cardiovascular-agents and Brugada-Syndrome

The Brugada syndrome is a rare but well-defined cause of sudden cardiac death. The key underlying abnormality is a decrease in net depolarising current due to a genetic defect, though recent evidence also implicates structural abnormalities in some patients. Diagnosis requires a Brugada-type ECG as well as typical clinical features: such clinical considerations are currently key in guiding risk stratification and hence management. Whilst pharmacological therapies are under investigation, the only intervention with a robust evidence base remains insertion of an implantable cardioverter defibrillator. Further research will be required to allow more effective risk stratification and hence more rational therapy.

Topics: Brugada Syndrome; Cardiovascular Agents; Death, Sudden, Cardiac; Defibrillators, Implantable; Electric Countershock; Electrocardiography; Heart Conduction System; Heart Rate; Humans; Risk Assessment; Risk Factors; Treatment Outcome

Drug-induced Brugada syndrome (BrS) represents a great challenge for the prescribing clinicians as well as for those involved in the development of novel pharmaceuticals and in the regulatory bodies responsible with monitoring drug safety. Apart from well-known cardiac agents (mainly Class I antiarrhythmics), an increasing number of noncardiac agents, including psychotropic and anesthetic drugs, have been shown to induce the characteristic Brugada electrocardiogram pattern predisposing to fatal ventricular arrhythmias. Up to now, both repolarization and depolarization abnormalities are thought to be related to the development of ventricular fibrillation in BrS patients. This review highlights the mechanisms and the noncardiac medical agents that unmask a genetic predisposition to BrS.

Topics: Anesthetics; Brugada Syndrome; Cardiovascular Agents; Electrocardiography; Genetic Predisposition to Disease; Humans; Psychotropic Drugs

Sodium (Na) channels are essential for cardiac electrical activity. Cardiac Na channel dysfunction, inherited or acquired, can induce life-threatening conduction and arrhythmia disorders. Inherited Na channel dysfunction may put affected patients at a greater risk for these complications when channel-modifying drugs are prescribed. This study addressed pharmacogenetic effects in three well-described Na channel-related diseases: long QT syndrome type 3, Brugada syndrome and inherited cardiac conduction disease. A review of the currently available literature on cardiac Na channel-modulating drugs was undertaken. An overview is given of the known risks of development of the previously mentioned complications of commonly prescribed drugs in patients affected with Na channel-related diseases and the underlying mechanisms.

Topics: Action Potentials; Arrhythmias, Cardiac; Brugada Syndrome; Cardiovascular Agents; Electrocardiography; Genetic Predisposition to Disease; Humans; Long QT Syndrome; Mutation; Myocardium; Pedigree; Pharmacogenetics; Protein Conformation; Risk Factors; Sodium Channels

of the progress in arrhythmias in 2020. RACE4 and ALL-IN indicated that integrated nurse-led care improves outcomes in AF patients.3,4 The same was reported for early rhythm control therapy15 and cryoablation as initial AF treatment.25,26 Subcutaneous ICD was non-inferior to classical transvenous ICD therapy in PRAETORIAN.54 One mechanistic study showed that autoantibodies against misexpressed actin, keratin, and connexin-43 proteins create a blood-borne biomarker profile enhancing diagnosis of Brugada syndrome.50 Another mechanistic study indicated that transseptal LV pacing yields similar improvement in contractility as His bundle pacing whilst being more easy to execute.44 In PRE-DETERMINE a simple-to-use ECG risk score improved risk prediction in patients with ischemic heart disease possibly enhancing appropriate ICD therapy in high risk patients.58.

Topics: Arrhythmias, Cardiac; Brugada Syndrome; Cardiovascular Agents; Defibrillators, Implantable; Humans; Treatment Outcome

Patients diagnosed as affected by Brugada syndrome (BrS) on the basis of a drug-induced type 1 ECG pattern (type1) are regarded as at low risk for cardiac arrest. We tested whether this assumption matches reality.. The study population included 26 patients from our group and 217 patients from three studies published between 2002 and 2013, all of them with aborted cardiac arrest (ACA) and in whom a previously unrecognized type1 (spontaneous or drug-induced) was discovered after the event, thus leading to the diagnosis of BrS.. Among our 26 patients, a drug-induced type1 was detected in 11 (42%) and only 1/11 showed a spontaneous pattern during follow-up; of 6 patients with syncope before ACA, 4 (67%) had only a drug-induced pattern. ICD shocks rates were similar in both spontaneous and drug-induced groups (57% and 45%). Early on, year 2002, the percentage of drug-induced type1 after ACA was much lower (14%) and has progressively increased to approximately 50%.. If drug-induced type1 carries low arrhythmic risk, it should seldom be the only marker for BrS after an ACA. In studies on patients after an unexpected ACA, a drug-induced type1 leads to the diagnosis of BrS more often than anticipated. This contrasts with prospective studies focusing on patients already diagnosed as BrS and which consider drug-induced type1 as a marker of low risk. Contrary to current views, it is possible that not all patients with a drug-induced BrS type1 are at low risk of future events.

Topics: Adult; Brugada Syndrome; Cardiovascular Agents; Cohort Studies; Electrocardiography; Female; Heart Arrest; Humans; Male; Middle Aged; Retrospective Studies; Risk Assessment

Topics: Acoustic Stimulation; Adrenergic Uptake Inhibitors; Animals; Anticonvulsants; Atomoxetine Hydrochloride; Blood Pressure; Brugada Syndrome; Cardiovascular Agents; Disease Models, Animal; Epilepsy; Female; Heart Rate; Male; Mice, Inbred DBA; Respiration; Respiratory System Agents; Seizures

Brugada syndrome is an inherited cardiac disorder associated with a specific electrocardiographic pattern, involving ST segment elevation in leads V1 to V3. When not spontaneously terminated, it can lead to ventricular fibrillation and sudden death. We present a case report of a young male whose brother suffered a sudden cardiac arrest while playing soccer. A novel mutation c.2678G>A was detected on the gene SCN5A through molecular diagnosis. The mutation was shown to be present in the individual, his daughter and his other brother. For patients with previous ventricular fibrillation and/or syncope, implantable cardiac device (ICD) is recommended. However, how can patients without symptoms but with a clear diagnosis prevent cardiac arrest?

Topics: Adult; Asymptomatic Diseases; Brugada Syndrome; Cardiovascular Agents; Child; Defibrillators, Implantable; Female; Humans; Male; Mutation; NAV1.5 Voltage-Gated Sodium Channel; Pedigree; Sodium Channels

A 31-year-old male patient was admitted to the emergency department with acute atrial fibrillation. After diltiazem infusion, a single oral dose of 600 mg propafenone was given to the patient for medical cardioversion. Approximately four hours later, sinus rhythym was restored. Re-evaluation of the admission ECG revealed right bundle branch block and saddleback-type ST-segment elevation of about 2 mm in V1-2 leads. Following propafenone, this type 2 Brugada ECG pattern turned to the coved type 1 Brugada pattern with ST elevation of more than 2 mm. After disappearance of propafenone effect, the ECG pattern turned to the type 2 Brugada pattern. Considering that the patient also had a family history of sudden cardiac death, electrophysiological study was conducted. During ventricular tachycardia stimulation, no ventricular arrhythmia was observed, thus the patient was scheduled to a close follow-up program.

Topics: Adult; Anti-Arrhythmia Agents; Atrial Fibrillation; Brugada Syndrome; Cardiac Electrophysiology; Cardiovascular Agents; Diltiazem; Electric Countershock; Electrocardiography; Humans; Male; Propafenone

Topics: Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Brugada Syndrome; Cardiac Conduction System Disease; Cardiovascular Agents; Heart Conduction System; Humans

Topics: Arrhythmias, Cardiac; Brugada Syndrome; Cardiac Conduction System Disease; Cardiovascular Agents; Digitalis; Heart Conduction System; Humans

Topics: Arrhythmias, Cardiac; Brugada Syndrome; Cardiac Conduction System Disease; Cardiovascular Agents; Heart Conduction System; Humans

Topics: Arrhythmias, Cardiac; Brugada Syndrome; Cardiac Conduction System Disease; Cardiovascular Agents; Heart Conduction System; Humans