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Simple Summary: Our body's reaction to acute emotional stress differs, depending on several factors, which include a small molecule called endothelin. Excessive responses are important, as they can trigger (sometimes serious) heartbeat disturbances. To further investigate the role of endothelin in this process, we compared the reactions to laboratory-induced stress in two groups of rats, known to have diverse baseline levels of endothelin in the blood. We found distinct responses leading to slow heartbeat disturbances in the latter group. This feature resembles that observed in people with a tendency to faint after strong emotions, a common problem with many unknown aspects. Our study calls for further research on the effects of endothelin on fainting and irregular heartbeat after acute emotional stress. The ubiquitous peptide endothelin is currently under investigation as a modulatory factor of autonomic responses to acute emotional stress. Baseline plasma levels of endothelin alter blood pressure responses, but it remains unclear whether autonomic activity and arrhythmogenesis (i.e., brady- or tachyarrhythmias) are affected. We recorded sympathetic and vagal indices (derived from heart rate variability analysis), rhythm disturbances, voluntary motion, and systolic blood pressure after acute emotional stress in conscious rats with implanted telemetry devices. Two strains were compared, namely wild-type and ETB-deficient rats, the latter displaying elevated plasma endothelin. No differences in heart rate or blood pressure were evident, but sympathetic responses were blunted in ETB-deficient rats, contrasting prompt activation in wild-type rats. Vagal withdrawal was observed in both strains at the onset of stress, but vagal activity was subsequently restored in ETB-deficient rats, accompanied by low voluntary motion during recovery. Reflecting such distinct autonomic patterns, frequent premature ventricular contractions were recorded in wild-type rats, as opposed to sinus pauses in ETB-deficient rats. Thus, chronically elevated plasma endothelin levels blunt autonomic responses to acute emotional stress, resulting in vagal dominance and bradyarrhythmias. Our study provides further insights into the pathophysiology of stress-induced tachyarrhythmias and syncope. [ABSTRACT FROM AUTHOR]

Fetal dysrhythmias are common abnormalities, which can be categorized into three types: rhythm irregularities, tachyarrhythmias, and bradyarrhythmias. Fetal arrhythmias, especially in high-risk pregnancies, require special monitoring and treatment. The aim of this study was to assess the stillbirth and early and late neonatal mortality rates for pregnancies complicated by fetal dysrhythmias from one single tertiary referral center from 2000 to 2022. Of the 1018 fetuses with congenital heart disease, 157 (15.42%) were evaluated in this analysis. Seventy-four (46.7%) fetuses had bradyarrhythmias, 51 (32.5%) tachyarrhythmias, and 32 (20.4%) had rhythm irregularities. Additional structural heart defects were detected in 40 (25.3%) fetuses and extracardiac anomalies in 29 (18.4%) fetuses. Thirteen (8.2%) families opted for termination of the pregnancy. Eleven (7.6%), out of 144 continued pregnancies ended in spontaneous intrauterine fetal death (IUFD). Neonatal death was observed in nine cases (5.7%), whereas three (1.9%) died within the first 7 days of life. Although most intrauterine fetal deaths occurred in pregnancies with fetal bradyarrhythmia, neonatal death was observed more often in fetuses with tachyarrhythmia (8.5%). The presence of extracardiac anomalies, congenital heart disease (CHD), and Ro-antibodies are predictive factors for the occurrence of IUFD. Rhythm irregularities without any other risk factor do not present higher risks of adverse perinatal outcome. [ABSTRACT FROM AUTHOR]

The ubiquitous peptide endothelin is currently under investigation as a modulatory factor of autonomic responses to acute emotional stress. Baseline plasma levels of endothelin alter blood pressure responses, but it remains unclear whether autonomic activity and arrhythmogenesis (i.e., brady- or tachyarrhythmias) are affected. We recorded sympathetic and vagal indices (derived from heart rate variability analysis), rhythm disturbances, voluntary motion, and systolic blood pressure after acute emotional stress in conscious rats with implanted telemetry devices. Two strains were compared, namely wild-type and ETB-deficient rats, the latter displaying elevated plasma endothelin. No differences in heart rate or blood pressure were evident, but sympathetic responses were blunted in ETB-deficient rats, contrasting prompt activation in wild-type rats. Vagal withdrawal was observed in both strains at the onset of stress, but vagal activity was subsequently restored in ETB-deficient rats, accompanied by low voluntary motion during recovery. Reflecting such distinct autonomic patterns, frequent premature ventricular contractions were recorded in wild-type rats, as opposed to sinus pauses in ETB-deficient rats. Thus, chronically elevated plasma endothelin levels blunt autonomic responses to acute emotional stress, resulting in vagal dominance and bradyarrhythmias. Our study provides further insights into the pathophysiology of stress-induced tachyarrhythmias and syncope.

Fetal dysrhythmias are common abnormalities, which can be categorized into three types: rhythm irregularities, tachyarrhythmias, and bradyarrhythmias. Fetal arrhythmias, especially in high-risk pregnancies, require special monitoring and treatment. The aim of this study was to assess the stillbirth and early and late neonatal mortality rates for pregnancies complicated by fetal dysrhythmias from one single tertiary referral center from 2000 to 2022. Of the 1018 fetuses with congenital heart disease, 157 (15.42%) were evaluated in this analysis. Seventy-four (46.7%) fetuses had bradyarrhythmias, 51 (32.5%) tachyarrhythmias, and 32 (20.4%) had rhythm irregularities. Additional structural heart defects were detected in 40 (25.3%) fetuses and extracardiac anomalies in 29 (18.4%) fetuses. Thirteen (8.2%) families opted for termination of the pregnancy. Eleven (7.6%), out of 144 continued pregnancies ended in spontaneous intrauterine fetal death (IUFD). Neonatal death was observed in nine cases (5.7%), whereas three (1.9%) died within the first 7 days of life. Although most intrauterine fetal deaths occurred in pregnancies with fetal bradyarrhythmia, neonatal death was observed more often in fetuses with tachyarrhythmia (8.5%). The presence of extracardiac anomalies, congenital heart disease (CHD), and Ro-antibodies are predictive factors for the occurrence of IUFD. Rhythm irregularities without any other risk factor do not present higher risks of adverse perinatal outcome.

We report a case of unusual and unexplained cardiac death in an 18-years old female patient with congenital neurosensorial deafness. The fatal event was characterized by an initial syncopal episode, associated with a wide QRS tachycardia (around 110 bpm) but stable hemodynamic conditions. The patient, however, subsequently developed severe hypotension and progressive bradyarrhythmias until asystole and lack of cardiac response to resuscitation maneuvers and ventricular pacing. [ABSTRACT FROM AUTHOR]

The incidence of bradyarrhythmias in patients with acute coronary syndrome (ACS) is 0.3% to 18%. It is caused by sinus node dysfunction (SND), high-degree atrioventricular (AV) block, or bundle branch blocks. SND presents as sinus bradycardia or sinus arrest. First-degree AV block occurs in 4% to 13% of patients with ACS and is caused by rhythm disturbances in the atrium, AV node, bundle of His, or the Tawara system. First- or second-degree AV block is seen very frequently within 24 h of the beginning of ACS; these arrhythmias are frequently transient and usually disappear after 72 h. Third-degree AV blocks are also frequently transient in patients with infero-posterior myocardial infarction (MI) and permanent in anterior MI patients. Left anterior fascicular block occurs in 5% of ACS; left posterior fascicular block is observed less frequently (incidence < 0.5%). Complete bundle branch block is present in 10% to 15% of ACS patients; right bundle branch block is more common (2/3) than left bundle branch block (1/3). In patients with bradyarrhythmia, intravenous (IV) atropine (1-3 mg) is helpful in 70% to 80% of ACS patients and will lead to an increased heart rate. The need for pacemaker stimulation (PS) is different in patients with inferior MI (IMI) and anterior MI (AMI). Whereas bradyarrhythmias are frequently transient in patients with IMI and therefore do not need permanent PS, there is usually a need for permanent PS in patients with AMI. In these patients bradyarrhythmias are mainly caused by septal necrosis. In patients with ACS and ventricular arrhythmias (VTA) amiodarone is the drug of choice; this drug is highly effective even in patients with defibrillation-resistant out-of-hospital cardiac arrest. There is general agreement that defibrillation and advanced life support is essential and is the treatment of choice for patients with ventricular flutter/fibrillation. If defibrillation is not available in patients with cardiac arrest due to VTA, cardiopulmonary resuscitation is mandatory.

Heart failure patients are predisposed to develop arrhythmias. Supraventricular arrhythmias can exacerbate the heart failure symptoms by decreasing the effective cardiac output and their control require pharmacological, electrical, or catheter-based intervention. In the setting of atrial flutter or atrial fibrillation, anticoagulation becomes paramount to prevent systemic or cerebral embolism. Patients with heart failure are also prone to develop ventricular arrhythmias that can present a challenge to the managing clinician. The management strategy depends on the type of arrhythmia, the underlying structural heart disease, the severity of heart failure, and the range from optimization of heart failure therapy to catheter ablation. Patients with heart failure, irrespective of ejection fraction are at high risk for developing sudden cardiac death, however risk stratification is a clinical challenge and requires a multiparametric evaluation for identification of patients who should undergo implantation of a cardioverter defibrillator. Finally, patients with heart failure can also develop symptomatic bradycardia, caused by sinus node dysfunction or atrio-ventricular block. The treatment of bradycardia in these patients with pacing is usually straightforward but needs some specific issue.

Cardiac arrhythmias are varied and very common. They are usually classified as bradyarrhythmias and tachyarrhythmias, which are treated according to their own common principle separately. There is no long term effective oral drugs that can be used to treat bradyarrhythmias effectively up to now. Pacemaker is still the only effective treatment for it. Now catheter ablation has already applied to almost every kind of tachyarrhythmias, and which is the first choice for treating supraventricular tachycardia and atrial flutter because of the satisfactory result. Most patients with other types of tachyarrhythmias, especially atrial fibrillation and all kinds of premature beats are still given drug therapy. Amiodarone, propafenone, sotalol and mexiletine are common used antiarrhythmic drugs in our country. This article overviewed the principle and the matters need to attention in the drug therapy of cardiac arrhythmias. [ABSTRACT FROM AUTHOR]

Abstract: Cardiac arrhythmias are a common cause of potentially life-threatening, haemodynamic compromise in critically ill patients. This article describes a systematic approach to the management of the four general characteristics of arrhythmia (broad or narrow complex and tachycardia or bradycardia) as it is important to treat the patient and the general type of rhythm rather than considering each disturbance in detail. Successful management of all cardiac arrhythmias should be approached in stages, each of which is covered in this article: rapidly assess the haemodynamic status of the patient; identify the origin of the arrhythmia; correct predisposing factors (e.g. hypoxia, electrolyte imbalance); consider specific therapy (e.g. drugs, DC cardioversion); prevent further arrhythmias. [Copyright &y& Elsevier]

Electrophysiologic testing represents a major advance in both the diagnosis and management of cardiac rhythm and conduction disturbances. It is a sophisticated but arduous and invasive technique that requires proper patient selection, trained personnel, and specialized equipment and facilities for its optimal application. Patients with serious or life-threatening rhythm disorders are most likely to benefit from electrophysiologic testing. Patients with cardiovascular disease and incapacitating symptoms such as syncope or near-syncope, for whom noninvasive testing fails to reveal an etiology, as well as those patients considered candidates for various pacemaker and antiarrhythmic surgical interventions, are also suitable candidates for electrophysiologic testing. This relatively young field is still rapidly evolving. The major advance to come in the field of electrophysiology will be the simple identification of patients at high risk for sudden cardiac death. It is unclear whether invasive electrophysiologic testing will ultimately fulfill this goal or whether it will be helpful instead in leading to the development of noninvasive methods which may satisfy this need. This symposium and the introductory article address the present status of electrophysiologic studies in clinical practice. [ABSTRACT FROM AUTHOR]