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Biomedical subjects

Arthur Wilde

Publications and source records attributed to Arthur Wilde.

5 recordsLinked to original sources

Diagnosis and management of very rare primary arrhythmia syndromes in children and adults: a Clinical Consensus Statement of the European Heart Rhythm Association of the ESC and the Association of Cardiovascular Nursing & Allied Professions of the ESC, endorsed by the Association for European Paediatric and Congenital Cardiology.

Very rare and ultra-rare primary inherited arrhythmia syndromes (IAS) represent a heterogeneous group of disorders associated with a significant risk of sudden cardiac death, often manifesting from foetal life to early adulthood. Current guidelines primarily address more common IAS and provide limited, non-specific recommendations for these rare entities, particularly in paediatric populations. This European Heart Rhythm Association Clinical Consensus Statement, developed in collaboration with the Association of Cardiovascular Nursing and Allied Professions and endorsed by the Association for European Paediatric and Congenital Cardiology, integrates available evidence with expert opinion. Recommendations were formulated through structured discussion and voting, following ESC consensus methodology, with a focus on clinically actionable gene-disease associations. The document provides a comprehensive framework for the diagnosis and management of very rare IAS, including calmodulinopathies, Andersen-Tawil syndrome, Timothy syndrome, TRDN-related disease, calcium release deficiency syndrome, and other atypical channelopathies. It highlights age-specific clinical presentations, the importance of genetic testing, and tailored therapeutic strategies, including pharmacological treatments, left cardiac sympathetic denervation, and selective use of implantable cardioverter-defibrillators. Special attention is given to paediatric considerations, foetal diagnosis, and the role of multidisciplinary care. The document also addresses arrhythmic risk in metabolic and cardiomyopathic conditions, as well as the importance of molecular autopsy and family screening in sudden unexplained death. This consensus document fills a critical gap by providing expert-driven, pragmatic guidance for the management of very rare IAS across the lifespan. It underscores the need for specialized care, international collaboration, and prospective registries to improve evidence generation, risk stratification, and patient outcomes in this vulnerable population.

Humans↗

Brugada syndrome: report of the second consensus conference: endorsed by the Heart Rhythm Society and the European Heart Rhythm Association.

Since its introduction as a clinical entity in 1992, the Brugada syndrome has progressed from being a rare disease to one that is second only to automobile accidents as a cause of death among young adults in some countries. Electrocardiographically characterized by a distinct ST-segment elevation in the right precordial leads, the syndrome is associated with a high risk for sudden cardiac death in young and otherwise healthy adults, and less frequently in infants and children. Patients with a spontaneously appearing Brugada ECG have a high risk for sudden arrhythmic death secondary to ventricular tachycardia/fibrillation. The ECG manifestations of Brugada syndrome are often dynamic or concealed and may be unmasked or modulated by sodium channel blockers, a febrile state, vagotonic agents, alpha-adrenergic agonists, beta-adrenergic blockers, tricyclic or tetracyclic antidepressants, a combination of glucose and insulin, hypo- and hyperkalemia, hypercalcemia, and alcohol and cocaine toxicity. In recent years, an exponential rise in the number of reported cases and a striking proliferation of articles defining the clinical, genetic, cellular, ionic, and molecular aspects of the disease have occurred. The report of the first consensus conference, published in 2002, focused on diagnostic criteria. The present report, which emanated from the second consensus conference held in September 2003, elaborates further on the diagnostic criteria and examines risk stratification schemes and device and pharmacological approaches to therapy on the basis of the available clinical and basic science data.

Arrhythmogenic Right Ventricular Dysplasia↗

Brugada syndrome: report of the second consensus conference.

Since its introduction as a clinical entity in 1992, the Brugada syndrome has progressed from being a rare disease to one that is second only to automobile accidents as a cause of death among young adults in some countries. Electrocardiographically characterized by a distinct ST-segment elevation in the right precordial leads, the syndrome is associated with a high risk for sudden cardiac death in young and otherwise healthy adults, and less frequently in infants and children. Patients with a spontaneously appearing Brugada ECG have a high risk for sudden arrhythmic death secondary to ventricular tachycardia/fibrillation. The ECG manifestations of Brugada syndrome are often dynamic or concealed and may be unmasked or modulated by sodium channel blockers, a febrile state, vagotonic agents, alpha-adrenergic agonists, beta-adrenergic blockers, tricyclic or tetracyclic antidepressants, a combination of glucose and insulin, hypo- and hyperkalemia, hypercalcemia, and alcohol and cocaine toxicity. In recent years, an exponential rise in the number of reported cases and a striking proliferation of articles defining the clinical, genetic, cellular, ionic, and molecular aspects of the disease have occurred. The report of the first consensus conference, published in 2002, focused on diagnostic criteria. The present report, which emanated from the second consensus conference held in September 2003, elaborates further on the diagnostic criteria and examines risk stratification schemes and device and pharmacological approaches to therapy on the basis of the available clinical and basic science data.

Arrhythmogenic Right Ventricular Dysplasia↗

Direct comparison of a contractility and activity pacemaker sensor during treadmill exercise testing.

There are limited data about the chronotropic capacity of the peak endocardial acceleration (PEA) sensor. This study directly compared the chronotropic function from the PEA and the activity (ACT) sensor. The study included 18 patients (age 73 +/- 7 years) with > or = 75% pacemaker-driven heart rate (HR) and a PEA sensor and 11 healthy controls (age 67 +/- 7 years) underwent a chronotropic assessment exercise protocol (CAEP) exercise test with the pacemaker patients in VVIR mode after programming the sensors in the default setting with adjustment of the upper sensor rate as an age related maximum value (220-age). The ACT sensor was externally strapped on the thorax. Achieved exercise duration for the patients and controls was, respectively, 9.2 +/- 3 vs 18.4 +/- 4 minutes (P <0.001). The maximal achieved HR with the PEA sensor was 124 +/- 25 beats/min, versus the ACT with 140 +/- 23, versus the controls with 153 +/- 26 beats/min (P <0.001 between the groups). For the PEA, ACT, and controls, the time to peak HR was, respectively, 11 +/- 3, 7 +/- 3.6, and 18 +/- 4 (P <0.001 between groups) and HR after 10 minutes recovery was, respectively, 80 +/- 20, 65 +/- 15, and 82 +/- 4 beats/min (P <0.001 between groups). The PEA sensor functions hypochonotroop during exercise programmed as a single sensor system. It is, therefore, preferable to combine the PEA sensor with an activity-based sensor in a dual sensor system. Although both groups had normal left ventricular functions, the exercise capacity of pacemaker patients is significantly lower than in the controls.

Aged↗

The 2373insG mutation in the MYBPC3 gene is a founder mutation, which accounts for nearly one-fourth of the HCM cases in the Netherlands.

AIMS: Hypertrophic cardiomyopathy (HCM) is caused by mutations in genes that encode sarcomeric proteins. In this study we investigated the involvement of the sarcomeric myosin binding protein C in the Dutch HCM population. METHODS AND RESULTS: We initially screened 22 Dutch index patients for mutations in the MYBPC3 gene, which revealed four different mutations in 14 patients. The 2373insG mutation was identified in 10 apparently unrelated patients. A subsequent screening for the 2373insG mutation in a group of another 237 unrelated HCM patients revealed 50 additional carriers of the same genetic defect. Genotyping with polymorphic repeat markers and intragenic SNPs of the 60 Dutch as well as two German and five North American 2373insG carriers indicated they all share the same haplotype. CONCLUSION: The 2373insG mutation accounts for almost one-fourth of all HCM cases in the Netherlands (60/259), which is predominantly present in the northwestern part of the country (22/66) and is a founder mutation probably originating from the Netherlands.

Cardiomyopathy, Hypertrophic, Familial↗