Interpolated junctional extrasystoles mimicking complex polymorphic ventricular arrhythmias in a healthy young athlete: a case report.

Background: In young competitive athletes, ventricular arrhythmias could be a reason for concern as they may represent the sign of a serious underlying cardiac condition. On the other hand, atrial or conduction system premature beats are usually benign. However, when the properties of the His-Purkinje system lead to conduction aberrancies, there is a risk of misinterpreting benign arrhythmias as potentially at risk ventricular ectopic beats. Case summary: We described the case of a healthy young athlete with asymptomatic interpolated junctional ectopic beats interpreted as polymorphic ventricular tachycardia during pre-participation screening. Discussion: Strange and rare electrocardiogram pictures may be observed during sport pre-participation screening. The small atrioventricular (AV) junction is made up of many specialized fibres with different conduction properties. Junctional arrhythmias can have a normal anterograde conduction or can be conducted with aberrancy. Rarely, they can be interpolated and cause PR prolongation or bundle branch block by increasing the refractory period of the AV node and/or the conduction system. When aberrancy occurs, they can be mistaken for 'atypical' ventricular arrhythmias. Prognosis of these events remains uncertain.

Delayed depolarization and histologic abnormalities underlie the Brugada syndrome.

Brugada syndrome (BrS) is a controversial disease whose pathophysiology is still far from being fully understood. Unlike other cardiological disorders, a definite etiology has not yet been established so that it could be summarized under two main chapters: "functional" or "organic", "repolarization" or "depolarization" disorder. Despite initial descriptions leaned towards the organic substrate and delayed depolarization features, functional and repolarization theories have attracted most of the Cardiological attention for many years. Data from electrocardiography, endocavitary tracings, electroanatomic mapping and histopathology, however, demonstrated that BrS is mainly characterized by structural myocardial changes mostly at the right ventricular outflow tract (RVOT), but also at the right ventricle (RV) and by delayed conduction at the same sites. Conduction disorders at different levels may also be present and identify patients at high risk for major arrhythmic events. The aim of the present review is to provide the current state of art of the pathophysiology of BrS, focusing on electro-vectorcardiography and electrophysiological features, histopathology, echocardiography, and cardiac magnetic resonance imaging (CMRI).

Arrhythmic Mitral Valve Prolapse in the Young: A Rare but Concerning Entity.

Arrhythmic mitral valve prolapse (MVP) is an increasingly recognized clinical entity, characterized by the association of myxomatous mitral valve, ventricular arrhythmias (VAs) and sudden cardiac death (SCD). Prevalence of MVP is reported ranging between 2% and 5% of the general population, and risk of SCD is estimated approximately 0.3% per year. Diagnosis of MVP and the occurrence of fatal events involve generally adults aged 30 to 50 years, whereas in younger and even pediatric individuals has rarely been described. Herein, we report two clinical cases of malignant MVP in young patients, with the aim to point out the clinical features and the challenge of clinical management and risk stratification.

Role of Provocable Brugada ECG Pattern in The Correct Risk Stratification for Major Arrhythmic Events.

The so-called Brugada syndrome (BS), first called precordial early repolarization syndrome (PERS), is characterized by the association of a fascinating electrocardiographic pattern, namely an aspect resembling right bundle branch block with a coved and sometime upsloping ST segment elevation in the precordial leads, and major ventricular arrhythmic events that could rarely lead to sudden death. Its electrogenesis has been related to a conduction delay mostly, but not only, located on the right ventricular outflow tract (RVOT), probably due to a progressive fibrosis of the conduction system. Many tests have been proposed to identify people at risk of sudden death and, among all, ajmaline challenge, thanks to its ability to enhance latent conduction defects, became so popular, even if its role is still controversial as it is neither specific nor sensitive enough to guide further invasive investigations and managements. Interestingly, a type 1 pattern has also been induced in many other cardiac diseases or systemic diseases with a cardiac involvement, such as long QT syndrome (LQTS), arrhythmogenic right ventricular cardiomyopathy (ARVC), hypertrophic cardiomyopathy (HCM) and myotonic dystrophy, without any clear arrhythmic risk profile. Evidence-based studies clearly showed that a positive ajmaline test does not provide any additional information on the risk stratification for major ventricular arrhythmic events on asymptomatic individuals with a non-diagnostic Brugada ECG pattern.

Right Ventricular Outflow Tract Tachycardia with Structural Abnormalities of the Right Ventricle and Left Ventricular Diverticulum.

A 43-year-old woman presented to the emergency room with a sustained ventricular tachycardia (VT). ECG showed a QRS in left bundle branch block morphology with inferior axis. Echocardiography, ventricular angiography, and cardiac magnetic resonance imaging (CMRI) revealed a normal right ventricle and a left ventricular diverticulum. Electrophysiology studies with epicardial voltage mapping identified a large fibrotic area in the inferolateral layer of the right ventricular wall and a small area of fibrotic tissue at the anterior right ventricular outflow tract. VT ablation was successfully performed with combined epicardial and endocardial approaches.

Body fat and the cognitive pattern: A population-based study.

OBJECTIVE: The relationship between body fatness and cognitive pattern at a population level was investigated. METHODS: Among 500 unselected subjects from the general population, the role of body mass index (BMI) and body fat mass (BFM) on a mini-mental state examination (MMSE) and on a battery of paper and pencil neuropsychological tests was analyzed. Multiple linear regressions, accounting for potential confounders, were used. RESULTS: In fully adjusted models, MMSE (coefficient +0.027, 95% confidence intervals, 0.017-0.177), the clock drawing test (+0.141, 0.053-0.226), and the trail making test A (+1.542, 0.478-2.607) were positively associated with BMI. Adding BFM to the models, no associations were observed. The tests were also positively associated with BFM (+0.056, 0.021-0.091; +0.063, 0.025-0.101; +0.592, 0.107-1.077; respectively). At analysis of covariance, the same tests were significantly better performed over 29.4 kg m(-2) of BMI. After adding BFM as further confounder, all differences in performance across BMI were no longer significant. The three tests were better performed over 34.6 kg of BFM. CONCLUSIONS: Higher BMI and particularly higher BFM are positively associated with better performance at the cognitive tasks exploring selective attention and executive functions.

Orthostatic hypotension does not increase cardiovascular risk in the elderly at a population level.

BACKGROUND: The general belief that orthostatic hypotension (OH) predisposes to cardiovascular events is based on sparse and contradictory data, rarely derived from population studies. METHODS: A total of 1,016 men and women aged ≥65 years was studied in a 12-year epidemiological population-based study. Cardiovascular events were detected in subjects with and without OH (blood pressure (BP) decrease ≥20mm Hg for systolic or ≥10mm Hg for diastolic), and Cox analysis was performed including OH as an independent variable. RESULTS: In univariate analysis, coronary (20.2% vs. 13.1%, P = 0.05), cerebrovascular (13.1% vs. 8.4%, P = 0.05), and heart failure (HF) events (20.2% vs. 13.8%, P = 0.03) were apparently more incidental in subjects with OH than in those without OH. Nevertheless, after adjusting for age, gender, and systolic BP as confounders, OH did not act as a cardiovascular predictor (relative risk for cerebrovascular events 1.33, 95% confidence interval (CI), 0.78-2.2, for coronary events 1.25, CI 0.82-1.88, for HF 1.07, CI 0.71-1.62, for arrhythmias 0.82, CI 0.40-1.37, and for syncope 0.58, CI 0.13-2.71). CONCLUSIONS: Although OH seems to be a predictor of coronary, cerebrovascular, and HF events, no predictive role was found in models that include biological confounders. Independent of the cause of OH, age and systolic BP, which are positively associated with OH, fully explain the greater incidence of cardiovascular events and the greater cardiovascular risk observed in subjects with OH.

Cognitive functions and cognitive reserve in relation to blood pressure components in a population-based cohort aged 53 to 94 years.

In 288 men and women from general population in a cross-sectional survey, all neuropsychological tests were negatively associated with age; memory and executive function were also positively related with education. The hypertensives (HT) were less efficient than the normotensives (NT) in the test of memory with interference at 10 sec (MI-10) (-33%, P = 0.03), clock drawing test (CLOX) (-28%, P < 0.01), and mini-mental state examination (MMSE) (-6%, P = 0.02). Lower MMSE, MI-10, and CLOX were predicted by higher systolic (odds ratio, OR, 0.97, P = 0.02; OR 0.98, P < 0.005; OR 0.95, P < 0.001) and higher pulse blood pressure (BP) (OR 0.97, P = 0.02; OR 0.97, P < 0.01; and 0.95, P < 0.0001). The cognitive reserve index (CRI) was 6% lower in the HT (P = 0.03) and was predicted by higher pulse BP (OR 0.82, P < 0.001). The BP vectors of lower MMSE, MI-10, and CLOX were directed towards higher values of systolic and diastolic BP, that of low CRI towards higher systolic and lower diastolic. The label of hypertension and higher values of systolic or pulse BP are associated to worse memory and executive functions. Higher diastolic BP, although insufficient to impair cognition, strengthens this association. CRI is predicted by higher systolic BP associated to lower diastolic BP.

The C825T GNB3 polymorphism, independent of blood pressure, predicts cerebrovascular risk at a population level.

BACKGROUND: The role of C825T polymorphism of the candidate GNB3 gene in predicting cerebrovascular outcome has been poorly explored in longitudinal setting at a population level. METHODS: In an epidemiological setting, 1,678 men and women from general population were genotyped for C825T polymorphism of GNB3 gene and follow-up for 10 years to detect nonfatal and fatal cerebrovascular events (CE). Established cerebrovascular risk factors were used to adjust the multivariate Cox analysis for confounders. RESULTS: Seventy-three nonfatal and 30 fatal CE were recorded. Incidence of CE was higher in TT than in C-carriers (fatal: 2.6 vs. 1.7%, P < 0.03; nonfatal: 7.8 vs. 3.9%, P < 0.03; fatal recurrences: 1.6 vs. 0.6%, P < 0.03). In Cox analysis, the TT genotype predicted nonfatal (hazard ratio 1.99, 95% confidence interval 1.05-3.79, P = 0.03), fatal (2.91, 1.05-8.12, P = 0.04), and fatal recurrent CE (6.82, 1.50-31.1, P = 0.02) also after adjustment for age, gender, systolic and diastolic blood pressure, body adiposity, atherogenetic blood lipids, serum uric acid, diabetes, calories, caffeine and ethanol intake, and coronary events at baseline. Further adjustment for historical CE made the association between TT genotype and incident fatal CE nonsignificant (hazard ratio 2.72, 95% confidence interval 0.96-7.22, P = 0.06). CONCLUSIONS: The TT genotype of GNB3 gene predicts incident CE independent of blood pressure and other established risk factors at a population level. Further studies are needed to clarify the nature and pathways of this association.