The principal findings of the present study were as follows. Firstly, AMI deaths were seasonal, with the maximum mortality recorded in winter and the minimum in summer. Secondly, the observed seasonal variation of AMI deaths originated almost exclusively in the seasonal variation of AMI deaths in the elderly. Thirdly, the average mean temperature of the preceding seven days was the most powerfully associated (highest R2) with daily AMI deaths. Lastly, monthly mean relative humidity values were independently correlated with monthly AMI deaths. Most studies of the relationship of climatic variables to mortality have used “cardiovascular mortality” or “ischaemic heart disease mortality” as end points, not providing data as to the specific causes of cardiovascular death (such as AMI, other coronary syndromes, embolisms and strokes). Our study used a much harder diagnosis as cause of death: AMI has well‐defined diagnostic criteria and is usually readily recognised and adequately documented, whereas cardiovascular mortality leaves more room for misclassifications.
Athens is a metropolitan city with a temperate Mediterranean climate, with mild winters and long, hot summers. Our findings of increased cardiovascular mortality during winter months are in accordance with most of the previously published studies.1,2,3,4,5,6,7,8,9,10
Winter mean daily AMI deaths were 31.8% higher than in summer, a figure strikingly similar to those previously reported: Kloner et al7
reported 33% higher death rates from coronary artery disease in winter, van Rossum et al9
recorded a 27% difference in death rates from ischaemic heart disease between January and July, and the Second National Registry of Myocardial Infarction survey reported 28–43% (depending on the geographical area) more AMIs in winter.22
In our study, this temporal variation mostly concerned older people, as the difference between summer and winter was most pronounced for people older than 70 years and much less notable for younger people.
We found that the temperature–AMI mortality relation is U‐shaped, indicating that, as temperature increases, the number of daily deaths declines, reaching a minimum corresponding to 23.3°C, then beginning to increase as the temperature rises. This finding agrees with previous reports.18,20,23,24
The finding that the average of the mean daily temperatures of the preceding seven days was the best predictor of daily mortality suggests that temperature has a cumulative physiological effect, which indicates that consecutive days of low or high temperatures have more prominent an impact on AMI mortality than the mean temperature of a single day. The finding of a relative increase of AMI mortality during hot weather may indicate that, despite the efforts of the authorities to provide air‐conditioned areas especially for older people on hot summer days, high temperatures still take their toll on older people.
The physiological mechanisms underlying the relationship between cold weather and cardiovascular events seem to be multifaceted. From a haemodynamic point of view, the stimulation of skin thermoreceptors results, through an increase in sympathetic activity and rise of plasma catecholamine concentrations, in peripheral vasoconstriction, tachycardia and increased blood pressure,25,26
thus raising cardiac workload. In addition to these haemodynamic alterations, plasma fibrinogen and factor VIIc activity levels are higher in winter,27
possibly indicating a cold‐related hypercoagulable state, which favours thrombotic phenomena.28
These responses to low temperatures probably constitute a substantial part of the pathophysiological interactions leading to increased rates of cardiovascular deaths in winter. Less studied is the relationship between high temperatures and cardiovascular mortality.
The relationship of ambient humidity to cardiovascular morbidity is unclear. Schwartz et al
in a study across 12 US cities, found no consistent relationship between ambient humidity and hospital admissions for cardiovascular diseases. On the other hand, Panagiotakos et al
in a study of emergency room admissions for non‐fatal acute coronary syndromes in the Athens area, found a correlation with relative humidity. To the best of our knowledge, the present study is the first to identify a relationship between relative humidity and AMI deaths. This relationship between monthly mean values of relative humidity and monthly AMI death rates was the only statistically important one in the regression model to which temperature and atmospheric pressure parameters were added. The biological substrate of this relationship is unclear. In temperate climates with less pronounced winter–summer temperature differences, relative humidity possibly has a more influential effect on cardiovascular mortality than that previously recognised. That this correlation is evident only in the monthly analysis of the data may suggest that the impact of relative humidity on AMI mortality is exerted over a broader range of time than that of temperature. More studies are needed to verify these findings and, possibly, affirm the relatively strong association between excess environmental humidity and cardiovascular mortality.
As far as atmospheric pressure is concerned, our data did not show any significant correlation with AMI deaths, contrary to the previous report of the World Health Organization MONICA (MONitoring trends and determinants In CArdiovascular disease) project in Lille,15
which described a U‐shaped relationship between atmospheric pressure and myocardial infarction incidence and mortality. This study was performed in a city with climatic conditions substantially different from those in Athens (Lille has a humid oceanic climate, as opposed to the dry Mediterranean climate of Athens), which may account for this difference in observations; however, this point deserves further research.
The findings of the present study, regarding the effects of ambient temperature on the day‐to‐day data and relative humidity on the monthly data, do not imply that these atmospheric variables are solely responsible for the observed seasonal distribution of AMI deaths. Such studies cannot plausibly account for other possible causes of seasonality, such as variations in physical exercise and eating habits. The markedly high incidence of AMI deaths in December, for example, may be partly attributable to the “Merry Christmas Coronary” phenomenon, as eloquently put by Kloner29
—that is, a constellation of circumstances, ranging from delay in seeking medical help, to overeating, overdrinking and increased emotional stress associated with the holiday period, that, combined, lead to increased cardiac mortality at that time of year.30
However, we believe that such specific circumstances cannot fully account for the pronounced seasonality of cardiovascular mortality and morbidity. In the case of the holiday period, for example, one would expect a similar peak, or at least a local maximum, in AMI deaths at the time of the Easter holidays (in April), which in Greece is celebrated with even more indulgence than Christmas and is associated with all the factors suggested to be responsible for the “Merry Christmas Coronary” phenomenon, apart from the weather conditions. We did not observe such a peak in the present study.
Our study did not assess atmospheric pollution variables, which may influence cardiovascular mortality in a seasonal manner (air pollution in Athens is heavier in winter than in summer31
). However, although associations of various air pollution determinants with cardiovascular mortality32,33
have been found, there is no established relationship to AMI deaths. In addition, in the largest surveys in this field, the authors do not report including air pollution in their analysis as a confounder.15,19
Moreover, it should be noted that among the numerous air pollutants, particulate matter (PM) (and more specifically the finest of airborne particles: PM10 and PM2.5—that is, particles with an aerodynamic diameter of less than 10 μm and 2.5 μm, respectively) has been shown to be the most significant pollutant associated with acute cardiovascular events.34,35,36
In fact, a large study of several US cities reported that airborne particles were the only air pollutant that independently affected daily deaths.37
It has also been shown that in Athens, although total PM mass varies significantly between seasons, the differences in PM10 and PM2.5 between summer and winter are very small.38
It is thus reasonable to suggest that their effect on AMI deaths should not have important seasonal variation.
Another possible confounder that we were not able to control for was influenza epidemics. However, an increase in temperature was associated with an increase in AMI deaths (U‐shaped curve) in periods of the year not associated with influenza (July and August), possibly indicating that the observed seasonality of AMI deaths is not totally attributable to influenza infections. Still, this constitutes a true limitation of our analysis.
The finding that the number of AMI deaths among the elderly was in December more than twofold the number in June indicates that educating the population of senior citizens about the hazards of exposure to cold is inadequate. It may also suggest that, although Athens is a modern city with mostly adequate housing and heating installations, unsatisfactory provisions for these factors for the elderly may be an issue. The relative increase in AMI deaths with higher temperatures in the summer (the right arm of the U shape of the AMI deaths–temperature curve; fig 3), observed in a quite temperate summer for Athens (maximum daily temperature did not exceed 39°C), suggests that a more effective policy of civil protection during hot weather is necessary. Lastly, including the association of relative humidity with AMI mortality may be necessary in healthcare and civil protection planning.