When a myocardial infarction comes out of the not-so-blue air.

Acute coronary syndromes such as unstable angina or myocardial infarction often develop unexpectedly and severely interrupt a patient’s life. Two main pathological processes, atherosclerosis and thrombosis, lead to acute coronary syndromes such as unstable angina and myocardial infarction.1,2 The typical atherosclerotic lesion is a fibrolipid plaque composed of a pool of lipids covered with a connective tissue cap. Although the plaque narrows the coronary arteries, acute coronary syndromes only occur when a plaque erodes, fissures, or ruptures and a thrombus is formed that partially or totally occludes the arteries and impedes blood flow. The sudden onset of the disease has led to research examining triggers of acute coronary syndromes. Among the factors that contribute to acute coronary syndromes in vulnerable patients1,2 are physical exertion, extreme anger, sexual activity, and drug abuse.3 These factors alter the shear stress at the arterial walls and increase the risk of thrombosis. Triggering of myocardial infarction caused by these stressors occurs within 1 or 2 hours of exposure, and the risk subsides rapidly after this time window. This further emphasizes the transient nature of the risks associated with triggers and distinguishes these factors from those risk factors promoting the gradual development of atherosclerosis over decades.