A catastrophic earthquake could affect the population at all levels. Following an earthquake, as well as human and economic losses, the public health and the rate of cardiovascular diseases (CVDs) can be negatively affected. In the 21^st century, there have been more than 20 earthquakes ranging in intensity from 6 to 9.3.^[1] After the Christchurch, New Zealand, the 2011 earthquake a significant increase in overall cardiovascular events (P = 0.003), ST elevation myocardial infarctions (P = 0.016) and stress cardiomyopathy admissions have been reported.^[2] In the first year, people living in the damaged areas had approximately 10% more cardiovascular hospitalizations.^[3]

Previous studies have showed that the prevalence of acute coronary syndrome, hypertension, heart failure and arrhythmias increase in areas after a high-impact earthquake.^[4-6] The post-traumatic mental stress is the central reason for increasing the risk of CVDs, especially (25% more) in the older population.^[7-9] The onset of acute cardiovascular events following earthquakes has been variable from the first day of the event to weeks and months [Figure 1]. Leor et al.^[10] have reported that there was an increase in sudden cardiac deaths on the day of the Northridge earthquake 1994, compared with the week before and after the earthquake. The 15 minutes after Noto Peninsula earthquake 2007, in Japan, an acute coronary syndrome and 72 h after the event the first case of stroke was reported by Tsuchida et al.^[11]

The pathophysiology of earthquake-related cardiovascular events is suggested to be triggered by the activation of the sympathetic nervous system (SNS), Hypothalamic-pituitary-adrenal (HPA) axis, endothelial dysfunction, abnormal circadian rhythms, increased platelet activation, and vascular thrombosis.^[12] The activation of the SNS and HPA axis cause releasing of catecholamines, corticotrophin hormone and, cortisol. Stress-induced mechanisms and excess hormones releasing lead to the progression of atherosclerosis, most etiology of the mortality.^[13] Stress can also activate the renin-angiotensin system and increase the production of circulating angiotensin II [Figure 2].^[14]

In conclusion, earthquake-induced CVDs are attributed to the abnormalities in the SNS, HPA axis, and neuroendocrine pathways triggered by mental and physical stresses. The rate and duration of the increases in cardiovascular events depend on the levels of earthquake damage, stress and, socio-economic stability.