"ST-elevation myocardial infarction associated with air pollution levels in Mexico City".

Background Coronary heart disease has multiple risk factors, including air pollution. Numerous pathophysiological mechanisms have been identified with increasing levels of air pollution, mainly with ozone (O3), nitrogen dioxide (NO2), sulphur dioxide (SO2), particulate matter (PM10), fine particulate matter (PM2.5) and carbon monoxide (CO). In Mexico, the pollution level is reported using an air quality index called IMECA. Methods All patients with STEMI admitted at Hospital Español were collected between 2012 and 2019 (N = 348). We conducted a retrospective analysis using the air pollution exposure at the time of each event (lag0), the previous 24 h (lag1), 48 h (lag2), 72 h (lag3) and 5-day cumulative lag. The level of air pollution was analyzed independently using IMECA and particle concentrations. The data was divided in two groups: days with one of more STEMI's (MI group) and days free of events (Control group), using ANCOVA to evaluate the difference between means of both groups taking into account confounders. Results: For days with one or more cardiovascular event, a significant increase in SO2 was observed at lag1; similar increase was found in CO, PM2.5, SO2 at lag2. For the 5-day cumulative lag, SO2 and PM2.5 showed a significant increase. No differences were found using the IMECA levels in both groups. Conclusions: The elevated concentrations levels of CO, SO2 and PM2.5 showed significant association with STEMI at different time points before the event. Ozone, PM10 and NO2 showed no difference between groups. IMECA levels showed no association with STEMI in our study.

[Atrial fibrillation. New views on an old disease]. / Fibrilación auricular. Nuevos aspectos sobre una vieja enfermedad.

Atrial fibrillation (Afib) is clinically the most common arrhythmia. Its main complications are recurrent embolic events and a variable deterioration of functional class. Atrial fibrillation induces changes in cellular ionic channels that self-perpetuate the arrhythmia. The pharmacologic treatment of Afib is directed toward correction of those changes and return to sinus rhythm. It is also intended to maintain adequate heart rates and prevent embolic events through anticoagulation or platelet antiagregation. There are presently several class IC or class III antiarrhythmics available for attempting a return to sinus rhythm. The success rates are irregular, the best achieved with flecainide or propafenone among patients without structural heart disease. Amiodarone is the best choice when there is such a problem. The combination possibilities are huge, so that each case must be individualized. The new class III antiarrhythmics are very effective, but have a relatively high rate of side effects including torsade de pointes. Anticoagulation should be the preferred treatment among the majority of patients, but each case should be individually evaluated. New therapies such as focal or linear catheter ablation techniques, atrial or biatrial programmed stimulation, and atrial cardioverter-defibrillator need longer follow-up and experience to be objectively evaluated, although there are reasons to be optimistic in the future, even if patients need antiarrhythmic support at present. Surgery has high morbi-mortality rates, so it is not the preferred approach.