Who says you are so sick? An investigation on individual susceptibility to cybersickness triggers using EEG, EGG and ECG.

In this research paper, we conducted a study to investigate the connection between three objective measures: Electrocardio-gram(EGG), Electrogastrogram (EGG), and Electroencephalogram (EEG), and individuals' susceptibility to cybersickness. Our primary objective was to identify which of these factors plays a central role in causing discomfort when experiencing rotations along three different axes: Roll, Pitch, and Yaw. This study involved 35 participants who were tasked with destroying asteroids using their eye gaze while undergoing passive rotations in four separate sessions. The results, when combined with subjective measurements (specifically, Fast motion sickness questionnaire (FMS) and Simulator sickness questionnaire (SSQ) score), demonstrated that EGG measurements were superior in detecting symptoms associated with nausea. As for ECG measurements, our observations did reveal significant changes in Heart Rate Variability (HRV) parameters. However, we caution against relying solely on ECG as a dependable indicator for assessing the extent of cybersickness. Most notably, EEG signals emerged as a crucial resource for discerning individual differences related to these rotational axes. Our findings were significant not only in the context of periodic activities but also underscored the potential of aperiodic activities in detecting the severity of cybersickness and an individual's susceptibility to rotational triggers.

Beat-to-beat cardiac repolarization lability increases during hypoxemia and arousals in obstructive sleep apnea patients.

Obstructive sleep apnea (OSA) is associated with the progression of cardiovascular diseases, arrhythmias, and sudden cardiac death (SCD). However, the acute impacts of OSA and its consequences on heart function are not yet fully elucidated. We hypothesized that desaturation events acutely destabilize ventricular repolarization, and the presence of accompanying arousals magnifies this destabilization. Ventricular repolarization lability measures, comprising heart rate corrected QT (QTc), short-time-variability of QT (STVQT), and QT variability index (QTVI), were calculated before, during, and after 20,955 desaturations from lead II electrocardiography signals of 492 patients with suspected OSA (52% men). Variations in repolarization parameters were assessed during and after desaturations, both with and without accompanying arousals, and groupwise comparisons were performed based on desaturation duration and depth. Regression analyses were used to investigate the influence of confounding factors, comorbidities, and medications. The standard deviation (SD) of QT, mean QTc, SDQTc, and STVQT increased significantly (P < 0.01), whereas QTVI decreased (P < 0.01) during and after desaturations. The changes in SDQT, mean QTc, SDQTc, and QTVI were significantly amplified (P < 0.01) in the presence of accompanying arousals. Desaturation depth was an independent predictor of increased SDQTc (ß = 0.405, P < 0.01), STVQT (ß = 0.151, P < 0.01), and QTVI (ß = 0.009, P < 0.01) during desaturation. Desaturations cause acute changes in ventricular repolarization, with deeper desaturations and accompanying arousals independently contributing to increased ventricular repolarization lability. This may partially explain the increased risk of arrhythmias and SCD in patients with OSA, especially when the OSA phenotype includes high hypoxic load and fragmented sleep.NEW & NOTEWORTHY Nocturnal desaturations are associated with increased ventricular repolarization lability. Deeper desaturations with accompanying arousals increase the magnitude of alterations, independent of confounding factors, comorbidities, and medications. Changes associated with desaturations can partially explain the increased risk of arrhythmias and sudden cardiac death in patients with OSA, especially in patients with high hypoxic load and fragmented sleep. This highlights the importance of detailed electrocardiogram analytics for patients with OSA.

Bariatric surgery mitigated electrocardiographic abnormalities in patients with morbid obesity.

Obesity can lead to cardiovascular dysfunctions and cause electrocardiographic disruptions. Bariatric surgery plays a significant role in weight loss. To assess its benefits, this study investigated electrocardiographic changes before and after bariatric surgery. The present article describes a retrospective cohort study with a 6-month follow-up period. Electrocardiograms were interpreted and compared before and six months after surgery. The relationships between weight loss, type of surgery, and electrocardiographic alterations were analyzed. A total of 200 patients participated in the study, with 34 (17%) men and 166 (83%) women. The mean age of the participants was 44.6 ± 8.6, and their mean body mass index was 43.8 ± 5.5 kg/m2. The mean of QTc decreased after the surgery, while the Sokolow-Lyon scores increased. The statistical analysis showed that QTc dispersion (> 40) (P < 0.001), right ventricular hypertrophy (P < 0.001), abnormal R wave progression (P < 0.001), QTc (P < 0.001) and Sokolow-Lyon criteria (P < 0.001) significantly changed postoperatively. In conclusion, bariatric surgery can reduce QTc, correct poor R wave progression, and resolve right ventricular hypertrophy (RVH) in patients with morbid obesity.

Diagnosis and treatment of recurrent syncope in a middle-aged women.

A 50-year-old female patient, presented with repeated syncope for more than 2 years. Prior assessments were conducted at different hospitals, but no definite abnormalities were found. The patient's fear and anxiety about possible future attacks were escalating. Through a Head-up tilt test, the cause was finally identified as vasovagal syncope. Following a 5-min administration of nitroglycerin, the patient reported palpitations, nausea, and deep, rapid breathing. The electrocardiogram initially showed a first-degree atrioventricular block, progressing swiftly to a second-degree type I atrioventricular block-high atrioventricular block. Immediate intervention was undertaken, but blood pressure was not instantly ascertainable, coinciding with an abrupt loss of consciousness. Subsequent electrocardiographic findings included paroxysmal third-degree atrioventricular block, sinus arrest, and complete cardiac arrest, prompting the initiation of external cardiac compressions. The longest recorded ventricular arrest approximated 15 s, with sinus rhythm resuming post 10 s of cardiac compressions and the patient regaining consciousness. The patient underwent vagal ablation and no longer experienced syncope.

QRS-T angle: is it a specific parameter associated with sudden cardiac death in type 2 diabetes? Results from the SURDIAGENE and the Mini-Finland prospective cohorts.

AIMS/HYPOTHESIS: Type 2 diabetes is associated with a high risk of sudden cardiac death (SCD), but the risk of dying from another cause (non-SCD) is proportionally even higher. The aim of the study was to identify easily available ECG-derived features associated with SCD, while considering the competing risk of dying from non-SCD causes. METHODS: In the SURDIAGENE (Survie, Diabete de type 2 et Genetique) French prospective cohort of individuals with type 2 diabetes, 15 baseline ECG parameters were interpreted among 1362 participants (mean age 65 years; HbA1c 62±17 mmol/mol [7.8±1.5%]; 58% male). Competing risk models assessed the prognostic value of clinical and ECG parameters for SCD after adjusting for age, sex, history of myocardial infarction, N-terminal pro b-type natriuretic peptide (NT-proBNP), HbA1c and eGFR. The prospective Mini-Finland cohort study was used to externally validate our findings. RESULTS: During median follow-up of 7.4 years, 494 deaths occurred including 94 SCDs. After adjustment, frontal QRS-T angle ≥90° (sub-distribution HR [sHR] 1.68 [95% CI 1.04, 2.69], p=0.032) and NT-proBNP level (sHR 1.26 [95% CI 1.06, 1.50] per 1 log, p=0.009) were significantly associated with a higher risk of SCD. Nevertheless, frontal QRS-T angle was the only marker not to be associated with causes of death other than SCD (sHR 1.08 [95% CI 0.84, 1.39], p=0.553 ). These findings were replicated in the Mini-Finland study subset of participants with diabetes (sHR 2.22 [95% CI 1.05, 4.71], p=0.04 for SCD and no association for other causes of death). CONCLUSIONS/INTERPRETATION: QRS-T angle was specifically associated with SCD risk and not with other causes of death, opening an avenue for refining SCD risk stratification in individuals with type 2 diabetes.

Case report of a child with long QT syndrome type 14 caused by CALM1 gene mutation and literature review.

OBJECTIVE: To analyze the clinical and genetic characteristics of a patient with long QT syndrome type 14 (long QT syndrome-14, LQT14, OMIM # 616247) caused by a de novo CALM1 mutation. METHODS: The clinical data of the patient were collected, next-generation sequencing technology was used to determine the exome gene sequence of the patient, and the suspected pathogenic locus was verified by Sanger sequencing. RESULTS: A 5-year and 9-month-old girl was admitted to the hospital due to a syncopal episode. During the attack, the main symptoms were loss of consciousness, cyanosis of the face and lips, and weakness of limbs. The child had multiple seizures in the past, all of which occurred after emotional excitement and activity. She was diagnosed with epilepsy for more than 3 years, but the effect of antiepileptic treatment was not satisfactory. The electrocardiogram was normal in the past. A month ago, convulsions occurred again after exercise, and the electrocardiogram showed QTc 496 ms. The treadmill test showed a significant prolongation of QTc after exercise, and the genetic results suggested a new heterozygous variant of CALM1, c.395A>G; p. (Asp132Gly). Consequently, she was diagnosed with LQT14 and treated with propranolol. During a follow-up of 15 months, there were no seizures or syncope. CONCLUSIONS: This patient had multiple episodes of convulsions or syncope after emotional stimulation or activity, with intermittent prolongation of the QTc on routine ECG, marked prolongation of the QTc after exercise, and T-wave alternans, which differed from the LQT14 phenotype caused by the previous CALM1 mutation.

Chagas disease stroke and associated risk factors: A case-control study.

INTRODUCTION: The intricate relationship between Chagas disease and ischemic stroke remains unclear. Limited evidence exists concerning secondary prophylaxis, etiological diagnosis, and stroke-related determinants. This study aims to discern factors linked to stroke in Chagas disease by contrasting patients with and without a history of ischemic stroke. METHODS: Retrospective data from all outpatient Chagas disease patients from two Brazilian hospitals - one Chagas center and one stroke clinic - were examined. Descriptive analyses were conducted to identify stroke-associated factors. Variables were compared between patients with and without ischemic stroke history. RESULTS: Among 678 subjects, 72 had experienced stroke. Univariate associations with stroke included male gender, heart failure, prior or ongoing alcoholism, electrocardiographic features (non-sinus rhythm, left bundle branch, right bundle branch block, left anterosuperior fascicular block, atrial fibrillation), as well as echocardiographic findings indicative of reduced left ventricular ejection fraction and segmental abnormalities. After logistic regression (multivariate analysis), congestive heart failure, right bundle branch block, left anterosuperior divisional block, and atrial fibrillation retained independent associations. CONCLUSION: In this study, cardiac involvement emerged as the predominant factor correlated with stroke in Chagas disease. While atherosclerosis-related risk factors were prevalent, their influence on ischemic stroke in Chagas disease appeared limited.

Electrocardiographic frontal QRS-T angle is independently associated with panic disorder.

OBJECTIVE: Panic disorder (PD) may cause serious cardiac arrhythmias by causing electrical abnormalities. Abnormal P-wave axis (aPwa), presence of fragmented QRS (fQRS), wide frontal QRS-T angle (fQRSTa), QRS duration corrected (QRSdc) and log/ logQRS duration/RR interval (log/logQRS/RR) have been correlated with increased risk of serious supraventricular and ventricular cardiac arrhythmias in a general population. The purpose of this study was to compare these newly explored atrial and ventricular arrhythmia indicators in patients with PD and in healthy subjects. METHOD: A total of 169 newly diagnosed PD patients and 128 healthy subjects were included in the study. The Panic and Agoraphobia Scale (PAS) was administered, and 12-lead electrocardiography (ECG) measurements were obtained. Electrocardiographic parameters including aPwa, fQRSTa, presence of fQRS, QRS duration corrected (QRSdc), and log/logQRS duration/RR distance (log/logQRS/RR) were compared between the two groups. RESULTS: aPwa and fQRS, in addition to fQRSTa, QRSdc, and log/ logQRS/RR ratio values, were significantly increased in the PD group compared to healthy controls. Correlation analyses revealed that wider fQRSTa, number of fQRS derivation, number of total fQRS, wider QRSdc, and log/logQRS/RR ratio significantly correlated with PAS score. Logistic regression analysis demonstrated that fQRSTa and the number of total fQRS were independently associated with PD. CONCLUSION: PD is associated with wider fQRSTa, QRSdc, and log/logQRS/RR in addition to the increased abnormal aPwa and presence of fQRS. These findings suggest that untreated PD patients may be susceptible to supraventricular and ventricular arrhythmia, indicating that ECG should be routinely obtained in the management of PD patients.

Canine Model of Ischemia-Induced Ventricular Tachycardia.

INTRODUCTION: Despite advances in antiarrhythmia therapies, ventricular tachycardia (VT) is a leading cause of sudden cardiac death. Investigation into the characteristics and new treatments for this arrhythmia is required to improve outcomes and a reproducible model of VT would be useful in these endeavors. We therefore created a canine model of ischemia-induced VT. MATERIALS AND METHODS: A pacing lead was implanted in the right ventricle in canines (n = 13) and the left anterior descending artery was occluded in two locations for 2 h and subsequently released to create an ischemia-reperfusion injury. In the 10 dogs that survived the first 48 h following the initial study, a terminal study was conducted 4-7 d later and VT was induced using premature stimulation or burst pacing through the right ventricle lead. The arrhythmia was terminated using either antitachycardia pacing or a defibrillatory shock. Multiple inductions into sustained VT were attempted. RESULTS: Sustained VT was induced in eight of 10 dogs with an average cycle length of 335 ± 70 bpm. Multiple episodes of VT were induced. Episodes of VT exhibited different electrocardiogram morphologies and cycle lengths in individual animals. CONCLUSIONS: This canine model provides a consistent technique for inducing multiple episodes of sustained VT. It may be useful for investigating VT mechanisms and testing novel therapeutics and treatments for patients with VT.

Association of abnormalities in electrocardiography and ultrasonic echocardiography with the occurrence of cardiovascular disease in patients with advanced chronic kidney disease.

BACKGROUND: In patients with chronic kidney disease (CKD), the incidence of cardiovascular disease (CVD) increases with disease progression. CVD screening tests in those with CKD were researched to determine whether abnormalities observed in electrocardiography (ECG) and ultrasonic echocardiography (UCG) were risk factors associated with the development of CVD. METHODS: This study included 604 patients with CKD G4 and G5, for whom both ECG and UCG were performed. They were divided into four groups: those without ECG- and UCG-indicated abnormalities (group A, n = 333), with only ECG abnormalities (group B, n = 106), with only UCG abnormalities (group C, n = 75), and with both ECG and UCG abnormalities (group D, n = 90). Multivariate analysis using Cox regression analysis of the occurrence of CVD was performed during a follow-up period. RESULTS: During the observation period, 124 patients had clinical events. Among them, 45 patients (13.5%) were in Group A, 25 patients (23.6%) in Group B, 19 patients (25.3%) in Group C, and 35 patients (38.9%) in Group D, respectively. CVD event occurrence was highest in Group D. The results of the multivariate analysis also showed that the CVD event rates were significantly higher in Group C (HR: 2.96, P = < .001) and D (HR: 4.22, P < .001) than in Group A. CONCLUSION: In patients with advanced CKD, there was a significant correlation of ECG and UCG abnormalities with CVD events. Additionally, those having both types of abnormalities may have a higher risk of coronary artery disease than other groups.

Electrophysiological study in chagasics with syncope and conduction disorder.

BACKGROUND: Investigation of syncope involves the use of electrophysiological study, particularly in patients with cardiac conduction disorder. There is conflicting evidence about the role of electrophysiological study in patients with Chagas disease. OBJECTIVE: The objective of this study was to evaluate the electrophysiological study findings in patients with Chagas disease and bundle branch block and/or divisional block presenting with syncope. METHODS: This is a retrospective study of patients with Chagas disease and cardiac conduction disorder who underwent electrophysiological study from 2017 to 2021 for the investigation of syncope in a tertiary hospital in São Paulo, Brazil. Those with non-interpretable ECG, known coronary artery disease, and/or other cardiomyopathies were excluded. HV interval and electrophysiological study-induced malignant ventricular arrhythmias data were analyzed. RESULTS: A total of 45 patients (60.2±11.29 years, 57.8% males) were included. The mean HV interval was 58.37 ms±10.68; 22.2% of the studied population presented an HV interval of ≥70 ms; and malignant ventricular arrhythmias were induced in 57.8% patients. The use of beta-blockers and amiodarone (p=0.002 and 0.036, respectively), NYHA functional class≥II (p=0.013), wide QRS (p=0.047), increased HV interval (p=0.02), Rassi score >6.5 (p=0.003), and reduced left ventricular ejection fraction (p=0.031) were associated with increased risk of inducible malignant ventricular arrhythmias. CONCLUSION: More than half of the patients with Chagas disease, syncope, and cardiac conduction disorder have inducible malignant ventricular arrhythmias. Prolonged HV interval was observed in only 20% of population. Wide QRS, prolonged HV, reduced ejection fraction, and higher Rassi score were associated with increased risk of malignant ventricular arrhythmias.

Increased circulating progranulin is not sufficient to induce cardiac dysfunction or supraventricular arrhythmia.

Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia, and the incidence of new-onset AF has been increasing over the past two decades. Several factors contribute to the risk of developing AF including age, preexisting cardiovascular disease, chronic kidney disease, and obesity. Concurrent with the rise in AF, obesity has followed the same two-decade trend. The contribution of circulating proteins to obesity-related AF is of particular interest in the field. In this study, we investigated the effects of increased circulating levels of the glycoprotein progranulin on the development of supraventricular arrhythmias and changes to cardiac function. AAV8-mediated overexpression of full-length mouse progranulin was used to increase plasma protein levels and determine susceptibility to supraventricular arrhythmias and changes in cardiac structure and function. C57Bl/6N mice were subjected to increased circulating levels of progranulin for 20 weeks. Cardiac conduction was evaluated by surface ECG with and without isoproterenol challenge, and cardiac structure and function were measured by echocardiography after 20 weeks of circulating progranulin overexpression. Increased circulating levels of progranulin were maintained throughout the 20-week study. The cardiac structure and function remained unchanged in mice with increased circulating progranulin. ECG indices (P wave duration, P amplitude, QRS interval) were unaffected by increased progranulin levels and no arrhythmogenic events were observed following the isoproterenol challenge. In our model, increased levels of circulating progranulin were not sufficient to induce changes in cardiac structure and function or elicit ECG abnormalities suggestive of susceptibility to supraventricular arrhythmias.

Predictors of Atrial Fibrillation Developing in Hospital Stage After Coronary Artery Bypass Surgery.

Aim    To identify independent predictors associated with in-hospital atrial fibrillation (AF) following coronary artery bypass grafting (CABG).Material and methods     The study included 80 patients (88.75 % men) who had elective CABG surgery at the Sklifosovsky Research Institute of Emergency Medicine. Based on the development of AF during the hospital stage of treatment (up to 10 days after CABG surgery), patients were divided into two groups. The group with AF consisted of 19 patients, and the group without AF consisted of 61 patients. All patients underwent electrocardiography (ECG), transthoracic echocardiography (EchoCG) with calculation of the left ventricular (LV) geometry type, and assessment of operational indexes. During surgery, biopsy of a part of the right atrial (RA) appendage was taken from 61 patients to verify the severity of myocardial fibrosis on a four-score scale where 0 is no interstitial fibrosis, 1 is slight fibrosis, 2 is moderate fibrosis, and 3 is severe fibrosis.Results    All included patients had a low risk of developing postoperative complications according to the EuroSCORE II scale. According to EchoCG data, patients with AF had significantly higher ratios of left ventricular myocardial mass to body surface area (LVMM / BSA) (p = 0.0006) and of left atrial volume to body surface area (LA volume / BSA), p = 0.008). The distribution of patients by type of LV geometry was as follows: in the group with AF, 52.63 % (n=10) of patients were diagnosed with concentric LV hypertrophy (LVH) whereas in the group without AF, the majority of patients (83.60 %, n=51) had normal LV geometry and concentric LV remodeling (LVR) (p<0.0001). According to the results of histological study, patients of the AF group more frequently had moderate and severe interstitial fibrosis in the AF appendage (p = 0.003). After multivariate regression and ROC analysis, the predictive value remained for concentric LVH (p=0.002), LVMM / BSA ratio ≥97 g / m2 (p=0.006), LA volume / BSA ratio ≥ 34.4 ml / m2 (p=0.04), and for RA appendage interstitial fibrosis score ≥2 (p=0.004). Based on the identified predictors, a regression model was developed to predict the development of AF at the hospital stage after CABG (p<0.0001). The sensitivity and specificity of the model were 86.67 % and 78.26 %, respectively.Conclusion    In patients at low perioperative risk, the LVMM / BSA ratio ≥97 g / m2, the LA volume ratio / BSA ≥34.4 ml / m2, a RA appendage interstitial fibrosis score ≥2, and the presence of LVH were independent predictors of the development of AF at the hospital stage after CABG operation.Conclusion In patients at low perioperative risk, a LVMM / BSA ratio ≥97 g / m2, a LA volume / BSA ratio ≥34.4 ml / m2, a RA appendage interstitial fibrosis score ≥2, and the presence of LVH were independent predictors of the development of AF at the hospital stage after CABG.

Association of lipoprotein(a) with left ventricular hypertrophy assessed by electrocardiogram in adults: a large cross-sectional study.

Background and aims: Increasing evidence supports a causal relationship between lipoprotein(a) [Lp(a)] and atherosclerotic cardiovascular disease, yet its association with left ventricular hypertrophy (LVH) assessed by electrocardiogram (ECG) remains unknown. The aim of this study was to explore the relationship between Lp(a) and LVH assessed by ECG in general population. Methods and results: In this cross-sectional study, we screened 4,052 adults from the participants of the third National Health and Nutrition Examination Survey for analysis. Lp(a) was regarded as an exposure variable. LVH defined by the left ventricular mass index estimated from ECG was considered as an outcome variable. Multivariate logistic regression and restricted cubic spline (RCS) were used to assess the relationship between Lp(a) and LVH. Individuals with LVH had higher Lp(a) compared to individuals without LVH (P< 0.001). In the fully adjusted model, Lp(a) was strongly associated with LVH when as a continuous variable (per 1-unit increment, OR: 1.366, 95% CI: 1.043-1.789, P = 0.024), and higher Lp(a) remained independently associated with a higher risk of LVH when participants were divided into four groups according to quartiles of Lp(a) (Q4 vs Q1, OR: 1.508, 95% CI: 1.185-1.918, P = 0.001). And in subgroup analysis, this association remained significant among participants< 60 years, ≥ 60 years, male, with body mass index< 30 kg/m2, with hypertension and without diabetes (P< 0.05). In addition, we did not observe a nonlinear and threshold effect of Lp(a) with LVH in the RCS analysis (P for nonlinearity = 0.113). Conclusion: Lp(a) was closely associated with LVH assessed by ECG in general population.

Visual or computer-based measurements: Which is important for the interpretation of an athlete's electrocardiography?

OBJECTIVE: Preparticipation screening of athletes by electrocardiography is the most crucial step in determining sudden cardiac death risk factors. Several electrocardiography interpretation software programs have been developed for physicians practicing in this field. Our study aimed to assess cardiopoint sudden death screening module by comparing its findings with two cardiologists using Seattle and International criteria. METHODS: A total of 303 licensed national athletes (37% females) were enrolled. electrocardiographies were examined by the cardiopoint sudden death screening module using Seattle criteria and cardiologists. The consistency between cardiologists and software was compared, and the confidence assessment of the module was tested. RESULTS: With regard to Seattle criteria, moderate consistency was found between the cardiopoint sudden death screening module and the 1st (κ=0.41) and 2nd cardiologist (κ=0.59). Consistency between two cardiologists was moderate (κ=0.55). When we applied International criteria, there was moderate consistency between the module and the 1st cardiologist (κ=0.42), and good consistency between the module and the 2nd cardiologist (κ=0.63). Consistency between the two cardiologists was good (κ=0.62). CONCLUSION: The cardiopoint sudden death screening module had similar agreement with cardiologists based on both criteria. However, the software needs to be updated according to International criteria. Using computer-based measurements for preparticipation screening will help to save time and provide standardization of electrocardiography interpretation.

Systemic primary carnitine deficiency induces severe arrhythmia due to shortening of QT interval.

BACKGROUND: Systemic primary carnitine deficiency (PCD) is characterized by cardiomyopathy and arrhythmia. Without carnitine supplementation, progression is usually towards fatal cardiac decompensation. While the cardiomyopathy is most likely secondary to energy deficiency, the mechanism of arrhythmia is unclear, and may be related to a short QT interval. OBJECTIVE: We aim to describe rhythmic manifestations at diagnosis and with carnitine supplementation. METHODS: French patients diagnosed for PCD were retrospectively included. Clinical and para clinical data at diagnosis and during follow-up were collected. Electrocardiograms with QT interval measurements were blinded reviewed by two paediatric cardiologists. RESULTS: Nineteen patients (median age at diagnosis 2.3 years (extremes 0.3-28.9)) followed in 8 French centres were included. At diagnosis, 21% of patients (4/19) had arrhythmia (2 ventricular fibrillations, 1 ventricular tachycardia and 1 sudden death), and 84% (16/19) had cardiomyopathy. Six electrocardiograms before treatment out of 11 available displayed a short QT (QTc < 340 ms). Median corrected QTc after carnitine supplementation was 404 ms (extremes 341-447) versus 350 ms (extremes 282-421) before treatment (p < 0.001). The whole QTc was prolonged, and no patient reached the criterion of short QT syndrome with carnitine supplementation. Three patients died, probably from rhythmic cause without carnitine supplementation (two extra-hospital sudden deaths and one non-recoverable rhythmic storm before carnitine supplementation), whereas no rhythmic complication occurred in patients with carnitine supplementation. CONCLUSION: PCD is associated with shortening of the QT interval inducing severe arrhythmia. A potential explanation would be a toxic effect of accumulated fatty acid and metabolites on ionic channels embedded in the cell membrane. Carnitine supplementation normalizes the QTc and prevents arrhythmia. Newborn screening of primary carnitine deficiency would prevent avoidable deaths.

[Electrocardiographic interval as a predictor of life-threatening arrhythmias in dilated cardiomyopathy patients]. / Intervalo electrocardiográfico como predictor de arritmias graves en pacientes con miocardiopatía dilatada.

Background: The Tpe interval (Tp-e) in the surface electrocardiogram represents ventricular repolarization, a key phase in the pathogenesis of severe ventricular arrhythmias. However, there are few studies evaluating changes in this electrocardiographic interval as a risk factor for serious arrhythmias in patients with dilated cardiomyopathy. Objective: To determine whether the Tp-e interval prolongation predicts the presence of life-threatening arrhythmias in patients with dilated cardiomyopathy (DCM) with implantable cardioverter-defibrillator (ICD). Material and methods: Analytical, cross-sectional study in patients with DCM with ICDs. The Tp-e interval was measured in the V2 electrocardiographic lead and correlated with the incidence of life-threatening arrhythmias identified by the ICD. Results: 53 patients were recruited, 10 (18.8%) presented life-threatening arrhythmias. Prolongation of Tp-e interval was related to an increase in the incidence of ventricular tachycardia/fibrillation tachycardia (VT/FT) with a mean of 93 ± 20.5 ms (p = 0.003), using ROC curves to determine the thereshold of 90 ms for increased risk of VT/VF with sensitivity of 70% and specificity of 84%, with an area under the curve of 0.798. Conclusion: The prolongation of the ITp-e interval greater than 90 ms in a population with dilated cardiomyopathy predicts the presence of arrhythmic episodes, such as VT and/or VT/FT.

Introducción: el intervalo Tpe (ITp-e) en el electrocardiograma de superficie representa la repolarización ventricular, fase clave en la patogénesis de arritmias ventriculares graves. Sin embargo, existen pocos estudios que evalúen la alteración de este intervalo electrocardiográfico como factor de riesgo de arritmias graves en pacientes con miocardiopatía dilatada. Objetivo: determinar si la prolongación del ITp-e predice la presencia de arritmias potencialmente mortales en pacientes con miocardiopatía dilatada (MCD) portadores de desfibrilador automático implantable (DAI). Material y métodos: estudio, transversal analítico en pacientes con MCD portadores de DAI. Se midió el ITp-e en la derivación electrocardiográfica V2 y se correlacionó con la incidencia de arritmias potencialmente letales identificadas por el DAI. Resultados: se incluyeron 53 pacientes, 10 (18.8%) presentaron arritmias potencialmente mortales. La prolongación del ITp-e se relacionó con aumento de incidencia de taquicardia ventricular/fibrilación ventricular (TV/FV) con media de 93 ± 20.5 ms (p = 0.003), por lo que se determinó mediante curvas ROC el punto de corte de 90 ms para el aumento de riesgo de TV/FV con sensibilidad de 70% y especificidad de 84%, con área bajo la curva de 0.798. Conclusión: la prolongación del intervalo ITp-e > 90 ms en población con miocardiopatía dilatada predice la presencia de episodios arrítmicos como TV o FV.