vasospastic angina that eventually progressed to non-ST elevation myocardial infarction (NSTEMI). During the episodes of chest pain, the electrocardiogram revealed ST segment depression rather than elevation. Coronary angiography revealed near normal coronary arteries with initial diffuse spasm of the left coronary system. The patient continues to be symptomatic despite treatment with different forms and doses of nitrates and calcium channel blockers. No financial support was needed or provided by any source.     

A most unusual acute coronary syndrome

A 60-year-old man, known for stable coronary artery disease, was admitted for suspected unstable angina. In the previous month, the patient presented with progressive dyspnea on light exertion. In the preceding four months, he had experience occasional episodes of flushing and diarrhea, and had inexplicably lost 22.7 kg. Night sweats and fever were absent. ST segment elevation in the inferior leads and ST segment depression in the precordial leads were documented during an episode of chest pain. The coronary angiogram showed diffuse disease with 70% stenosis of the left anterior descending coronary artery and 50% stenosis on the second diagonal (D(2)). An echocardiogram showed a patent foramen ovale. Balloon angioplasty and stenting were performed on the two lesions. Two days later, prolonged chest pain recurred. Cardiac catheterization was repeated and showed occlusive thrombus within the stent on the D(2). Angioplasty was repeated. Symptoms recurred 36 h later, with the electrocardiogram showing ST segment elevation. The first angiogram was reviewed and vasospasm was suspected on a branch of the D(2), on the second marginal and in the distal circumflex artery. The diagnosis of vasospastic angina was retained. Beta-blockers were replaced by high doses of a calcium channel blocker with an excellent clinical response. The case described is of a patient with an acute coronary syndrome, vasospastic angina, in-stent thrombosis and carcinoid disease. Coronary vasospasm was attributed to serotonin, which was secreted by the carcinoid tumour that reached an atherosclerotic coronary vasculature through a patent foramen ovale, thereby avoiding pulmonary inactivation.     

A case of vasospastic angina: development of transient collateral circulation lessen the degree of myocardial ischemia during coronary artery spasm

A 57-year-old man was admitted to our hospital because he had had attacks of chest pain at rest for more than a year, in spite of daily oral diltiazem (90 mg/day) and isosorbide dinitrate (15 m/day). The diagnosis of variant angina was made for him based on ST elevation in chest leads of the electrocardiogram during his first attack. However, one year later, the electrocardiograms during attacks showed only ST depression or T wave inversion in chest leads. The coronary arteriogram during spontaneous chest pain revealed that the left anterior descending artery was totally occluded at its middle portion, and that its peripheral portion was perfused by collateral circulation from the right coronary artery. The coronary arteriograms after administration of nitroglycerin were apparently normal, and no signs of collateral circulation were observed. These findings indicated that the transient collateral circulation could develop after repetitive coronary artery spasms even in the absence of significant coronary stenosis, and that it could lessen the degree of myocardial ischemia during coronary artery spasm.     

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Two patients complained of chest pain while at rest and during physical activities. However there seemed to be no direct relation between exertional angina and an increasing level of work performed, indicating that these patients had a variable threshold of angina during exercise. In one patient spontaneous chest pain was associated with transient S-T segment changes in precordial leads, and during coronary arteriography the administration of ergonovine induced spasm of the left anterior descending coronary artery. The other patient showed S-T segment elevation in inferior leads during an ergonovine-induced anginal attack and coronary arteriography revealed a spontaneous spasm of the right coronary artery. In both patients repeated exercise tests yielded different results, because the chest pain and S-T segment depression occurred at different work loads with large differences in heart rate-systolic blood pressure product.It is concluded that a variable threshold of angina during exercise is a clinical manifestation in some patients with vasospastic angina and is probably due to the difference in coronary arterial tone at the onset of exercise.     

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.     

Multivessel variant angina after a radical nephrectomy operation

A case of multivessel variant angina after an open radical nephrectomy operation (RNO) is presented. A 52-year-old man was admitted to the coronary care unit with recurrent chest pain and dynamic ST-T wave changes on electrocardiogram early after an RNO. The first diagnosis of the clinical condition was non-ST segment elevation acute coronary syndrome. However, recurrent angina with ST segment elevation occurred after the standard medical therapy, which included beta-blockers. Emergency coronary angiography showed diffuse and multiple narrowing of all the three major coronary arteries during the chest pain, which was relieved by intracoronary nitroglycerine injection. Variant angina was suspected, and beta-blocker therapy was replaced with calcium channel blocker treatment. No angina attacks were observed during the clinical follow-up. Although a direct relationship between the type of surgery and variant angina was not established, coronary vasospasm after an RNO should be kept in mind, especially in the differential diagnosis of a patient with recurrent angina and dynamic ST-T changes on electrocardiogram. Although beta-blocker therapy is a first-line treatment for all acute coronary syndromes, it can be harmful in patients with variant angina and should be stopped immediately after verification of diagnosis.     

Reversible left ventricular apical ballooning associated with jet lag in a Taiwanese woman: A case report

Reversible left ventricular apical ballooning, without coronary artery stenosis, is a novel heart syndrome mimicking acute myocardial infarction, and is very rare in Taiwan. A 74-year-old Taiwanese woman returned from travelling abroad for one week and suffered from persistent, severe jet lag with sleep disturbance. She had a cold exacerbated by bronchial asthma for three days. She presented with sudden onset of chest pain after drinking three cups of coffee and taking a sauna for more than 1 h. On admission, an electrocardiogram showed ST segment elevation in leads II, III, aVF and V(3-6), and cardiac enzyme tests revealed minimal elevation. An echocardiogram showed apical ballooning and basal hyperkinesias of the left ventricle (LV) in systole. A coronary angiogram on the second day was normal, while the ST segment was still elevated, and the patient continued to experience chest pain. A negative T wave developed three days later. The electrocardiogram abnormality and LV dysfunction resolved completely six months later. A takotsubo (ampulla) cardiomyopathy was diagnosed. The activated myocardial adrenergic nervous system, stimulated by acute and marked stress in this patient, with more adrenergic innervations distributed in the apex of the LV, may be the trigger for this novel cardiac syndrome.     

Two cases of primary artery dissection

We experienced two cases of primary coronary artery dissection. (Case 1) 55-year-old man had frequent episodes of chest oppression at early morning and midnight. During chest oppression, electrocardiogram showed transient ST-segment elevation in leads II, III, and a VF. Then, he was diagnosed as having angina pectoris. This diagnosis was based on the fact that he presented coronary spastic syndrome. Right coronary angiogram demonstrated an intimal flap and false lumen at segment 3, and primary coronary dissection was confirmed. (Case 2) A 27-year-old woman complained of back pain while taking a bath. Electrocardiogram showed ST-segment elevation and abnormal Q in leads V2, V3 and V4. She was diagnosed as having acute anterior wall myocardial infarction. Presence of coronary artery dissection at segment 6 was identified by left coronary angiogram. Primary coronary artery dissection is clinically diagnosed by coronary angiogram very rarely. Only 27 such cases have been reported. It was speculated that, in case 1, vasospastic angina may be associated with primary coronary artery dissection. Case 2 had primary coronary artery dissection at segment 6 of the left anterior descending artery. Thus, her clinical picture was similar to those of previously reported cases.     

Acute coronary syndrome induced by oral capecitabine

A 41-year-old woman who was undergoing oral chemotherapy with capecitabine for metastatic breast cancer presented with recurrent episodes of chest pain associated with electrocardiographic signs of diffuse ST segment elevation. After spontaneous pain relief, the electrocardiogram showed ischemic evolution in the anterior precordial leads. Coronary and ventricular angiography, performed 24 h later, showed normal coronary arteries and normal left ventricular function. After therapy with capecitabine was discontinued, the patient did not experience further episodes of chest pain. After a nine-month follow-up, she remains alive, with a good performance status and without clinical evidence of persistent ischemia.     

Value of the bipolar lead CM5 in electrocardiography

Only bipolar lead recording are available during ambulatory monitoring. Their sensitivity in detecting ST segment changes in relation to standard electrocardiographic leads is not known. The magnitude and direction of ST segment changes in the bipolar lead CM5 were compared with those in standard electrocardiographic leads in patients during exercise testing and percutaneous transluminal coronary angioplasty. Thirty patients with coronary artery disease were studied during exercise tests in which ST segment depression (greater than 0.5 mm) occurred in one or more standard electrocardiographic leads and 13 patients were studied during angioplasty that resulted in ST segment change in one or more leads (I, II, III, V2, V5, and CM5). Lead CM5 was the most sensitive lead (93%) during exercise testing and also showed the greatest magnitude of ST segment change below the isoelectric line in 93% of the patients. Only two patients, one with ST segment elevation in inferior leads and one with changes restricted to septal leads, had no ST segment depression in lead CM5. When ST segment shift from the baseline electrocardiogram was measured the magnitude of depression was greatest in lead CM5 in only 63% of the patients. During angioplasty of the left anterior descending coronary artery, lead CM5 showed ST segment depression in seven patients, ST segment elevation in two, and a biphasic response in one. Two of the three patients with balloon inflation in right coronary artery developed ST segment elevation in lead CM5. Thus lead CM5 is a reliable lead for detecting subendocardial ischaemia experienced during everyday activities in anginal patients. During total occlusion of coronary arteries (as in variant angina or myocardial infarction) lead CM5 commonly shows ST segment depression and changes due to right coronary artery occlusion may not be detected.     

不稳定型心绞痛并发的室性心动过速及介入治疗对其的影响

目的探讨不稳定型心绞痛并发的室性心动过速(简称室速)特点以及经皮冠状动脉(简称冠脉)介入治疗对其的影响。方法对10例不稳定型心绞痛患者并发的室速,通过心电图观察室速发生前ST段的变化。行冠脉造影及介入治疗,了解室速特点与冠脉病变的关系。通过临床随访包括动态心电图观察室速发作情况。结果6例变异型心绞痛患者并发的室速在冠脉闭塞期出现,均为单一前降支病变;4例混合型心绞痛患者并发的室速,2例出现在ST段压低最深时,另2例则出现ST段逐渐变浅时,均为多支冠脉病变。10例均成功地接受了介入治疗。在10个月至4.1年的随访过程中,10例均未出现室速和临床再狭窄。结论不稳定型心绞痛并发的室速可能是缺血及再灌注损伤引起,ST段下移所致室速的患者冠脉病变可能更为复杂、严重。介入治疗可控制这类室速的发作。     

Value of the bipolar lead CM5 in electrocardiography.

Only bipolar lead recording are available during ambulatory monitoring. Their sensitivity in detecting ST segment changes in relation to standard electrocardiographic leads is not known. The magnitude and direction of ST segment changes in the bipolar lead CM5 were compared with those in standard electrocardiographic leads in patients during exercise testing and percutaneous transluminal coronary angioplasty. Thirty patients with coronary artery disease were studied during exercise tests in which ST segment depression (greater than 0.5 mm) occurred in one or more standard electrocardiographic leads and 13 patients were studied during angioplasty that resulted in ST segment change in one or more leads (I, II, III, V2, V5, and CM5). Lead CM5 was the most sensitive lead (93%) during exercise testing and also showed the greatest magnitude of ST segment change below the isoelectric line in 93% of the patients. Only two patients, one with ST segment elevation in inferior leads and one with changes restricted to septal leads, had no ST segment depression in lead CM5. When ST segment shift from the baseline electrocardiogram was measured the magnitude of depression was greatest in lead CM5 in only 63% of the patients. During angioplasty of the left anterior descending coronary artery, lead CM5 showed ST segment depression in seven patients, ST segment elevation in two, and a biphasic response in one. Two of the three patients with balloon inflation in right coronary artery developed ST segment elevation in lead CM5. Thus lead CM5 is a reliable lead for detecting subendocardial ischaemia experienced during everyday activities in anginal patients. During total occlusion of coronary arteries (as in variant angina or myocardial infarction) lead CM5 commonly shows ST segment depression and changes due to right coronary artery occlusion may not be detected.     

‘Action potential-like’ ST elevation following pseudo-Wellens' electrocardiogram

Coronary artery vasospasm is an important cause of chest pain syndromes that can lead to myocardial infarction, ventricular arrhythmias, and sudden death. In 1959, Prinzmetal et al described a syndrome of nonexertional chest pain with ST-segment elevation on electrocardiography. Persistent angina is challenging, and repeated coronary angioplasty may be required in this syndrome. Calcium antagonists are extremely effective in treating and preventing coronary spasm, and may provide long-lasting relief for the patient. Whereas the Wellens'' syndrome is characterized by symmetrically inverted T-waves with preserved R waves in the precordial leads suggestive of impending myocardial infarction due to a critical proximal left anterior descending stenosis, the pseudo-Wellens'' syndrome caused by coronary artery spasm has also rarely been reported in literature. We present a pseudo-Wellens syndrome as a cause of vasospastic angina, and a diffuse ST segment elavation on electrocardiogram resembling the Greek letter lambda, called also ''action potential-like'' ECG in a patient with vasospastic-type Printzmetal angina.