Sudden cardiac arrest is a leading cause of cardiovasculardeath. In the last ten days, I encountered two cases of out-of-hospital cardiac arrest; the first was a 28-year-old on 25 mg olanzapine and the second was a 70-year-old post-bypass. In the first case the PM 2.5 levels were > 300 in the preceding few days and in the second case the PM 2.5 levels were > 400 in the preceding two days.I request all our readers to share all cases of sudden out-of-hospital card
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Sudden cardiac arrest is a leading cause of cardiovasculardeath. In the last ten days, I encountered two cases of out-of-hospital cardiac arrest; the first was a 28-year-old on 25 mg olanzapine and the second was a 70-year-old post-bypass. In the first case the PM 2.5 levels were > 300 in the preceding few days and in the second case the PM 2.5 levels were > 400 in the preceding two days.
I request all our readers to share all cases of sudden out-of-hospital cardiac arrest. There may be more such cases, which were considered as routine deaths. However, I am convinced that the reason is air pollution.
Here is why:
This study identified out-of-hospital cardiac arrest (OHCA) cases that occurred in Seoul between 2006 and 2013 from the nationwide emergency medical service database. The association of the daily incidence of OHCA with airpollutants including PM2.5 (particles ≤ 2.5 μm), PM10, CO, O3, NO2, and SO2 was analyzed. A total of 21,509 OHCAs of presumed cardiac origin were identified. An elevation in PM2.5 by 10 μg/m3at a moving average of lag 1 and 2 days was shown to increase the risk of OHCA by 1.30%. An exposure-response relationship was present: the risk of OHCA increased significantly with even a mild elevation of PM2.5 (10-15 μg/m3) and further increased with higher levels. While PM10, NO2, CO, and SO2 also showed significant associations with OHCA in single-pollutant models, only PM2.5 remained significant after adjustment for other pollutants. Subgroup analyses showed male sex, advanced age, hypertension, diabetes, heart disease, and history of stroke were risk factors for OHCA in response to elevations in PM2.5. The study concluded that increased ambient levels of PM2.5 were significantly associated with increased risk of OHCA within 1 to 2 days of exposure, which had a dose-response relationship. Subjects with conventional cardiovascular risk factors were more susceptible to harm of PM2.5 (Int J Cardiol.2016;203:1086-92).
A case-crossover study design, at Brigham Young University, USA, was used to analyze ischemic events in 12,865 patients who lived on the Wasatch Front in Utah. Increase in ambient fine particulate pollution PM 2.5 by 10 μg/m3 was associated with increased risk of acute ischemic coronary events (unstable angina and myocardial infarction) equal to 4.5%. Effects were larger for those with angiographically-demonstrated coronary artery disease (Circulation. 2006;114(23):2443).
Relative risks (RRs) and 95% CIs were calculated for each increment of 10μg/m3 in pollutant concentration, with the exception of carbon monoxide, for which an increase of 1 mg/m3 was considered. After a detailed screening of 117 studies, 34 studies were identified. All the main air pollutants, with the exception of ozone, were significantly associated with an increase in heart attack risk (carbon monoxide, nitrogen dioxide, sulfur dioxide, PM10 and PM2.5: 1.025. (JAMA. 2012;307(7):713).
All heart patients with underlying blockages or patients with arrhythmias should consult their doctors for risk modification in conditions of high pollution levels.
Dr KK Aggarwal
Padma Shri Awardee
President Elect Confederation of Medical Associations in Asia and Oceania (CMAAO)