Cocaine-induced pseudo-Wellens' syndrome: a Wellens' phenocopy.

Wellens' syndrome represents critical occlusion of the proximal left anterior descending coronary artery. Electrocardiographic changes similar to Wellens' wave are not exceptional to acute coronary occlusion and can also be seen in cardiac and non-cardiac conditions, such as left ventricular hypertrophy, persistent juvenile T wave, bundle branch blocks, cerebral haemorrhage, pulmonary oedema, pulmonary embolism, pheochromocytoma, Takotsubo syndrome, digitalis and cocaine-induced coronary vasospasm. Cocaine-induced pseudo-Wellens' syndrome should be considered as one of the differentials, since cocaine is used frequently by young adults and can cause left anterior descending coronary vasospasm mimicking Wellens' syndrome. Initiation of the beta-blocking agent in pseudo-Wellens' syndrome as a part of acute coronary syndrome management can be disastrous. We illustrated a case of cocaine-induced pseudo-Wellens' syndrome presented with typical chest pain associated with Wellenoid ECG.

Verapamil-sensitive idiopathic left ventricular tachycardia in a 6-month-old: unique considerations in diagnosis and management in an infant.

Idiopathic left ventricular tachycardia of the Belhassen type is rare in infants. We present a 6-month-old infant girl with a wide-complex tachycardia with right bundle branch block QRS morphology, a superior axis, and atrioventricular dissociation, consistent with a left anterior fascicular tachycardia. Initial echocardiogram revealed depressed ventricular function. The tachycardia was unresponsive to therapeutic trials of adenosine, esmolol, procainamide, and lidocaine. There was brief conversion of the tachycardia to sinus rhythm with transesophageal atrial overdrive pacing, suggesting a reentrant mechanism of the arrhythmia. Ultimately, the judicious administration of intravenous verapamil resulted in termination of the arrhythmia, which has been sustained on oral therapy.

[Cannabis and acute coronary syndrome with ST segment elevation]. / Cannabis et syndromes coronariens aigus avec sus-décalage de ST.

Cannabis is the most common substance of drug abuse in the world and has euphoric and hallucinogenic effects. Its cardiovascular effects are well-known. However, there is limited information concerning cannabis-induced acute coronary syndrome and the exact contribution of cannabis smoking to coronary artery disease. We report and discuss a case of ST-Elevation acute coronary syndrome occurring in a young patient aged 24 years, who was a heavy cannabis smoker.

Sodium channel blockade with QRS widening after an escitalopram overdose.

INTRODUCTION: Escitalopram is rarely associated with prolongation of the QTc interval; however, there are no reported cases of QRS complex widening associated with escitalopram overdose. We report a case of a patient who presented with both QRS complex widening and QTc interval prolongation after an escitalopram overdose. CASE: A 16-year-old girl presented to the emergency department after ingestion of escitalopram, tramadol/acetaminophen, and hydrocodone/acetaminophen. Laboratory results were significant for 4-hour acetaminophen 21.1 µg/mL. Serum electrolytes including potassium, magnesium, and calcium were all normal. Initial electrocardiogram (ECG) revealed a widened QRS with an incomplete right bundle branch pattern. After administration of 100-mEq sodium bicarbonate, a repeat ECG revealed narrowing of the QRS complex and a prolonged QTc interval. Magnesium sulfate 2 g intravenous and sodium bicarbonate drip were initiated. A repeat ECG, 1 hour after the second, revealed normalization of the QRS complex and QTc interval. DISCUSSION: Prolongation of the QTc interval is an expected effect of escitalopram. Both escitalopram and citalopram are metabolized to the cardiotoxic metabolite S-didesmethylcitalopram and didesmethylcitalopram, respectively, which have been implicated in numerous cardiac abnormalities including widening of the QRS complex. Although never previously described with escitalopram, this mechanism provides a reasonable explanation for the QRS complex widening and incomplete right bundle branch block that occurred in our patient. CONCLUSIONS: Both QRS complex widening and QTc interval prolongation should be monitored in cases of escitalopram and citalopram overdoses.

Arrhythmogenic effect of flecainide toxicity.

Flecainide is a class 1C antiarrhythmic drug especially used for the management of supraventricular arrhythmia. In overdose cases, flecainide can induce life treating ventricular arrhythmias and cardiogenic shock. We report the case of a 72-year-old woman admitted to our intensive care unit for a regular monomorphic wide complex tachycardia (QRS duration 240 ms, right bundle branch block and superior axis morphology) without apparent P waves. Clinical examination showed slight left congestive heart failure signs without cardiogenic shock. An intravenous bolus of 10 mg adenosine 5'-triphosphate (ATP) was ineffective to stop the tachycardia. The diagnosis of ventricular tachycardia induced by flecainide overdose was considered. 500 mL of intravenous 84‰ sodium bicarbonate was administrated. The patient's QRS narrowed immediately and 12-lead ECG showed sinus rhythm. Blood samples confirmed the flecainide overdose and the clinical status progressively improved.

Clinical spectrum of fascicular tachycardia.

AIMS: Ventricular tachycardia spreading from the anterior or posterior division of the left bundle branch is generally called fascicular tachycardia (FT). We will present our experience with FT, a type of ventricular tachycardia not necessarily implying the absence of heart disease and/or sensitivity to selective antiarrhythmic drugs, but only particular routes of left ventricular depolarization. METHODS: Since 1981 we have had the opportunity to study 10 cases of FT (nine men and one woman; aged 28-77 years, mean ±â€ŠSD 55 ±â€Š18.6 years) by means of echocardiography, coronary angiography (seven cases), endomyocardial biopsy (five cases), signal-averaged electrocardiogram (SAECG, nine patients), electrophysiological and electropharmacological evaluation. RESULTS: Seven patients had paroxystic, extrastimulus inducible FT that was sensitive to verapamil given intravenously (group A); three patients, on the other hand, showed repetitive or incessant FT, not modifiable by stimulation techniques and sensitive to class 1 antiarrhythmic drugs (group B). Patients presented histologic substrates ranging from the absence of heart disease to previous myocardial infarction or myocarditis. FT spontaneously disappeared within 2 years in group B, while frequently persisted in the long term in group A. CONCLUSIONS: FT is not a homogeneous group of ventricular tachycardia, as patients may differ according to clinical presentation, mechanisms that are involved in the genesis of the arrhythmia and natural history; the histologic substrate is highly variable, ranging from the total absence of heart disease to severe forms of myocardial involvement.

Acute left bundle branch block as a complication of brachytherapy for lung cancer.

Endoluminal brachytherapy for lung cancer ensures the delivery of a maximal therapeutic radiation dose to the tumor with a minimal effect on normal surrounding tissues. We report on a 62-year-old man, who acutely developed LBBB and heart failure 48 hours after the second course of combined endoluminal and external beam radiation therapy. After administration of angiotensin converting enzyme inhibitors, diuretics, and anti-inflammatory drugs, electrocardiographic changes resolved and patient completely recovered. Radiotherapy was reintroduced after ten days.

Ischemic etiology for adenosine-sensitive fascicular tachycardia.

Adenosine-responsive ventricular tachycardias (VTs) typically occur in patients without structural heart disease; and thus, its association with myocardial ischemia is rare. In this case report, we describe a patient who had demonstrable ischemia along the anterolateral wall of the left ventricle and who developed a VT that was clinically terminated with adenosine. Surface electrocardiogram demonstrated a monomorphic VT with a right bundle-branch block morphology and a rightward axis configuration, and electrophysiologic testing showed atrioventricular dissociation upon atrial pacing and retrograde His waves following induction of VT. These findings localized the patient's VT to the left anterior fascicle, an anatomical region that coincided with the patient's territory of ischemia. We describe the electrophysiologic testing involved in elucidating the patient's tachyarrhythmia, and we provide a brief discussion of the pathogenesis and clinical features of adenosine-sensitive VT. Our case demonstrates that heterogeneous mechanisms of VT are operative in patients with ischemic heart disease.

Gemcitabine-induced acute coronary syndrome: a case report.

OBJECTIVES: To report a case of metastatic leiomyosarcoma, in which a patient developed chest pain accompanied by acute left bundle-branch block (LBBB) after gemcitabine infusion. CLINICAL PRESENTATION AND INTERVENTION: A 59-year-old woman admitted with bilateral pulmonary nodules had classic risk factors for coronary heart disease and coronary stenosis as demonstrated by previous coronary angiography. She was treated with gemcitabine infusion, and 30 min later she experienced severe chest pain accompanied by acute LBBB confirmed by ECG. We suspected gemcitabine-induced coronary vasospasm exacerbated by the preexisting coronary artery disease as the cause of the acute coronary syndrome. The patient was subsequently treated with antianginal therapy and percutaneous coronary intervention. Her chest pain resolved and LBBB disappeared. She was discharged 2 days later without any further cardiac events. No additional cancer therapy was given and she died 5 months later, due to disease progression. CONCLUSION: This case showed that chemotherapeutic agents must be administered with intensive cardiac monitoring especially in patients with cardiac disease and well-known risk factors to prevent the development of cardiac complications, despite an agent not being known to be 'cardiotoxic'.

Serial reevaluation for ARVD/C is indicated in patients presenting with left bundle branch block ventricular tachycardia and minor ECG abnormalities.

INTRODUCTION: Diagnosis of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is based on a set of criteria proposed by the International Task Force (TF) for Cardiomyopathies in 1994. To fulfill these criteria, presence of both electrocardiographic and anatomical abnormalities must be assessed with ECG and imaging techniques, respectively. This may be difficult in patients with early/mild forms of the disease as detectable structural abnormalities may still be absent. We evaluated in which patients presenting with right ventricular tachycardia (VT) serial reevaluation for ARVD/C is indicated. METHODS AND RESULTS: Sixty consecutive patients (41 men, mean age 40+/-15 years) were evaluated by the TF criteria for possible ARVD/C because of presentation with a left bundle branch block (LBBB) VT, representing 1 minor criterion. The presence on the ECG of a T-wave inversion beyond lead V2 (1 minor), right precordial QRS prolongation (1 major), or an epsilon wave (1 major) was assessed together with the visualization of severe regional/global right ventricle dysfunction (1 major) or mild segmental dilatation/regional hypokinesia (1 minor) by standard imaging techniques. Initially, 22 (37%) patients were diagnosed as having ARVD/C. After 47+/-39 (range 6-146) months, 23 initially TF-negative patients were reevaluated because of recurrent symptoms, with 12 (52%) additional patients now meeting the TF criteria. Eleven of these 12 (92%) patients presented initially with ECG abnormalities only, but developed structural abnormalities on imaging at follow-up. CONCLUSION: ECG abnormalities may precede structural abnormalities warranting serial reevaluation for ARVD/C in initially TF-negative patients presenting with LBBB VT with only ECG abnormalities.

Successful use of quinidine in treatment of electrical storm in Brugada syndrome.

We report an adolescent with a malignant form of Brugada syndrome who presented with 15 episodes of ventricular fibrillation (VF) over 10 days, shortly after implantation of an implantable cardioverter defibrillator. Oral quinidine bisulphate at a dose of 1000 mg/day successfully suppressed the electrical storm and recurrence of VF over 18-month follow-up. It also normalized the ST-segment elevation in his right precordial leads, suppressed all ambient unifocal ventricular extrasystoles and induction of VF on programmed electrical stimulation. This case suggests that quinidine, by virtue of its blocking action on Ito, may be useful as adjunctive therapy in Brugada syndrome.

[Intermittent complete left bundle branch block during general anesthesia].

We report a case of intermittent complete left bundle branch block (CLBBB) which occurred during general anesthesia. An 83-year-old female was scheduled for upper lobectomy of the right lung under general anesthesia. Her preoperative 12-lead ECG showed atrial fibrillation and ST-depression in V4-6. Anesthesia was induced with propofol and pentazocine, and maintained with 0.5-1.5% isoflurane, 0-50% nitrous oxide in oxygen under close monitoring and appropriate respiratory management. The operation was performed uneventfully. Several minutes after the end of surgery, on converting her into the supine position from the left lateral decubitus position, widened QRS complexes, later diagnosed as CLBBB, appeared on ECG. At that time, heart rate was 92 beats x min(-1). After the administration of esmolol hydrochloride, heart rate decreased rapidly in a few minutes and ECG returned to normal conduction from CLBBB. We diagnosed this as rate-dependent intermittent CLBBB. Although intermittent CLBBB continued until the next day, the patient was asymptomatic and cardiac enzymes were within normal ranges. The intermittent CLBBB, which occasionally occurs during anesthesia, makes the diagnosis of myocardial ischemia and acute myocardial infarction difficult. The present case suggests that esmolol can be used effectively and safely to distinguish CLBBB as a benign disorder from myocardial ischemia in a patient with CLBBB.

Prenatal diagnosis and treatment of fetal long QT syndrome: a case report.

We report a case of a fetus presenting with bradycardia, intermittent atrioventricular (AV) block, ventricular tachycardia (VT) and the signs of fetal congestive heart failure (ascites and scrotal hydrocele) during mid-gestation. Prenatal treatment with beta-adrenergic blocker (propranolol) and digitalis glycosides was prescribed because of suspicion of long QT syndrome occurring with fetal congestive heart failure. The male baby was born at 39 weeks of gestation and showed a prolonged QT interval (QTc = 492 ms) and frequent variable AV block or alternating left and right bundle branch block, depending on the atrial rate. Prenatal administration of lidocaine failed to correct the fetal VT. Conversely, propranolol decreased the attack frequency of fetal VT. Postnatal administration of the K(+) channel opener (nicorandil) successfully shortened the QT interval and improved the outcome.

Long-term follow-up of individuals with the electrocardiographic pattern of right bundle-branch block and ST-segment elevation in precordial leads V1 to V3.

BACKGROUND: The electrocardiographic pattern of right bundle-branch block with ST-segment elevation in leads V1 to V3 is increasingly recognized among patients who have aborted sudden cardiac death, but also in asymptomatic individuals, raising questions about its prognostic significance. METHODS AND RESULTS: The clinical, electrophysiological, and follow-up data of 334 patients with the Brugada phenotype were analyzed. A total of 79 women and 255 men with a mean age at diagnosis of 42+/-16 years were studied. The abnormal ECG was recognized after a resuscitated cardiac arrest in 71 patients (group A), after a syncopal episode in 73 patients (group B), and in 190 asymptomatic individuals (group C). Sustained ventricular arrhythmias were inducible in 83%, 63%, and 33% of patients in group A, group B, and group C, respectively. During 54+/-54 and 26+/-36 months of follow-up, respectively, 62% of patients in group A and 19% of group B patients had a new arrhythmic event. Inducibility of ventricular arrhythmias was the only predictor of arrhythmia occurrence in both groups. During a mean follow-up of 27+/-29 months, 8% of group C individuals had a first arrhythmic event. In these individuals, inducibility of ventricular arrhythmias and a basal abnormal ECG were predictors of arrhythmia occurrence. CONCLUSIONS: An ECG showing right bundle-branch block and ST-segment elevation in the right precordial leads is a marker of malignant ventricular arrhythmias and sudden death. Recurrence of malignant arrhythmias is high after the occurrence of symptoms. Among asymptomatic individuals, those with a spontaneously abnormal ECG and inducible to ventricular arrhythmias have the poorer prognosis.

Ventricular arrhythmias with left bundle branch block pattern and inferior axis: assessment of their mechanisms on the basis of response to ATP, nicorandil and verapamil.

The present study investigated the mechanism of ventricular arrhythmias showing left bundle branch block (LBBB) pattern with an inferior axis. The effects of 3 drugs, adenosine triphosphate (ATP), nicorandil and verapamil, were evaluated in 17 patients. ATP suppressed the arrhythmias in 14 patients and nicorandil suppressed them in 8 of those 14. Verapamil suppressed 5 of the 6 ATP-nicorandil-sensitive arrhythmias. Four patients with ATP- or nicorandil-sensitive arrhythmias were not sensitive to verapamil. On the other hand, 3 of the ATP-insensitive arrhythmias were sensitive to neither nicorandil nor verapamil. The QT intervals and QTc were shortened by nicorandil in 5 of the 6 patients who were sensitive to all 3 drugs. One mechanism of suppression by nicorandil could be related to less Ca++ entering the myocardium, which would decrease the duration of the action potential as indicated by the shortened QT intervals. The results suggest that the mechanism of some ventricular arrhythmias is related to triggered activity. Arrhythmias that are sensitive to ATP or nicorandil, but not to verapamil, may be caused by abnormal automaticity. On the other hand, arrhythmias that are insensitive to all 3 drugs might be related to reentry. The features of ventricular arrhythmias with LBBB pattern and inferior axis differ and therefore the causative mechanisms are not the same.

Is the Brugada syndrome a distinct clinical entity?

In 1992, Brugada and Brugada described a syndrome characterized by right bundle branch block pattern with ST elevation in leads V1 through V3 and a history of sudden death due to polymorphic ventricular tachycardia or ventricular fibrillation. Since these patients had no evidence of cardiac disease, these findings were ascribed to a distinct clinical entity. Further experience has shown that this same pattern may be mimicked by patients with right ventricular dysplasia, acute ischemia of the right ventricle, other infiltrative cardiomyopathies, as well as tricyclic drug overdose. The pathogenesis of these changes may be due to loss of the dome configuration in the transmembrane potential of right ventricular epicardial cells, which would result in a voltage gradient producing ST elevation. Other explanations involve delayed conduction in a dysplastic right ventricle. The clinical importance of this syndrome is that it calls attention to patients at risk for sudden cardiac death. In addition, these observations have sparked the interest of basic electrophysiologists relative to the relationship of these ECG waveforms and malignant ventricular arrhythmias. Finally, the clinician must exclude other organic diseases before diagnosing this entity.