Early Repolarization: A Rare Primary Arrhythmic Syndrome and Common Modifier of Arrhythmic Risk

Despite longstanding beliefs, early repolarization is not always a benign electrocardiographic observation. Its association with increased arrhythmic events has been observed in 2 strikingly different groups of individuals, retrospectively in young subjects with idiopathic ventricular fibrillation and in long‐term cohort studies from the general population. This form of primary electrical disease is now referred to as the early repolarization syndrome and has mechanistically been demonstrated to occur secondary to a transmural gradient of early cellular repolarization, resulting in the presence of an ST‐elevation pattern and J‐waves merged within or offset from the terminal QRS complex. In addition to creating a milieu of increased arrhythmic risk in isolation, an increasing number of studies have highlighted that the presence of early repolarization and J‐waves may provide a baseline electrical substrate that modifies the risk of malignant arrhythmias in other clinical settings, such as acute myocardial ischemia. The challenge ahead lies in discerning when early repolarization may represent an ominous ECG marker, as opposed to a benign entity.     

Air Pollution and the Risk of Cardiac Defects: A Population-Based Case-Control Study

Previous epidemiologic studies have assessed the role of the exposure to ambient air pollution in the development of cardiac birth defects, but they have provided somewhat inconsistent results. To assess the associations between exposure to ambient air pollutants and the risk of cardiac defects, a population-based case-control study was conducted using 1087 cases of cardiac defects and a random sample of 10,870 controls from 1,533,748 Taiwanese newborns in 2001 to 2007.Logistic regression was performed to calculate odds ratios for 10 ppb increases in O₃ and 10 μg/m³ increases in PM₁₀. In addition, we compared the risk of cardiac defects in 4 categories-high exposure (>75th percentile); medium exposure (75th to 50th percentile); low exposure (<50th–25th percentile); reference (<25th percentile) based on the distribution of each pollutant. The risks of ventricular septal defects (VSD), atrial septal defects (ASD), and patent ductus arteriosus (PDA) were associated with 10 ppb increases in O₃ exposure during the first 3 gestational months among term and preterm babies. In comparison between high PM₁₀ exposure and reference category, there were statistically significant elevations in the effect estimates of ASD for all and terms births. In addition, there was a negative or weak association between SO_2, NO₂, CO, and cardiac defects_.The study proved that exposure to outdoor air O₃ and PM₁₀ during the first trimester of gestation may increase the risk of VSD, ASD, and PDA.     

Arrhythmic syncope: From diagnosis to management

Syncope is a concerning symptom that affects a large proportion of patients. It can be related to a heterogeneous group of pathologies ranging from trivial causes to diseases with a high risk of sudden death. However, benign causes are the most frequent, and identifying high-risk patients with potentially severe etiologies is crucial to establish an accurate diagnosis, initiate effective therapy, and alter the prognosis. The term cardiac syncope refers to those episodes where the cause of the ce...     

Air Pollution and Arrhythmias

Air pollution is commonly defined as the contamination of the air we breathe by any chemical, physical, or biological agent that is potentially threatening to human and ecosystem health. The common pollutants known to be disease-causing are particulate matter, ground-level ozone, sulphur dioxide, nitrogen dioxide, and carbon monoxide. Although the association between increasing concentrations of these pollutants and cardiovascular disease is now accepted, the association of air pollution and arrhythmias is less well established. In this review we provide an in-depth discussion of the association of acute and chronic air pollution exposure and arrhythmia incidence, morbidity, and mortality, and the purported pathophysiological mechanisms. Increases in concentrations of air pollutants have multiple proarrhythmic mechanisms including systemic inflammation (via increases in reactive oxygen species, tumour necrosis factor, and direct effects from translocated particulate matter), structural remodelling (via an increased risk of atherosclerosis and myocardial infarction or by affecting the cell-to-cell coupling and gap junction function), and mitochondrial and autonomic dysfunction. Furthermore, we describe the associations of air pollution and arrhythmias. There is a strong correlation of acute and chronic air pollutant exposure and the incidence of atrial fibrillation. Acute increases in air pollution increase the risk of emergency room visits and hospital admissions for atrial fibrillation and the risk of stroke and mortality in patients with atrial fibrillation. Similarly, there is a strong correlation of increases of air pollutants and the risk of ventricular arrhythmias, out-of-hospital cardiac arrest, and sudden cardiac death.     

空气污染与心律失常的相关性研究

常见的空气污染物主要包括颗粒物、臭氧、二氧化氮和二氧化硫、一氧化碳等.吸入污染的空气不仅诱发呼吸系统疾病,同时还会诱发心血管疾病.流行病学调查发现人体暴露于污染物中可促进缺血性心脏病、心力衰竭、心律失常和心脏骤停在内的心脏事件的发生,增加心血管病发病率和病死率.现对国内外空气污染与心律失常的相关文献进行综述.     

The Effects of Air Pollution and Temperature on COPD

Chronic Obstructive Pulmonary Disease (COPD) affects 12–16 million people in the United States and is the third-leading cause of death. In developed countries, smoking is the greatest risk factor for the development of COPD, but other exposures also contribute to the development and progression of the disease. Several studies suggest, though are not definitive, that outdoor air pollution exposure is linked to the prevalence and incidence of COPD. Among individuals with COPD, outdoor air pollutants are associated with loss of lung function and increased respiratory symptoms. In addition, outdoor air pollutants are also associated with COPD exacerbations and mortality. There is much less evidence for the impact of indoor air on COPD, especially in developed countries in residences without biomass exposure. The limited existing data suggests that indoor particulate matter and nitrogen dioxide concentrations are linked to increased respiratory symptoms among patients with COPD. In addition, with the projected increases in temperature and extreme weather events in the context of climate change there has been increased attention to the effects of heat exposure. Extremes of temperature—both heat and cold—have been associated with increased respiratory morbidity in COPD. Some studies also suggest that temperature may modify the effect of pollution exposure and though results are not conclusive, understanding factors that may modify susceptibility to air pollution in patients with COPD is of utmost importance.