What was done
The authors examined the relationship between temperature and cardiac-related deaths in King County, Washington, USA, over the period 1980-2000 using Poisson regression analysis, based on information provided by the Washington State Department of Health on out-of-hospital deaths of all adults over the age of 54, plus historical meteorological data obtained from the National Climate Data Center for the Seattle-Tacoma International Airport.

What was learned
Cagle and Hubbard determined there were an average of 2.86 cardiac-related deaths per day for all days when the maximum temperature fell within the broad range of 5-30°C. For days with maximum temperatures less than 5°C, however, the death rate rose by 15% to a mean value of 3.30, while for days with maximum temperatures greater than 30°C death rates rose not at all, actually dropping by 3% to a mean value of 2.78. In addition, they found that "the observed association between temperature and death rate is not due to confounding by other meteorological variables," and they learned that "temperature continues to be statistically significantly associated with death rate even at a 5-day time lag."

What it means
Very simply, cold kills; and it is generally much more effective in doing its deadly work than is heat. So how does it do it?

Cagle and Hubbard mention a number of human haematological changes that occur upon exposure to cold, including a decrease in blood plasma volume (Bass and Henschel, 1956; Chen and Chien, 1977; Fregley, 1982; Collins et al., 1985) that is accompanied by "a sympathetic nervous system reflex response to cold-induced stress (LeBlanc et al., 1978; Collins et al., 1985; LeBlanc, 1992)," as well as "an increase in packed cell volume due to increased numbers of red cells per unit volume (Keatinge et al., 1984), increased platelet counts and platelet volume (Finkel and Cumming, 1965; Keatinge et al., 1984), increased whole blood viscosity (Keatinge et al., 1984), increased serum lipid levels (Keatinge et al., 1984; Woodhouse et al., 1993; Neild et al., 1994), and increased plasma fibrinogen and factor VII clotting activity values (Keatinge et al., 1984; Woodhouse et al., 1994)." These various haemodynamic and vasoconstrictive factors combine, in their words, "to produce what Muller et al. (1994) refer to as 'acute risk factors' that may trigger a cardiac event." Vasoconstriction and concomitant increases in central blood volume and systolic blood pressure, for example, "put additional workload on the heart which may lead to increased arrhythmias (Amsterdam et al., 1987), decreased thresholds for angina and abnormal myocardial contractions (De Lorenzo et al., 1999) as well as increasing the risk of dislodging a vulnerable plaque which could lead to thrombosis (Muller et al., 1994)," which "may occur through increased cardiac filling pressure and stroke volume which in turn increases cardiac oxygen requirements while lessening cardiac access to oxygen (Muza et al., 1988; De Lorenzo et al., 1999)." In addition, the Washington researchers report that "greater blood viscosity also works to increase the load on the heart through greater resistance to flow (Frisancho, 1993) and increasing blood pressure (Keatinge et al., 1984)."

References
Amsterdam, E.A., Laslett, L. and Holly, R. 1987. Exercise and sudden death. Cardiology Clinics 5: 337-343.

Bass, D.E. and Henschel, A. 1956. Responses of body fluid compartments to heat and cold. Physiology Review 36: 128-144.

Chen, R.Y.Z. and Chien, S. 1977. Plasma volume, red cell volume and thoracic duct lymph flow in hypothermia. American Journal of Physiology 233: 605-612.

Collins, K.J., Easton, J.C., Belfield, H.-Smith, Exton, A.N.-Smith and Pluck, R.A. 1985. Effects of age on body temperature and blood pressure in cold environments. Clinical Science 69: 465-470.

De Lorenzo, F., Kadziola, Z., Mukherjee, M., Saba, N. and Kakkar, V.V. 1999. Haemodynamic responses and changes of haemostatic risk factors in cold-adapted humans. Quarterly Journal of Medicine 92: 509-513.

Finkel, A. and Cumming, G.R. 1965. Effects of exercise in the cold on blood clotting and platelets. Journal of Applied Physiology 20: 423-424.

Fregley, M.J. 1982. Water and electrolyte balance during exposure to cold. Pharmacology and Therapeutics 18: 199-231.

Frisancho, A.R. 1993. Human Adaptation and Accommodation. University of Michigan Press, Ann Arbor, Michigan, USA.

Keatinge, W.R., Coleshaw, S.R., Cotter, F., Mattock, M.B., Murphy, M. and Chelliah, R. 1984. Increases in platelet and red cell counts, blood viscosity and arterial pressure during mild surface cooling: Factors in mortality from coronary and cerebral thrombosis in winter. British Medical Journal 289: 1405-1408.

LeBlanc, J. 1992. Mechanisms of adaptation to cold. Journal of Sports Medicine 13: S169-S172.

LeBlanc, J., Cote, J., Dulac, S. and Dulong, F.-Turcot. 1978. Effects of age, sex and physical fitness on responses to local cooling. Journal of Applied Physiology 44: 813-817.

Muller, J.E. and Mangel, B. 1994. Circadian variation and triggers of cardiovascular disease. Cardiology 85(Supplement 2): 3-10.

Muza, S.R., Young, A.J., Sawka, M.N., Bogart, J.E. and Pandolf, K.B. 1988. Respiratory and cardiovascular responses to cold stress following repeated cold water immersion. Undersea Biomedical Research 15: 165-178.

Neild, P.J., Syndercombe-Court, D., Keatinge, W.R., Donaldson, G.C., Mattock, M. and Caunce, M. 1994. Cold-induced increases in erythrocyte count, plasma cholesterol and plasma fibrinogen of elderly people without a comparable rise in protein C or factor X. Clinical Science (London) 86: 43-48.

Woodhouse, P.R., Khaw, K.T. and Plummer, M. 1993. Seasonal variation of serum lipids in an elderly population. Age and Ageing 22: 273-278.