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Brugada syndrome (BrS) is a hereditary clinical-electrocardiographic arrhythmic entity with low worldwide prevalence. The syndrome is caused by changes in the structure and function of certain cardiac ion channels and reduced expression of Connexin 43 (Cx43) in the Right Ventricle (RV), predominantly in the Right Ventricular Outflow Tract (VSVD), causing electromechanical abnormalities. The diagnosis is based on the presence of spontaneous or medicated ST elevation, characterized by boost of the J point and the ST segment ≥2 mm, of superior convexity "hollow type" (subtype 1A) or descending rectilinear model (subtype 1B). BrS is associated with an increased risk of syncope, palpitations, chest pain, convulsions, difficulty in breathing (nocturnal agonal breathing) and/or Sudden Cardiac Death (SCD) secondary to PVT/VF, unexplained cardiac arrest or documented PVT/VF or Paroxysmal atrial fibrillation (AF) in the absence of apparent macroscopic or structural heart disease, electrolyte disturbance, use of certain medications or coronary heart disease and fever. In less than three decades since the discovery of Brugada syndrome, the concept of Mendelian heredity has come undone. The enormous variants and mutations found mean that we are still far from being able to concretely clarify a genotype-phenotype relationship. There is no doubt that the entity is oligogenetic, associated with environmental factors, and that there are variants of uncertain significance, especially the rare variants of the SCN5A mutation, with European or Japanese ancestors, as well as a spontaneous type 1 or induced pattern, thanks to gnomAD (coalition) researchers who seek to aggregate and harmonize exome and genome sequencing data from a variety of large-scale sequencing projects and make summary data available to the scientific community at large). Thus, we believe that this in-depth analytical study of the countless mutations attributed to BrS may constitute a real cornerstone that will help to better understand this intriguing syndromeKeywords: androgen-insensitivity syndrome, dihydrotestosterone receptor deficiency, sex differentiation disorders, hernia, child. [ABSTRACT FROM AUTHOR]

Background: Previous population studies have presented conflicting results regarding the prognostic impact of intraventricular conduction delays (IVCD). Methods: We studied long‐term prognostic impact and the association with comorbidities of eight IVCDs in a random sample of 6,299 Finnish subjects (2,857 men and 3,442 women, mean age 52.8, SD 14.9 years) aged 30 or over who participated in the health examination including 12‐lead ECG. For left bundle branch block (LBBB) and non‐specific IVCD (NSIVCD), two different definitions were used. Results: During 16.5 years' follow‐up, 1,309 of the 6,299 subjects (20.8%) died and of these 655 (10.4%) were cardiovascular (CV) deaths. After controlling for known clinical risk factors, the hazard ratio for CV death, compared with individuals without IVCD, was 1.55 for the Minnesota definition of LBBB (95% confidence interval 1.04–2.31, p =.032) and 1.27 (95% confidence interval 0.80–2.02, p =.308) for the Strauss' definition of LBBB. Subjects with NSIVCD were associated with twofold to threefold increase in CV mortality depending on the definition. While right bundle branch block, left anterior fascicular block and incomplete bundle branch blocks were associated with seemingly higher mortality, this was no longer the case after adjustment for age and sex. The presence of R‐R' pattern was not associated with any adverse outcome. Conclusions: In a population study with long‐term follow‐up, NSIVCD and Minnesota definition of LBBB were independently associated with CV mortality. Other IVCDs had no significant impact on prognosis. The prognostic impact of LBBB and NSIVCD was affected by the definition of the conduction disorder. [ABSTRACT FROM AUTHOR]

Electrocardiographic artifacts are defined as electrocardiographic alterations, not related to cardiac electrical activity. As a result of artifacts, the components of the electrocardiogram (ECG) such as the baseline and waves can be distorted. Motion artifacts are due to shaking with rhythmic movement. Examples of motion artifacts include tremors with no evident cause, Parkinson's disease, cerebellar or intention tremor, anxiety, hyperthyroidism, multiple sclerosis, and drugs such as amphetamines, xanthines, lithium, benzodiazepines, or shivering (due to hypothermia, fever (rigor due to shaking), cardiopulmonary resuscitation by chest compression (oscillations of great amplitude) and patients who move their limbs during the test, causing sudden irregularities in the ECG baseline that may resemble premature contractions or interfere with ECG wave shapes, or other supraventricular and ventricular arrhythmias. When the skeletal muscles experience shaking, the ECG is "bombarded" by apparently random electrical activity. [ABSTRACT FROM AUTHOR]

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Left septal fascicular block, or blockage of the middle fibers of the left bundle branch, is known to be suggestive of a critical proximal obstruction of the left anterior descending coronary artery before its first septal perforator branch. We describe the case of a 68-year-old male who exhibited this transient intraventricular dromotropic disturbance following alcohol septal ablation for hypertrophic obstructive cardiomyopathy. [ABSTRACT FROM AUTHOR]

Introduction: All drugs and techniques that induce the anesthetic state act in some way in the Autonomic Nervous System (ANS). The administration of local anesthetics in the subarachnoid space produces motor, sensitive and sympathetic block, with latencies and variable and independent block levels. The motor block is the first to install, followed by the sympathetic and the sensitive. Sympathetic blockage affects 2 to 6 dermatomes above the sensory block. The recovery of spinal anesthesia is assessed through a scale defined in 1979 by Bromage and is based exclusively on the return of motor function and does not take into account the recovery of ANS activity. The persistence of sympathetic block may imply a higher incidence of urinary retention, bradycardia and hypotension. Objective: To assess cardiac autonomic modulation during perioperative hypotension caused by subarachnoid anesthesia Methods: A randomised, double-blind clinical trial will be performed in a large hospital located in the southern region of Ceará, Brazil and at the HUJB in Cajazeiras, Paraíba. Sixty patients from the anaesthesia outpatient clinic were enrolled. Patients were divided into two groups: one group received Bupivacaine with clonidine, and the other group received only bupivacaine at a dose of 15 mg. The sample consisted of 60 ASA patients I to III, submitted to orthopedic surgery of lower limbs and lower abdomen under spinal anesthesia. The Heart Rate Variability will be evaluated in three moments: rest, before anesthesia; 20 min after the blockade was installed, and at the time of motor function recovery according to the Bromage criteria and prognostic indices will be evaluated in the development of perioperative hypotension in two groups. Linear methods will be used in the frequency domain and nonlinear in chaos domain, Poincaré plot, approximate entropy, Detrended Fluctuation Analysis (DFA) and Correlation Dimension. The data will be collected through a Polar V800® heart rate meter and properly submitted for analysis and filtering by Kubios 3.0® software. Discussion: In the literature we find data evaluating the installation of sympathetic block through HRV using linear methods however, there is a lack of studies using methods based on the domain of chaos. Some studies address the value of HRV as a predictor of hypotension following subarachnoid anesthesia, mainly using linear methods in the frequency domain. It is understood to be important to analyze these factors using methods already validated in the domain of chaos, complexity and fractality, more compatible with the complexity of the behavior of biological systems, in the characterization of the autonomic function during the subarachnoid anesthesia. Registry: The clinical trial was registered in the Brazilian Registry of Clinical Trials (ReBEC) under the number RBR-4Q53D6. [ABSTRACT FROM AUTHOR]

Mid-ventricular hypertrophic obstructive cardiomyopathy with secondary formation of apical aneurysm is a rare variant of hypertrophic cardiomyopathy. They have a unique behavior because unlike other variants it causes sustained monomorphic ventricular tachycardia, which makes it particularly severe. [ABSTRACT FROM AUTHOR]

In the 12-lead electrocardiogram (ECG), the time from the onset of the QRS complex (Q or R wave) to the apex or peak of R or to R' (when present), using indirect or semidirect surface unipolar precordial leads, bipolar limb leads or unipolar limb leads, is called ventricular activation time (VAT), R wave peak time (RWPT), R-peak time or intrinsicoid deflection (ID). The R-peak time in a specific ECG lead is the interval from the earliest onset of the QRS complex, preferably determined from multiple simultaneously recorded leads, to the peak (maximum) of the R wave or R' if present. Irrespective of the relative height of the R and R' waves, the R-peak time is measured to the second peak. The parameter corresponds to the time of the electrical activation occurring from the endocardium to the epicardium as reflected by the recording electrode located at a variable distance on the body surface, depending on the lead type: a unipolar precordial lead, a bipolar or unipolar limb lead. In normal conditions, the R-peak time for the thinner-walled right ventricle is measured from lead V1 or V2 and its upper limit of normal is 35 ms. The R-peak time for the left ventricle (LV) is measured from leads V5 to V6 and 45 ms is considered the upper limit of normal. In this manuscript, we review the clinical applications of this parameter. [ABSTRACT FROM AUTHOR]

Summary: Background: Functional training is a new training vision that was prepared from the gesture imitation of daily activities. Although your use has become popular in clinical practice, the influence of the several cardiorespiratory adjustments performed during the functional training in different populations and conditions is unknown. So, the aim of this systematic review was to gather information in the literature regarding the influence of functional training on cardiorespiratory parameters. Methods: We conducted search strategies on MEDLINE, PEDro, EMBASE, SportDiscus and Cochrane to identify randomized controlled trials investigating the effects of functional training on cardiorespiratory parameters. Methodological quality of the included studies was assessed using the PEDro scale. Grading of Recommendations Assessment, Development and Evaluation (GRADE) summarized the evidence. Results: Five original studies were included. Effects favoured functional training on oxygen consumption (VO2) at intermediate‐term follow‐up: weighted mean difference −1·0 (95% CI: 5·4–3·3), P = 0·642, and a small and not clinically important effect observed on VO2 favouring control at intermediate‐term follow‐up (i.e. mean difference of 1·30 (95% CI 1·07–1·53), P<0·001). Conclusion: According to the GRADE system, there is very low quality evidence that functional training is better than other interventions to improve cardiovascular parameters. This result encourages new searches about the theme. [ABSTRACT FROM AUTHOR]