Letter to the Editor Seasonal distribution of acute myocardial infarction: A need for a broader perspective Viktor C ˇ ulic ´ Division of Cardiology, Department of Medicine, University Hospital Split, S ˇ oltanska 1, 21000 Split, Croatia Received 19 March 2005; accepted 26 March 2005 Available online 23 May 2005 To date, a large body of evidence describing seasonal variation in the occurrence of acute myocardial infarction (AMI) has been accumulated [1–3]. In last year’s journal issues, two studies corroborated the seasonal pattern of AMI with a peak incidence in winter [4,5]. The fact that weather may influence the occurrence of AMI by causing a higher incidence during the winter period has been mainly attributed to cold exposure, an external trigger of sympathetic triggering pattern [6,7], and more frequent respiratory infections [5]. In his commentary, Cheng noted that investigations of seasonal distribution should take meteorological parameters into consideration [8]. Various kinds of meteorological stress have been associated with approximately 4% of AMI onsets [6]. Recently, relative humidity has been found to positively correlate with hospital admissions for acute coronary syndromes [9], and several meteorological conditions have been associated with the likelihood of ventricular tachycar- dia [10]. Weather-associated factors assuredly are related in a multifaceted way to the seasonal pattern of AMI with differing effects from climate to climate. A major shortcoming of the investigations concerning seasonal distribution of AMI is that the available method- ology does not permit control for a large number of endogenous and exogenous factors. Undoubtedly, there are multiple interfering relations among such factors and the key question is: What do we actually detect through the distribution of AMI? There are two additional possibilities that have not as yet been fully explored. One possibility is the existence of a variation of plaque vulnerability throughout the year. In that case, regardless of the occurrence of external triggers, the likelihood of interaction between the vulnerable plaques and externally provoked internal triggering mechanisms would be higher in wintertime. Recent evidence on seasonal variability in cholesterol levels may support such a hypothesis [11,12]. Another possibility is that there is an independent seasonal rhythm of external triggers, and that seasonal distribution of AMI mainly results from concentration or superimposition of triggering circumstances that may occur in winter. Although elevated concentrations of fine particle air pollutants have been described to transiently elevate the risk of AMI [13], the contributory role of air pollution in the seasonal distribution of AMI and possible interactions with other triggers remain unknown. The phenomenon called ‘‘seasonality’’ may also contrib- ute to the seasonal distribution of AMI [14]. One aspect of seasonality is winter depression, characterized by anxiety, social withdrawal, sadness, sleep disturbances, irritability, and decreased activity and libido. Such psychological factors have been associated with the progression of cardiovascular diseases [15,16]. In contrast to that, nonde- pressed periods are summer and spring. Another aspect of seasonality is changes in appetite and food preferences [15] and may partly underlie the reason for higher cholesterol levels during winter. An unequal seasonal distribution of AMI has been described in different subgroups of the same population [3,5], suggesting some biological variations due to racial or genetic differences, or that some cultural, religious, and lifestyle factors may be involved. Moreover, it has been proposed that individual characteristics may predispose to AMI onset triggered by different external triggers through diverse internal triggering mechanisms [6,7,17,18]. At the 0167-5273/$ - see front matter D 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2005.03.074 E-mail address: viktor.culic@st.htnet.hr. International Journal of Cardiology 109 (2006) 265 – 266 www.elsevier.com/locate/ijcard