Intravenous administration of class I antiarrhythmic drugs induced T wave alternans in a patient with Brugada syndrome

A 71-year-old man who experienced aborted sudden death was referred to our hospital. Coronary artery disease and cerebral accident were ruled out by conventional tests. The 12-lead ECG obtained at rest showed a right bundle branch block pattern and ST segment elevation in leads V1 to V3. Double ventricular extrastimuli at coupling intervals >180 msec induced ventricular fibrillation (VF) twice during electrophysiologic study. Intravenous administration of procainamide accentuated ST segment elevation in leads V1 to V3, and visible T wave alternans was induced in leads V2 and V3 at a dose of 450 mg. Initiation of T wave alternans was not associated with changes of the cardiac cycle or development of premature beats. When procainamide infusion was discontinued, T wave alternans disappeared before the elevated ST segment returned to the control level. Pilsicainide also accentuated ST segment elevation and induced similar T wave alternans in leads V2 and V3. Class I antiarrhythmic drug-related T wave alternans has been reported rarely in Brugada syndrome, but it may represent enhanced arrhythmogenicity of VF. We need to monitor closely and study the clinical implications of T wave alternans in Brugada syndrome.     

Spontaneous T wave alternans and premature ventricular contractions during febrile illness in a patient with Brugada syndrome

A 69-year-old man who had experienced syncope and ventricular fibrillation was referred to our hospital. ECG showed a right bundle branch block pattern with ST segment elevation in the right precordial leads. When the patient presented to the hospital with febrile illness, spontaneous T wave alternans and premature ventricular contractions were observed. When the patient became afebrile, ST segment elevation improved, and T wave alternans and premature ventricular contractions disappeared.     

心电图对非ST段抬高型急性冠脉综合征危险分层的价值

目的探讨心电图变化对非ST段抬高型急性冠状动脉综合征患者危险分层的价值。方法自2006年1月-2007年7月，在我院因急性胸痛拟诊不稳定型心绞痛及非ST段抬高心肌梗死而收入住院且记录资料完整的616例患者。人院后采集病史、查体，并在10min内完成常规18导联心电图检查，将患者人院时心电图的改变分为ST段压低组（包括伴有T波倒置者）、单纯T波倒置组、尚不能诊断的心电图组及正常心电图组；又将ST段压低组分为：胸前导联（V4-V6）ST段压低合并负向T波、胸前导联ST段压低合并正向T波、其他导联ST段压低合并正向T波、其他导联ST段压低合并负向T波4组。观察各组住院期主要心血管事件（心脏性死亡、非致命性心肌梗死、反复缺血性心绞痛发作），并随访1-12（7．2±3．8）个月，观察主要心血管事件变化。结果与正常心电图组比较；ST段压低组的复合心血管事件明显增多。胸前导联ST段压低合并T波倒置组的患者较其他导联ST段压低合并或不合并T波倒置组的复合心血管事件明显增多。结论．心电图的ST段变化对非ST段抬高型急性冠状动脉综合征患者的危险分层及心血管事件预测均有重要价值。     

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)     

Giant R wave, convex ST-segment elevation, and negative T wave during exercise treadmill test

The giant R wave syndrome is characterized by giant R wave accompanied by widening of the QRS complex, marked ST segment elevation, QRS axis deviation, and the formation of monophasic QRS-ST complex with obliteration of S wave in leads facing the ischemic zone. This report describes a 65-year-old-man with variant angina who had a transient giant R wave syndrome during an exercise treadmill test. Initially, at peak exercise, there was a convex ST segment elevation ending in a negative T wave in the same (inferior) leads which showed giant R waves. Later, in the recovery period and coinciding with an amelioration of myocardial ischemia, there was a less marked increase of R wave amplitude associated with concave ST segment elevation and positive T wave in the inferolateral leads. Subsequently, a ST segment depression in the inferolateral leads preceded the ECG normalization. The patient had also a concave ST segment elevation and positive T wave in inferolateral leads during a spontaneous episode of variant angina at rest. An emergency coronary arteriography showed a dominant right coronary artery with an 80% and a 75% diameter stenosis of the middle and distal segment, respectively; the other arteries and left ventriculogram were normal. The underlying mechanisms of the different shapes of ST segment elevation and T waveform in the setting of acute transmural myocardial ischemia are discussed.     

Atypical behavior of QTc and ST-T intervals in a patient with the Brugada syndrome

We present a 56-year-old man who was admitted to an emergency service after receiving an electric shock. The ECG showed a J point and ST segment elevation of up to 5 mm in leads V1 to V3, which normalized in 24 hours. The ajmaline test caused elevation of the J point and of the ST segment up to 12 mm in leads V1 to V3, QTc lengthening, and QTc and T wave alternans. These results denoted alterations in the duration of myocardial action potentials, a common finding in patients with Brugada syndrome and long QT syndrome.     

Spontaneous T wave alternans in a patient with Brugada syndrome--responses to intravenous administration of class I antiarrhythmic drug, glucose tolerance test, and atrial pacing

Spontaneous T wave alternans in Brugada syndrome. A 43-year-old man with an episode of syncope showed ECG patterns of coved-type ST elevation in leads V1-V3 and right bundle branch block pattern. The patient had spontaneous T wave alternans at baseline, and T wave alternans diminished with distinct development of ST elevation after administration of Na+ channel blocker, and during oral glucose load and atrial pacing. Na+ channel mutation may contribute to the genesis of his ECG changes.     

Unusual ST-t changes in Ebstein's anomaly with occlusion of a nondominant coronary artery

We present a case report of a patient of Ebstein's anomaly presenting with unusual ECG changes during acute coronary syndrome. The patient had undergone radiofrequency ablation of right posteroseptal accessory pathway. Two years later, he presented with acute chest pain. His ECG revealed ST elevation of 6-7 mm in leads III, aVF. V3R and V1-V4 with atrioventricular dissociation. He was thrombolysed for the same. He subsequently underwent an angiogram for continuing angina. His angiogram showed a nondominant right coronary artery with a 95% stenosis. The left circumflex artery was dominant but without any stenosis. The left anterior descending artery was also normal. Angiogplasty and stenting were done for the right coronary artery lesion and the patient did well on follow-up. The ST segment elevation in the anterior precordial leads resulting from occlusion of a nondominant right coronary artery is unusual. The possible reason for this is the isolated right ventricular infarction in the absence of any left ventricular infarction. Thus the electrical current of injury resulting from the right ventricular infarction was unopposed by any counterbalancing current of injury from the inferior surface of the left ventricle.     

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.     

Vasospastic angina accompanied by Brugada-type electrocardiographic abnormalities

Brugada Syndrome and Vasospastic Angina. We present two patients with vasospastic angina and Brugada-type ECG abnormalities. The first patient complained of chest pain, and transient ST segment elevation was confirmed on ECG. Coronary angiogram showed no organic stenosis. The second patient had syncopal episodes following anginal chest pain, and the same symptoms were reproduced by intracoronary acetylcholine injection that induced vasospasm. In both patients, ECG at rest showed ST segment elevation in leads V1 and V2 and a right bundle branch block pattern that were accentuated by a Class I antiarrhythmic drug. Ventricular fibrillation also was induced by programmed electrical stimulation. Susceptibility to ventricular fibrillation can be modulated by the interaction of coronary vasospasm with Brugada syndrome or vice versa; therefore, it is important to study the clinical implications of the coexistence of the two diseases in such patients.     

Electrocardiographic alterations in leads V1 to V3 in the diagnosis of right and left ventricular infarction

As Q wave and ST segment elevation in leads V1 to V3 may be due either to right ventricular infarction (RVI) or to anterior left ventricular infarction (ALVI), 72 autopsy patients with acute myocardial infarction who had had conventional 12-lead ECG records were studied to determine the accuracy of these ECG criteria, both for the diagnosis of RVI (29 patients, group A) and of ALVI (43 patients, group B). The accuracy of three ECG criteria (Q wave, ST segment elevation greater than or equal to 0.05 mV, and ST segment elevation greater than or equal to 0.1 mV) in diagnosing group A and group B patients was determined in each precordial lead (V1, V2, and V3) and the three criteria were found to be significantly more accurate in diagnosing group B than group A patients. In conclusion, although Q wave and ST segment elevation in leads V1, V2, and V3 may be present in some cases of RVI, their accuracy is too low to be considered useful diagnostic criteria in these patients.     

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.     

The effect of coronary vasospasm on the direction of ST-segment deviation in patients with both hypertrophic cardiomyopathy and vasospastic angina

BACKGROUND: There has been no report of ECG changes during anginal attacks in patients with coexistent hypertrophic cardiomyopathy (HCM) and vasospastic angina. STUDY OBJECTIVES: To elucidate the change in ST-segment during anginal attacks in patients with coexistent HCM and vasospastic angina (the HCM group) in comparison with that of patients with vasospastic angina and no left ventricular hypertrophy (the non-HCM group). DESIGN: Retrospective study. PATIENTS: Twelve patients in the HCM group, and 28 patients in the non-HCM group. MEASUREMENTS: The direction of ST segment shift, either ST-segment elevation or depression, on the ECGs recorded during vasospastic anginal attacks with severe vasoconstriction in the epicardial coronary artery after intracoronary injection of acetylcholine. RESULTS: Age, male gender, and distribution of coronary arteries in which the vasospasm occurred were similar between the two groups. Collateral circulation to the affected arteries was absent in all the study patients. The prevalence of anginal attacks associated with ST-segment elevation was 2.7 times higher in the non-HCM group than in the HCM group (51. 5% [17 of 33 attacks] vs 18.8% [3 of 16 attacks], respectively; p = 0.03). CONCLUSIONS: In the HCM group, myocardial ischemia associated with a transmural injury pattern seen on the ECG, which is represented as ST-segment elevation, seldom develops during vasospastic anginal attacks because of marked left ventricular hypertrophy.     

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.     

Polymorphic ventricular tachycardia in patients with vasospastic angina--clinical and electrocardiographic characteristics and long-term outcome.

There have been few clinical studies exploring the characteristics of spontaneous polymorphic ventricular tachycardia (VT) during a vasospastic angina attack. During a 4-year recruitment period, Holter ECG recordings were monitored for 42+/-24 h during a drug-free period in 60 consecutive patients with vasospastic angina (VSA) and of these, 8 patients had at least one episode of polymorphic VT during monitoring. Ischemic ST segment elevation was immediately preceded the spontaneous polymorphic VT in all 8 patients, 4 of whom had silent coronary vasospasm. Immediately before the onset of polymorphic VT, both R-on-T and long-short sequences were observed in 4 of the 8 patients and ST wave alternans were recorded in 2 patients. VT exhibited a pattern of torsade de pointes in 4 of the 8 patients. Five patients underwent electrophysiologic testing during a drug-free asymptomatic phase, and polymorphic VT was induced in 2 of the 5 patients, with one developing ventricular fibrillation. During a follow-up period of 73+/-17 months, there was a significant difference in the incidence of sudden death between patients with and without VT (2/8 cases [25%] vs 0/52 [0%]; p<0.01). Thus, vasospastic attacks, even if asymptomatic, that immediately precede the development of polymorphic VT may be associated with a repolarization abnormality and an increased risk of sudden death.     

Recurrence of Prinzmetal angina seven years following aortocoronary bypass surgery: a clinical and angiographic follow-up.

A patient with Prinzmetal angina and ST segment elevation in the anterior ECG leads became asymptomatic after a 50% left anterior descending coronary artery stenosis was bypassed. However, seven years later Prinzmetal angina recurred but with ST segment elevation in the inferior ECG leads. Although the coronary bypass graft had remained patent, the proximal and distal left anterior descending coronary artery was occluded. No significant stenosis was present in the right coronary artery. Perhexiline maleate controlled his symptoms but when the drug was stopped because of side effects an acute inferior myocardial infarction occurred.     

Recurrence of prinzmetal angina seven years following aortocoronary bypass surgery: A clinical and angiographic follow-up

A patient with Prinzmetal angina and ST segment elevation in the anterior ECG leads became asymptomatic after a 50% left anterior descending coronary artery stenosis was bypassed. However, seven years later Prinzmetal angina recurred but with ST segment elevation in the inferior ECG leads. Although the coronary bypass graft had remained patent, the proximal and distal left anterior descending coronary artery was occluded. No significant stenosis was present in the right coronary artery. Perhexiline maleate controlled his symptoms but when the drug was stopped because of side effects an acute inferior myocardial infarction occurred.     

Marked alternans of the elevated ST segment during occlusion of the left anterior descending coronary artery in percutaneous transluminal coronary angioplasty: clinical background and electrocardiographic features.

To investigate the clinical background and the electrocardiographic features of marked alternans of the elevated ST segment during coronary angioplasty, we examined 12-lead electrocardiograms recorded continuously during occlusion of the left anterior descending coronary artery by balloon inflation in 41 patients. The incidence of marked ST alternans was 27% of 41 patients and 15% of 117 balloon occlusions. The incidence decreased progressively from the first to the third occlusion. The time course of ST alternans was determined. Compared with patients without ST alternans, patients with ST alternans had a shorter history of angina, less severe stenosis of the target lesion before coronary angioplasty, more leads showing ST elevation during occlusion, higher ST elevation during occlusion and lower incidence of previous myocardial infarction in the left anterior descending coronary arterial area. ST alternans recorded on the surface electrocardiogram may thus be considered a marker of acute severe and extensive myocardial ischemia.     

Wellens' syndrome and other electrocardiographic changes in a patient with a left anterior descending artery subocclusion associated with a left main coronary artery subocclusion

Changing axis deviation has been reported also during atrial fibrillation or atrial flutter. Changing axis deviation has been also reported during acute myocardial infarction associated with atrial fibrillation too or at the end of atrial fibrillation during acute myocardial infarction. Patients with unstable angina have a higher incidence of left main coronary artery (LMCA) and proximal left anterior descending (LAD) coronary artery disease compared to patients with stable angina pectoris. In 1982, Wellens and colleagues described two electrocardiographic patterns that were predictive of critical narrowing of the proximal LAD artery, and were subsequently termed Wellens' syndrome. The criteria were: a) prior history of chest pain, b) little or no cardiac enzyme elevation, c) no pathologic precordial ST segment elevation, d) no loss of precordial R waves, and e) biphasic T waves in leads V2 and V3, or asymmetric, often deeply inverted T waves in leads V2 and V3. The ECG changes are best recognized outside the episode of anginal pain. Lead aVR and lead v1 ST segment elevation, during chest pain, has been reported in patients with LMCA disease with ST segment depression in leads V3, V4 and V5 (with maximal depression in V4).We present a case of changing axis deviation in a 37-year-old Italian man with a LAD coronary artery subocclusion associated with a LMCA subocclusion. This case focuses attention on the importance of the recognition of the patterns suspected for LAD coronary artery disease or for LMCA disease.     

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.