Meteorological parameters and seasonal variations in pulmonary thromboembolism.
ABSTRACT In recent years, circannual variations in incidence and mortality for venous thromboembolic disease have been demonstrated, with a peak in winter. However, several investigators have observed no seasonal variation in these diseases. The aim of our study was to investigate whether a seasonal variation, in terms of atmospheric pressure, humidity, and temperature, exists for pulmonary thromboembolism.
We retrospectively included 206 patients with a diagnosis of pulmonary embolism (PE) between 1 June 2001 and 31 May 2006.
The highest number of cases in the 5 years concerned occurred in May (29 cases). Although PE occurred most commonly in the spring (72 cases) and autumn (51 cases), the difference was statistically significant (P = .003). There were no case correlations with months and pressure, temperature, or humidity. However, there was a statistically significant positive correlation between case incidence and atmospheric pressure (r = 0.53, P < .0005) and humidity (r = 0.57, P < .0005). In terms of risk factors, seasonal distribution was not statistically significant as regards cases of embolism occurring for surgical or nonsurgical reasons (r = 0.588).
In terms of the relationship between seasons and embolism cases, despite the determination of an insignificant positive correlation, a statistically significant positive correlation was determined between air pressure and humidity and case incidence. There is now a need for further wide-ranging prospective studies including various hematological parameters to clarify the correlation between PE and air pressure.
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ABSTRACT: The occurrence of several adverse cardiovascular events, eg, myocardial infarction and stroke, is not randomly distributed over time, but shows definite seasonal patterns. The temporal pattern for pulmonary embolism (PE) is known, whereas the data concerning deep vein thrombosis (DVT) are not conclusive. The aim of our study was to investigate whether a seasonal variation exists also for DVT, together with the possible influence of different comorbid risk factors. We observed 1164 consecutive cases of DVT at the General Hospital of Ferrara, Italy, from 1998 to 2002. The total sample was divided into subgroups by gender, and by the most common comorbid conditions. For statistical analysis, the distribution of symptom onset was tested for uniformity by the chi 2 test for goodness of fit, and partial Fourier series were used to assess rhythmicity. Seasonal analysis showed a significantly reduced frequency of DVT events in summer and increased in winter, for the total population (p<0.0001), men (p=0.003), women (p=0.007), subjects with PE (p=0.001), and hypertension (p=0.001). Similarly, chronobiological analysis yielded a significant seasonal variation, with a peak in December for the total population (p<0.001), men and women (p<0.001 and p=0.02, respectively), PE (p=0.006), and hypertension (p=0.028). This study shows the existence of a highly significant seasonal pattern in the occurrence of DVT, characterized by a winter peak. Thus, colder months and relative hypercoagulability could be considered a supplementary high risk condition when prescribing an anticoagulant regimen.Medical science monitor: international medical journal of experimental and clinical research 06/2004; 10(5):CR191-6. · 1.36 Impact Factor
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ABSTRACT: Results for biochemical and haematological variables have been correlated with data on atmospheric temperature in order to identify possible mechanisms through which low environmental temperature may increase mortality from myocardial infarction and cerebrovascular disease. With the exception of cholesterol, there were no associations in the case of several clinical chemistry variables, or of haemoglobin and related indices. With varying degrees of consistency among the sex and age groups studied, temperature was positively correlated with factor VII, antithrombin III, and cholesterol, and negatively correlated with fibrinolytic activity. The correlations were all low but may offer some clues to mechanisms whereby air temperature influences ischaemic heart and cerebrovascular disease mortality.Journal of Clinical Pathology 02/1979; 32(1):16-20. · 2.44 Impact Factor
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ABSTRACT: Previous publications have highlighted seasonal variations in the incidence of thrombosis and pulmonary embolism, and that weather patterns can influence these. While medical risk factors for pulmonary thrombo-embolism such as age, obesity, hypercoagulable states, cancer, previous thrombo-embolism, immobility, limb paralysis, surgery, major illness, trauma, hypotension, tachypnoea and right ventricular hypokinesis are not directly implicated regarding environmental factors such as weather, they could be influenced indirectly by these. This would be especially relevant in polluted areas that are associated with a higher pulmonary embolism risk. Routine nuclear medicine lung ventilation/perfusion studies (V/Q scans) of 2071 adult patients referred to the nuclear medicine department of the Royal Surrey County Hospital in Guildford, UK, between January 1998 and October 2002 were reviewed and 316 of these patients were classified as positive for pulmonary embolism with high probability scan on PIOPED criteria. The occurrence of positive scans was compared to environmental factors such as temperature, humidity, vapour pressure, air pressure and rainfall. Multiple linear regression was used to establish the significance of these relations. The incidence of pulmonary embolism was positively related to vapour pressure and rainfall. The most significant relation was to vapour pressure (p=0.010) while rainfall was less significant (p=0.017). There was no significant relation between pulmonary embolism and air pressure, humidity or temperature. It is postulated that rainfall and water vapour may be contributary factors in thrombosis and pulmonary embolism by way of pollutants that are carried as condensation nuclei in micro-droplets of water. In particular, fossil fuel pollutants are implicated as these condensation nuclei. Pollutants may be inhaled by populations exposed to windborne vapour droplets in cities or airports. Polluted vapour droplets may be absorbed by the lung to hasten coagulation cascades in the blood. This may lead to thrombosis and increased pulmonary embolism under high vapour pressure conditions. With combined factors such as pre-existing ill health or immobility on long flights, the risk of thrombosis and consequent embolism might increase substantially.Medical Hypotheses 02/2005; 64(6):1198-201. · 1.05 Impact Factor