Introduction
It is known that acute cardiovascular events can be triggered by external factors among susceptible individuals. Previous studies have shown an increased risk of acute cardiac events following psychosocial and environmental triggers such as warfare, national sporting events and natural disasters. Earthquakes are well documented to cause cardiac complications. This topic is perhaps the hardest to study due to the unpredictable nature of the disaster. Often, severe destruction of the infrastructure and medical facilities hinders stringent study methodology. Christchurch, New Zealand, was struck by 2 major earthquakes at 4:36am on 4 September 2010, magnitude 7.1 and at 12:51pm on 22 February 2011, magnitude 6.3. Both events caused widespread destruction. Christchurch Hospital, the region’s only acute care hospital, was fortunate to have escaped major damage. It remained functional following both earthquakes. We sought to examine thoroughly the effects of the 2 earthquakes on acute cardiac presentations and their sequelae. We hypothesised that there would be an increase in overall chest pain admission, a surge of acute myocardial infarction and stress cardiomyopathy cases and that major earthquakes of different intensity, occurring at different times of the day would result in different cardiovascular presentation patterns.
Methods
Patients admitted under Cardiology in Christchurch Hospital 3 weeks prior to and 5 weeks following both earthquakes were analysed, with corresponding control periods in September 2009 and February 2010. Patients were categorised based on diagnosis: ST elevation myocardial infarction, Non ST elevation myocardial infarction, stress cardiomyopathy, unstable angina, stable angina, non-cardiac chest pain, arrhythmia and other. A sub-group analysis as well as a follow up study at 12 months was done for patients who presented with stress cardiomyopathy following the February 2011 earthquake.
Results
In the first 2 weeks following the early morning September earthquake, there was a significant increase in overall cardiovascular admissions (mean 75 admissions per week during the control periods, 120 admissions in week 1 and 100 admissions in week 2, p=0.003), ST elevation myocardial infarction (mean 5 cases per week during the control periods, 9 cases in week 1 and 11 cases in week 2, p=0.016), and non-cardiac chest pain (mean 29 cases per week during the control periods, 46 cases in week 1 and 36 cases in week 2, p=0.022). This pattern was not seen after the early afternoon February earthquake. Instead, there was a very large number of stress cardiomyopathy admissions with 21 cases (95% CI 2.6-6.4) in 4 days compared to only 6 stress cardiomyopathy cases after the first earthquake (95% CI 0.44 – 2.62; p<0.05). At 12 months, a follow-up study of the 21 patients with stress cardiomyopathy triggered by the second earthquake showed 100% survival rate with the majority free from cardiovascular, other medical or psychological sequelae.
Conclusion
The early morning September 2010 earthquake triggered a large increase in ST elevation myocardial infarction and a few stress cardiomyopathy cases. The early afternoon February earthquake, although smaller in Richter scale, was far more destructive compared to the first event given its shallow depth and closeness to the city centre. It caused significantly more stress cardiomyopathy in an already vulnerable population that may have been sensitised by the first earthquake. Two major earthquakes of different intensity, occurring at different times differed in their effect on acute cardiac events. Patients who had stress cardiomyopathy as the result of earthquakes had excellent prognosis in the intermediate follow-up period.
