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1.  Acute Exposure to Air Pollution Triggers Atrial Fibrillation 
The aim of the present study is to evaluate the association of air pollution with the onset of atrial fibrillation (AF).
Air pollution in general and more specifically particulate matter has been associated with cardiovascular events. Although ventricular arrhythmias are traditionally thought to convey the increased cardiovascular risk, AF may also contribute.
Patients with dual chamber implantable cardioverter defibrillators (ICDs) were enrolled and followed prospectively. The association of AF onset with air quality including ambient PM2.5, black carbon, sulfate, particle number, NO2, SO2, and O3 in the 24 hours prior to the arrhythmia was examined utilizing a case-crossover analysis. In sensitivity analyses, associations with air pollution between 2 and 48 hours prior to the AF were examined.
Of 176 patients followed for an average of 1.9 years, 49 patients had 328 episodes of AF lasting ≥ 30 seconds. Positive but nonsignificant associations were found for PM2.5 in the prior 24 hours, but stronger associations were found with shorter exposure windows. The odds of AF increased by 26% (95% CI 8% to 47%) for each 6.0 µg/m3 increase in PM2.5 in the 2 hours prior to the event (p=0.004). The odds of AF was highest at the upper quartile of mean PM2.5.
Particulate matter was associated with increased odds of AF onset within hours following exposure in patients with known cardiac disease. Air pollution is an acute trigger of AF, likely contributing to the pollution-associated adverse cardiac outcomes observed in epidemiological studies.
PMCID: PMC3752319  PMID: 23770178
Air pollution; Atrial fibrillation; Particulate matter; Traffic
3.  Air Pollution and the Triggering of Cardiac Arrhythmias 
Current opinion in cardiology  2010;25(1):16-22.
Purpose of Review
The last five years have witnessed an explosion in interest regarding cardiac arrhythmias and air pollution. The data have been strongest with respect to ventricular arrhythmias but there is accumulating evidence that air pollution is also associated with supraventricular arrhythmias.
Recent Findings
There is clear epidemiological evidence linking air pollution and cardiac mortality. Whether the cardiac mortality was from myocardial ischemia, congestive heart failure or arrhythmic, or all of these pathways is not clear from the epidemiological data. There is a large body of evidence that air pollution can modify autonomic tone. More recent data, utilizing patients with cardiac disease and implantable cardioverter defibrillators (ICDs) has clarified the association of air pollution and arrhythmias. Data is also accumulating that air pollution may be associated with atrial arrhythmias.
The incremental risk of air pollution in triggering arrhythmias or other acute cardiac events is greatest for those patients with underlying cardiac disease. Cardiovascular patients and those at high risk of cardiovascular disease should be educated about the risks for triggering of arrhythmias and other cardiac events by air pollution. These patients should monitor the local forecasted Air Quality Index and follow the recommendations to reduce exposures and limit activities.
PMCID: PMC3750956  PMID: 19881339
Air pollution; Ventricular arrhythmias; Atrial fibrillation; Sudden cardiac death
4.  Short-Term Effects of Ketamine and Isoflurane on Left Ventricular Ejection Fraction in an Experimental Swine Model 
ISRN Cardiology  2011;2011:582658.
Background. General anesthesia is an essential element of experimental medical procedures. Ketamine and isoflurane are agents commonly used to induce and maintain anesthesia in animals. The cardiovascular effects of these anesthetic agents are diverse, and the response of global myocardial function is unknown. Methods. In a series of 15 swine, echocardiography measurements of left ventricular ejection fraction (LVEF) were obtained before the animals received anesthesia (baseline), after an intramuscular injection of ketamine (postketamine) and after inhaled isoflurane (postisoflurane). Results. The mean LVEF of an unanesthetized swine was 47 ± 3%. There was a significant decrease in the mean LVEF after administration of ketamine to 41 + 6.5% (P = 0.003). The addition of inhaled isoflurane did not result in further decrease in mean LVEF (mean LVEF 38 ± 7.2%, P = 0.22). Eight of the swine had an increase in their LVEF with sympathetic stimulation. Conclusions. In our experimental model the administration of ketamine was associated with decreased LV function. The decrease may be largely secondary to a blunting of sympathetic tone. The addition of isoflurane to ketamine did not significantly change LV function. A significant number of animals had returned to preanesthesia LV function with sympathetic stimulation.
PMCID: PMC3262505  PMID: 22347646
5.  Commotio Cordis 
Sports Health  2009;1(2):174-179.
Commotio cordis is blunt, nonpenetrating trauma to the chest resulting in irregular heart rhythm and often leading to sudden death. This article presents the epidemiology, variables leading to commotio cordis, theories on predisposing factors, diagnosis, treatment, treatment outcomes, and return-to-play recommendations.
Evidence Acquisition:
A PubMed (MEDLINE) search for commotio cordis was conducted on July 1, 2008, and it yielded 106 results, of which 26 were used for this review, including experimental models, simulation studies, case analysis studies, case reports, general recommendation, review articles, and editorials.
There are more than 190 reported cases of commotio cordis in the United States. Forty-seven percent of reported cases occurred during athletic participation. Commotio cordis is the second-most common cause of sudden cardiac death in athletes. Occurrence of commotio cordis is related to time of impact during the cardiac cycle, direct impact over the heart, the hardness and speed of the projectile, and the ineffectiveness of chest barriers. As a result, the US Consumer Product Safety Commission recommends that softer “safety” baseballs be used for youth baseball. Resuscitation using defibrillation was effective in only 15% of cases. Resuscitation within 3 minutes resulted in a survival rate of 25% (17 of 68 cases). Survival drops to 3% when resuscitation is delayed beyond 3 minutes. Survival of commotio cordis has risen from 10% to 15% since 2001. Reduced ventricular ejection fraction has been identified in some commotio cordis survivors.
Preventive measures, such as using soft “safety” balls and making automated external defibrillators available at sporting venues, can reduce commotio cordis morbidity and mortality. Chest protector designs can be improved to enhance protection. Return to play is best left to clinical judgment given that data are lacking with regard to susceptibility for reoccurrence.
PMCID: PMC3445066  PMID: 23015869
athlete; commotio cordis; sudden cardiac death
6.  Parasympathetic response in chick myocytes and mouse heart is controlled by SREBP 
Parasympathetic stimulation of the heart, which provides protection from arrhythmias and sudden death, involves activation of the G protein–coupled inward rectifying K+ channel GIRK1/4 and results in an acetylcholine-sensitive K+ current, IKACh. We describe a unique relationship between lipid homeostasis, the lipid-sensitive transcription factor SREBP-1, regulation of the cardiac parasympathetic response, and the development of ventricular arrhythmia. In embryonic chick atrial myocytes, lipid lowering by culture in lipoprotein-depleted serum increased SREBP-1 levels, GIRK1 expression, and IKACh activation. Regulation of the GIRK1 promoter by SREBP-1 and lipid lowering was dependent on interaction with 2 tandem sterol response elements and an upstream E-box motif. Expression of dominant negative SREBP-1 (DN–SREBP-1) reversed the effect of lipid lowering on IKACh and GIRK1. In SREBP-1 knockout mice, both the response of the heart to parasympathetic stimulation and the expression of GIRK1 were reduced compared with WT. IKACh, attenuated in atrial myocytes from SREBP-1 knockout mice, was stimulated by SREBP-1 expression. Following myocardial infarction, SREBP-1 knockout mice were twice as likely as WT mice to develop ventricular tachycardia in response to programmed ventricular stimulation. These results demonstrate a relationship between lipid metabolism and parasympathetic response that may play a role in arrhythmogenesis.
PMCID: PMC2104475  PMID: 18060044
7.  Commotio Cordis 
Sudden arrhythmic death as a result of a blunt chest wall blow has been termed Commotio Cordis (CC). CC is being reported with increasing frequency with more than 180 cases now described in the United States Commotio Cordis Registry. The clinical spectrum is diverse; however young athletes tend to be most at risk, with victims commonly being struck by projectiles regarded as standard implements of the sport. Sudden death is instantaneous and victims are most often found in ventricular fibrillation (VF). Chest blows are not of sufficient magnitude to cause any significant damage to overlying thoracic structures and autopsy is notable for the absence of any structural cardiac injury. Development of an experimental model has allowed for substantial insights into the underlying mechanisms of sudden death. In anesthetized juvenile swine, induction of VF is instantaneous following chest impacts that occur during a vulnerable window before the T wave peak. Other critical variables, including the impact velocity and location, and the hardness of the impact object have also been identified. Rapid left ventricular pressure rise following chest impact likely results in activation of ion channels via mechano-electric coupling. The generation of inward current through mechano-sensitive ion channels results in augmentation of repolarization and non-uniform myocardial activation, and is the cause of premature ventricular depolarizations that are triggers of VF in CC. Currently available chest protectors commonly used in sport are not adequately designed to prevent CC. The development of more effective chest protectors and the widespread availability of automated external defibrillators at youth sporting events could improve the safety of young athletes.
PMCID: PMC2018736  PMID: 17957272
Commotio cordis; Ventricular Fibrillation; Athletes; Sudden Death; Mechano-electric coupling
8.  Inter-Association Task Force Recommendations on Emergency Preparedness and Management of Sudden Cardiac Arrest in High School and College Athletic Programs: A Consensus Statement 
Journal of Athletic Training  2007;42(1):143-158.
Objective: To assist high school and college athletic programs prepare for and respond to a sudden cardiac arrest (SCA). This consensus statement summarizes our current understanding of SCA in young athletes, defines the necessary elements for emergency preparedness, and establishes uniform treatment protocols for the management of SCA.
Background: Sudden cardiac arrest is the leading cause of death in young athletes. The increasing presence of and timely access to automated external defibrillators (AEDs) at sporting events provides a means of early defibrillation and the potential for effective secondary prevention of sudden cardiac death. An Inter-Association Task Force was sponsored by the National Athletic Trainers' Association to develop consensus recommendations on emergency preparedness and management of SCA in athletes.
Recommendations: Comprehensive emergency planning is needed for high school and college athletic programs to ensure an efficient and structured response to SCA. Essential elements of an emergency action plan include establishment of an effective communication system, training of anticipated responders in cardiopulmonary resuscitation and AED use, access to an AED for early defibrillation, acquisition of necessary emergency equipment, coordination and integration of on-site responder and AED programs with the local emergency medical services system, and practice and review of the response plan. Prompt recognition of SCA, early activation of the emergency medical services system, the presence of a trained rescuer to initiate cardiopulmonary resuscitation, and access to early defibrillation are critical in the management of SCA. In any collapsed and unresponsive athlete, SCA should be suspected and an AED applied as soon as possible for rhythm analysis and defibrillation if indicated.
PMCID: PMC1896083  PMID: 17597956
sudden cardiac death; athletes; emergency action plan; automated external defibrillators
9.  Increased Risk of Paroxysmal Atrial Fibrillation Episodes Associated with Acute Increases in Ambient Air Pollution 
Environmental Health Perspectives  2005;114(1):120-123.
Objectives: We reported previously that 24-hr moving average ambient air pollution concentrations were positively associated with ventricular arrhythmias detected by implantable cardioverter defibrillators (ICDs). ICDs also detect paroxysmal atrial fibrillation episodes (PAF) that result in rapid ventricular rates. In this same cohort of ICD patients, we assessed the association between ambient air pollution and episodes of PAF.
Design: We performed a case–crossover study.
Participants: Patients who lived in the Boston, Massachusetts, metropolitan area and who had ICDs implanted between June 1995 and December 1999 (n = 203) were followed until July 2002.
Evaluations/Measurements: We used conditional logistic regression to explore the association between community air pollution and 91 electrophysiologist-confirmed episodes of PAF among 29 subjects.
Results: We found a statistically significant positive association between episodes of PAF and increased ozone concentration (22 ppb) in the hour before the arrhythmia (odds ratio = 2.08; 95% confidence interval = 1.22, 3.54; p = 0.001). The risk estimate for a longer (24-hr) moving average was smaller, thus suggesting an immediate effect. Positive but not statistically significant risks were associated with fine particles, nitrogen dioxide, and black carbon.
Conclusions: Increased ambient O3 pollution was associated with increased risk of episodes of rapid ventricular response due to PAF, thereby suggesting that community air pollution may be a precipitant of these events.
PMCID: PMC1332666  PMID: 16393668
air pollution; arrhythmias; fibrillation; epidemiology; case—crossover; ozone
10.  Association of Air Pollution with Increased Incidence of Ventricular Tachyarrhythmias Recorded by Implanted Cardioverter Defibrillators 
Environmental Health Perspectives  2005;113(6):670-674.
Epidemiologic studies have demonstrated a consistent link between sudden cardiac deaths and particulate air pollution. We used implanted cardioverter defibrillator (ICD) records of ventricular tachyarrhythmias to assess the role of air pollution as a trigger of these potentially life-threatening events. The study cohort consisted of 203 cardiac patients with ICD devices in the Boston metropolitan area who were followed for an average of 3.1 years between 1995 and 2002. Fine particle mass and gaseous air pollution plus temperature and relative humidity were measured on almost all days, and black carbon, sulfate, and particle number on a subset of days. Date, time, and intracardiac electrograms of ICD-detected arrhythmias were downloaded at the patients’ regular follow-up visits (about every 3 months). Ventricular tachyarrhythmias were identified by electrophysiologist review. Risk of ventricular arrhythmias associated with air pollution was estimated with logistic regression, adjusting for season, temperature, relative humidity, day of the week, patient, and a recent prior arrhythmia. We found increased risks of ventricular arrhythmias associated with 2-day mean exposure for all air pollutants considered, although these associations were not statistically significant. We found statistically significant associations between air pollution and ventricular arrhythmias for episodes within 3 days of a previous arrhythmia. The associations of ventricular tachyarrhythmias with fine particle mass, carbon monoxide, nitrogen dioxide, and black carbon suggest a link with motor vehicle pollutants. The associations with sulfate suggest a link with stationary fossil fuel combustion sources.
PMCID: PMC1257589  PMID: 15929887
air pollution; arrhythmias; epidemiology; fibrillation; heart arrest
11.  New Concepts in Pacemaker Syndrome 
After implantation of a permanent pacemaker, patients may experience severe symptoms of dyspnea, palpitations, malaise, and syncope resulting from pacemaker syndrome. Although pacemaker syndrome is most often ascribed to the loss of atrioventricular (A-V) synchrony, more recent data may also implicate left ventricular dysynchrony caused by right ventricular pacing. Previous studies have not shown reductions in mortality or stroke with rate-modulated dual-chamber (DDDR) pacing as compared to ventricular-based (VVI) pacing. The benefits in A-V sequential pacing with the DDDR mode are likely mitigated by the interventricular (V-V) dysynchrony imposed by the high percentage of ventricular pacing commonly seen in the DDDR mode. Programming DDDR pacemakers to encourage intrinsic A-V conduction and reduce right ventricular pacing will likely decrease heart failure and pacemaker syndrome. Studies are currently ongoing to address these questions.
PMCID: PMC1502063  PMID: 16943933
VVI = ventricular-based; VVIR = rate modulated ventricular-based; A-V = atrioventricular; V-V = interventricular; V-A = ventricular-atrial; LBBB = left bundle branch block; LVEF = left ventricular ejection fraction; DDDR = rate modulated dual-chamber; SND = sinus node dysfunction; AAI = single-chamber atrial; AF = atrial fibrillation; LV = left ventricular; RV= right ventricular

Results 1-11 (11)