Myocardial infarction-related arrhythmia after rehabilitation treatment in a sanatorium]

The study involved 100 patients (80 men and 20 women), aged between 27 and 69 years treated at the Department of Cardiology, Medical Academy in Lublin for the first myocardial infarction, and classified for a 4-week rehabilitation in sanatorium. A 24-hours ECG recording with Holter technique (Medilog 3000 manufactured by Oxford Medilog Timed) was performed twice. In the first record cardiac arrhythmias ( extrasystole both supra- and ventricular, ventricular tachycardia) were more frequent in comparison with the results of the second recording carried out after a 4-week rehabilitation.     

Sex differences to myocardial ischemia and beta-adrenergic receptor blockade in conscious rats

We recently documented sex differences in the susceptibility to reperfusion-induced sustained ventricular tachycardia and beta-adrenergic receptor blockade in conscious rats. However, the effect of sex on ischemia-induced ventricular arrhythmias and beta-adrenergic receptor blockade is under-investigated. Therefore, we tested the hypothesis that gonadal hormones influence the ventricular arrhythmia threshold (VAT) induced by coronary artery occlusion as well as the response to beta-adrenergic receptor blockade. The VAT was defined as the time from coronary occlusion to sustained ventricular tachycardia resulting in a reduction in arterial pressure. Male and female intact and gonadectomized (GnX) rats were instrumented with a radiotelemetry device for recording arterial pressure, temperature, and ECG, as well as a Doppler ultrasonic flow probe to measure cardiac output and a snare around the left main coronary artery. The VAT was determined in conscious rats by pulling on the snare. The VAT was significantly longer in intact females (5.56 +/- 0.19) vs. intact males (4.31 +/- 0.14 min). This sex difference was abolished by GnX. Specifically, GnX decreased the VAT in females (4.55 +/- 0.22) and increased the VAT in males (5.14 +/- 0.30 min). Thus male sex hormones increase and female sex hormones decrease the susceptibility to ischemia-induced sustained ventricular tachycardia. beta-Adrenergic receptor blockade increased the VAT in intact males and GnX females only. Thus gonadal hormones influence the response to beta-adrenergic receptor blockade. Uncovering major differences between males and females in the pathophysiology of the cardiovascular system may result in sex-specific optimization of patient treatments.     

Study of cardiac arrhythmias and other forms of conduction abnormality in newborn infants.

In an unselected population of 2030 newborn infants studied by electrocardiography (ECG) between April 1975 and April 1977, 35 were found to have arrhythmias or other cardiac conduction abnormalities. Further investigation by means of 24-hour ECG monitoring showed that apparently serious tachyarrhythmias, such as ventricular tachycardia and slow heart rates associated with sinoatrial block, may be present without clinical disturbance in some newborn babies. Six infants had both bradycardia and tachycardia in the 24-hour recording, although the screening ECG had shown only one of these abnormalities. The alarming ECG appearance of some of the arrhythmias suggested a possible aetiological link with some unexplained sudden infant deaths: a multicentre study could determine this more readily and is therefore recommended.     

Confounding factors leading to misdiagnosing ventricular tachycardia as supraventricular in the emergency room

Studies conducted during the last 50 years have proposed electrocardiographic criteria and algorithms to determine if a wide QRS tachycardia is ventricular or supraventricular in origin. Sustained ventricular tachycardia is an uncommon reason for consultation in the emergency room. The latter and the complexity of available electrocardiographic diagnostic criteria and algorithms result in frequent misdiagnoses. Good hemodynamic tolerance of tachycardia in the supine position does not exclude its ventricular origin. Although rare, ventricular tachycardia in patients with and without structural heart disease may show a QRS duration <120 ms. Interruption of tachycardia by coughing, carotid sinus massage, Valsalva maneuver, or following the infusion of adenosine or verapamil should not discard the ventricular origin of the arrhythmia. In patients with regular, uniform, sustained broad QRS tachycardia, the presence of structural heart disease or A-V dissociation strongly suggest its ventricular origin. Occasionally, ventricular tachycardia can present with AV dissociation without this being evident on the 12-lead ECG. Cardiac auscultation, examination of the jugular venous pulse, and arterial pulse palpation provide additional clues for identifying A-V dissociation during tachycardia. This paper does not review the electrocardiographic criteria for categorizing tachycardia as ventricular but rather why emergency physicians misdiagnose these patients.     

Every face tells a story-unravelling a case of bidirectional ventricular tachycardia

Bidirectional ventricular tachycardia is a rare form of tachycardia. We hereby report a case of bidirectional ventricular tachycardia in an 8-year-old boy wherein careful clinical exami-nation led to the diagnosis of Andersen Tawil syndrome. The case also demonstrates the efficacy of flecainide in managing bidirectional ventricular tachycardia in the setting of Andersen Tawil syndrome.     

Coexistence of atrioventricular nodal reentrant tachycardia and idiopathic left ventricular outflow-tract tachycardia

Double tachycardia is a relatively rare condition. We describe a 21 year old woman with history of frequent palpitations. In one of these episodes, she had wide complex tachycardia with right bundle branch and inferior axis morphology. A typical atrioventricular nodal tachycardia was induced during electrophysiologic study, aimed at induction of clinically documented tachycardia. Initially no ventricular tachycardia was inducible. After successful ablation of slow pathway, a wide complex tachycardia was induced by programmed stimulation from right ventricular outflow tract. Mapping localized the focus of tachycardia in left ventricular outflow tract and successfully ablated via retrograde aortic approach. During 7 month's follow-up, she has been symptom free with no recurrence. This work describes successful ablation of rare combination of typical atrioventricular nodal tachycardia and left ventricular outflow tract tachycardia in the same patient during one session.     

兔右室流出道室速对L型钙通道α1c蛋白表达的影响

目的：通过建立右室流出道室速（RVOT-VT）的动物模型,以L型钙通道α1c蛋白作为观察指标,观察RVOT-VT时对L型钙通道α1c蛋白表达的影响,旨在探讨L型钙通道在RVOT-VT中的作用。方法：健康新西兰大耳白兔30只,随机分三组,分别为对照组（10只）、室速组（10只）、室速加维拉帕米干预组（10只）。采用免疫组织化学的方法对三组实验动物的右室流出道心肌组织进行L型钙通道cdc蛋白表达的检测。结果：1、高频刺激主动脉与肺动脉交界处均诱发了起源于右室流出道部位的室速,且室速持续时间均大于4小时。2、室速组L型钙通道α1c蛋白表达量明显下降;干预组L型钙通道α1cc蛋白的表达下降,但与对照组比较无显著差异。结论：1、室速组的心肌L型钙通道α1c蛋白表达发生了重构。2、维拉帕米可以改善心肌L型钙通道α1c蛋白的重构。3、L型钙通道在RVOT-VT发生、持续中起重要作用。     

Brugada ECG Pattern Unmasked by IV Flecainide in an Individual with Idiopathic Fascicular Ventricular Tachycardia

A 45-year old man presents with stable monomorphic ventricular tachycardia. He had previously been diagnosed with idiopathic fascicular ventricular tachycardia. Intravenous flecainide results in termination of his tachycardia but unmasks a latent type 1 Brugada ECG pattern not seen on his resting ECG. We discuss his subsequent management and the need to consider an alternative diagnosis in individuals with a Brugada type ECG pattern who present with stable monomorphic ventricular tachycardia.     

Ventricular tachycardia due to cardiac ischaemia: assessment by exercise electrocardiography

Although ventricular tachycardia is a well-known complication of myocardial ischaemia and may be provoked by exercise, many patients may appreciate only the angina and be unaware of the unduly rapid heart rate that precipitates it. Exercise testing is needed to show this arrhythmia and to enable treatment to be started.Twenty-three patients were found to have chronic ischaemic heart disease complicated by ventricular tachycardia. Six patients with old myocardial infarction had ventricular tachycardia at rest which required conversion to sinus rhythm; 17 patients developed ventricular tachycardia only when they exercised. In 12 of these 17 patients coronary angiography showed disease of the anterior descending branch of the left coronary artery; other vessels were usually also affected. Although beta-adrenergic blocking drugs increased exercise tolerance, ventricular tachycardia still occurred when the heart rate on exercise reached a level similar to that before treatment. In five patients coronary artery bypass surgery was performed because of angina and exercise-induced ventricular tachycardia. Exercise tolerance was increased in all three patients who underwent exercise tests after operation, and in two of these patients, both of whom were known to have patent grafts, ventricular tachycardia was abolished.If part of the beneficial effect of coronary bypass surgery is preventing life-threatening ventricular arrhythmias it is essential to detect these, and ambulatory monitoring and stress testing have a complementary role.     

Premature Ventricular Contractions and Non-sustained Ventricular Tachycardia: Association with Sudden Cardiac Death,Risk Stratification,and Management Strategies

Premature ventricular contractions (PVCs) and non-sustained ventricular tachycardia (NSVT) are frequently encountered and a marker of electrocardiomyopathy. In some instances, they increase the risk for sustained ventricular tachycardia, ventricular fibrillation, and sudden cardiac death. While often associated with a primary cardiomyopathy, they have also been known to cause tachycardia-induced cardiomyopathy in patients without preceding structural heart disease. Medical therapy including beta-blockers and class III anti-arrhythmic agents can be effective while implantable cardiac defibrillators (ICD) are indicated in certain patients. Radiofrequency ablation (RFA) is the preferred, definitive treatment in those patients that improve with anti-arrhythmic therapy, have tachycardia-induced cardiomyopathy, or have certain subtypes of PVCs/NSVT. We present a review of PVCs and NSVT coupled with case presentations on RFA of fascicular ventricular tachycardia, left-ventricular outflow tract ventricular tachycardia, and Purkinje arrhythmia leading to polymorphic ventricular tachycardia.     

The effects of sympathetic denervation on spontaneous ventricular defibrillation in the rat.

Ventricular tachycardia or ventricular fibrillation was electrically induced in 38 normal rats (group 1) and 24 sympathetically denervated rats (6-hydroxydopamine) (group 2). The time for spontaneous reversion to sinus rhythm was measured during (1) control, (2) isoproterenol, and (3) the combination of isoproterenol and phenylephrine. The time for spontaneous reversion was the same in both groups in the three states. The reversion time was prolonged threefold by isoproterenol, and restored to control values when phenylephrine was added to the infusion of isoproterenol. The tachycardia duration and the refractory period were inversely related: log10 (tachycardia duration) = 3.466-0.091 (refractory period). Ventricular tachycardia/fibrillation induction was examined as follows: (i) Ventricular tachycardia/fibrillation was induced in 100% of normal rats (group 1), but only 42% of the denervated rats (group 2, p less than 0.001); (ii) during isoproterenol, ventricular tachycardia/fibrillation was induced in 100% of rats of both groups; and (iii) when phenylephrine was added to isoproterenol, ventricular tachycardia/fibrillation was induced in 100% of group 1 rats versus 82% of group 2 rats, (p = NS). These observations suggest (1) the induction of ventricular tachycardia/fibrillation is highly dependent on intact sympathetic innervation, and (2) exogenous adrenergic agonists modulate the duration of ventricular fibrillation through their effects on ventricular refractory period, independent of sympathetic innervation.     

Ventricular arrhythmias.

Sudden cardiac death claims thousands of Canadians annually. Ventricular tachycardia and fibrillation account for up to 85% of these deaths. Identifying the patients at risk remains a major challenge. Those who have recurrent ventricular tachycardia or have been resuscitated from ventricular fibrillation are generally considered to be at highest risk. Although ventricular premature beats in the absence of previous ventricular tachycardia or fibrillation are not helpful in identifying such patients in most cases, they can indicate increased risk for sudden cardiac death in the presence of a structural cardiac abnormality, particularly recent myocardial infarction; however, the need for treatment in such cases is speculative and is being investigated. Treatment is mandatory for survivors of an episode of ventricular fibrillation and those with recurrent sustained ventricular tachycardia or torsade de pointes ventricular tachycardia. The approach to management is either invasive or noninvasive. Selection of an antiarrhythmic agent is facilitated by knowledge of some basic electrophysiologic features of the heart and of the classification of antiarrhythmic drugs. However, drug therapy has to be individualized on the basis of efficacy, left ventricular function and adverse effects or potential adverse effects of the drug. Amiodarone therapy or nonpharmacologic therapy should be considered if a suitable antiarrhythmic agent cannot be found.     

Ambulatory electrocardiographic records in patients with transient cerebral attacks or palpitation.

Continuous electrocardiographic (ECG) records were made over 24 hours in 130 ambulant outpatients complaining of syncope, dizzy turns, or palpitation. In all these patients resting ECGs had failed to show significant dysrhythmias. Exercise testing was performed on 64 patients and also failed to reveal any dysrhythmias. Analysis of the tape recordings, however, showed appreciable dysrhythmias in 74% of the group. In most cases the dysrhythmias were complex mixtures of rapid supraventricular and ventricular rhythms. bouts of ventricular tachycardia were seen in seven patients, all of whom were women. Episodic complete heart block was seen in only two patients, but prolonged ventricular gaps (greater than 1-5 s), not associated with ectopic beats, were found in 26. No episodes of ventricular fibrillation were recorded. We conclude that many patients with vague symptoms suggestive of transient cerebral ischaemia or irregular heart action have significant and often dangerous dysrhythmias which can be diagnosed only by long-term recording of the ECG under fully ambulant conditions.     

Long-Standing Undiagnosed Sheehan Syndrome Presenting as Polymorphic and Monomorphic Ventricular Tachycardia: A Case Series of 2 Patients

ObjectiveTo describe 2 cases of Sheehan syndrome presenting with ventricular tachycardia.MethodsIn this case series, we present 2 cases of Sheehan syndrome presenting with ventricular tachycardia, which is an extremely rare complication of Sheehan syndrome. We review the literature for cases of panhypopituitarism presenting with ventricular tachycardia and also review the pathophysiologic mechanisms underlying development of ventricular tachycardia in these patients.ResultsTwo female patients presented with ventricular tachycardia. One patient had monomorphic and the other had polymorphic ventricular tachycardia. On further workup, both patients were found to have panhypopituitarism. Due to past history of postpartum hemorrhage, both patients were suspected of having Sheehan syndrome as the cause of panhypopituitarism. Electrocardiogram revealed prolonged QT interval. Both patients were started on hormone replacement therapy. Both patients responded well initially and were discharged home. One of the patients is alive and healthy at the time of this report. However, the other patient was readmitted with seizures a few days after discharge and unfortunately died of sudden cardiac arrest.ConclusionUntreated cases of Sheehan syndrome can present with fatal ventricular tachycardia. Hormone replacement in these patients can treat and prevent fatal arrhythmias. (Endocr Pract. 2014;20:e211-e214)     

Idiopathic Ventricular Tachycardia Arising From the Right Ventricular Apex

We present a rare case of idiopathic ventricular tachycardia arising from the right ventricular apex. The electrocardiographic and electrophysiological characteristics of this tachycardia are discussed.     

Effect of atrial dilatation on the tendency of atrial arrhythmias

The arrhythmogenic effect of atrial dilatation was studied by electrophysiological investigations carried out on 24 dogs. Atrial distension was evoked by increasing the pressure in the right atrium (12 to 14 mm Hg) or by the balloon dilatation of the left atrium. Programmed electrical stimulation of the heart was used for the electrophysiological investigations. In addition to the superficial ECG leads also atrial and ventricular epicardial electrograms were obtained for the ECG recording. Acute atrial dilatation led to shortening of the atrial refractory period, whereas neither impulse conduction of the heart, nor pacemaker activity of the sinus node exhibited any alteration. Atrial dilatation resulted in pathological atrial irritability, and early or frequent atrial stimulation caused atrial tachycardia of shorter (non sustained) or longer (sustained) duration. Repetitive atrial extrasystoles in response to early stimuli could also frequently be observed during atrial dilatation. The obtained results indicate that atrial dilatation is arrhythmogenic and may lead to the development of atrial tachycardia.     

Role of catheter ablation in arrhythmogenic right ventricular dysplasia

Arrhythmogenic right ventricular dysplasia/cardiomyopathy is a disorder characterized by frequent ventricular tachycardia originating from the right ventricle and fibro-fatty replacement of right ventricular myocardium. Though the disorder was originally described during surgical ablation of refractory ventricular tachycardia, catheter ablation of tachycardia is one of the options for patients not responding to anti arrhythmic agents. Direct current fulguration was used in the initial phase followed by radiofrequency catheter ablation. In the present day scenario, all patients with risk for sudden cardiac death should receive an implantable cardioverter defibrillator. Radiofrequency catheter ablation remarkably reduces the frequency of defibrillator therapies. Direct current fulguration can still be considered in cases when radiofrequency ablation fails, though it requires higher expertise, general anesthesia and carries a higher morbidity. Newer mapping techniques have helped in identification of the site of ablation. In general, the success rate of ablation in arrhythmogenic right ventricular dysplasia is less than in other forms of right ventricular tachycardias like right ventricular outflow tract tachycardia.     

Cardiomyopathy induced by incessant ventricular tachycardia originating in the vicinity of the His bundle

A 04-year-old boy was referred to our institution with severe, progressive heart failure of 4-months duration associated with a persistent wide QRS tachycardia with left bundle branch block and severe left ventricular dysfunction. Because of incessant wide QRS tachycardia refractory to antiarrhythmic drugs, he was referred for electrophysiological study. The ECG was suggestive of VT arising from the right ventricle near the His area. Electrophysiological study revealed that origin of tachycardia was septum of the right ventricle, near His bundle, however the procedure was not successful and an inadvertent complete atrioventricular conduction block occurred. The same ventricular tachycardia recurred. A second procedure was performed with a retrograd aortic approach to map the left side of the interventricular septum. The earliest endocardial site for ablation was localized in the anterobasal region of left ventricle near His bundle. In this location, one radiofrequency pulse interrupted VT and rendered it not inducible. The echocardiographic evaluation showed partial reversal of left ventricular function in the first 3 months. The diagnosis was idiopathic parahisian left ventricular tachycardia leading to a tachycardia mediated cardiomyopathy, an extremely rare clinical picture in children.     

Ischemic Ventricular Tachycardia Presenting as a Narrow Complex Tachycardia

This report describes a patient presenting with a narrow complex tachycardia in the context of prior myocardial infarction and impaired ventricular function. Electrophysiological studies confirmed ventricular tachycardia and activation and entrainment mapping demonstrated a critical isthmus within an area of scar involving the His-Purkinje system accounting for the narrow QRS morphology. This very rare case shares some similarities with upper septal ventricular tachycardia seen in patients with structurally normal hearts, but to our knowledge has not been seen previously in patients with ischemic heart disease.     

Polymorphic Ventricular Tachycardia Due to Acute Coronary Ischemia: A Case Report

Acute myocardial ischemia can cause ventricular tachycardia (VT) in patients with structurally normal heart. Contrary to the fact that in patients with chronic myocardial scarring the ventricular tachycardia is monomorphic, in patients with acute ischemia the ventricular tachycardia is polymorphic and is reversible with coronary revascularization.We are reporting a 40 year old male who presented with recurrent syncope due to polymorphic ventricular tachycardia in the context of normal QT interval in baseline ECG and normal left ventricular function without any evidence of myocardial injury. Due to recurrent fatal ventricular arrhythmia despite medical management, urgent coronary angiography was done which showed critical obstruction of right coronary artery (RCA). Considering the critical obstruction of RCA responsible for polymorphic VT, emergency PCI of RCA was done. After successful PTCA and stenting to RCA, he had another episode of polymorphic VT which was terminated with intravenous phenytoin. Seven days after the PCI, 24 hours Holter monitoring was done which showed normal sinus rhythm with infrequent ventricular premature complexes and no evidence of VT. He was asymptomatic at six months follow-up.