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Important Associations between Temperature and Cardiovascular Death
Two large epidemiologic studies have confirmed a significant link between cold weather and higher incidence of heart attacks. Numerous prior studies have looked at associations between climate and mortality rates, and there is a clear trend of increased cardiovascular mortality during cold weather especially when abrupt reductions in outdoor temperatures occur. Why?
Temperature has a profound, direct effect on the viscosity of blood. A good rule of thumb is: Each 1°C reduction in temperature causes the viscosity of blood to increase by about 2 percent. Blood viscosity is an emerging cardiovascular risk factor, which is highly sensitive to cold temperatures and explains the increased cardiovascular risk during the winter months. Marc Claeys, the cardiovascular researcher at the University of Antwerp in Belgium who led an authoritative study analyzing data from 107,090 European participants, said, “Increased platelet aggregation and blood viscosity during cold exposure promotes thrombosis and clot formation.”1
Epidemiologic Studies of Seasonal Temperatures and Cardiovascular Risk
Winter cold brings with it a higher incidence of death, and cardiovascular death accounts for between 50 to 70% of excess deaths in winter months.2 Separately, hospitalization rates and admissions due to myocardial infarction (MI) have both been linked to lower temperatures. An observational study of 259,891 total acute MI cases in the second National Registry of Myocardial Infarction study showed a 53% increase in acute MI during winter months when compared to summer months.3
A prior study of 1,217 MI cases, conducted in India and published in the International Journal of Cardiology, showed a significantly higher rate of MI when air-temperatures were 16°C (60.8°F) or less (p<0.001).4 Indeed, MI has been shown to occur more frequently on colder days, regardless of the season. A large analysis of mortality data in 50 U.S. cities from 1989 to 2000, covering nearly 8 million total deaths, showed a higher overall risk of cardiovascular deaths (OR = 1.053; 95% CI, 1.036-1.070) and heart attack deaths (OR = 1.137; 95% CI, 1.051-1.230) on extremely cold days.
Extremely hot temperatures, on the other hand, are also associated with increased hospitalizations and health-related issues, but importantly, these increased adverse events were only linked to a marginal increase in mortality and only in patients with existing atrial fibrillation (OR = 1.059; 95%, 0.996-1.125).5
An analysis of approximately 24,000 sudden adult deaths in from 1987-1991 in West Berlin showed an 18.7% relative increase in sudden death during winter months than in summer months.6 This effect was most pronounced in patients older than 65 years, a population known to be at risk for many health complications, especially cardiovascular and cerebrovascular diseases (see Blood Thickens as You Get Older).
Despite numerous advances in treatment and prevention of cardiovascular events, cold-related cardiovascular deaths in elderly Americans at high risk of sudden cardiac death have remained steady, while heat-related cardiovascular deaths have been steadily declining. 7 It is therefore helpful to investigate and understand the physiological alterations which contribute to sudden cold-related cardiac death.
Etiologic Perspective on Increased Cardiovascular Death in Winter Cold
Microcirculatory blood flow is governed by perfusion pressure, vessel radius and length, and blood viscosity. Of these parameters, blood viscosity is by far the most sensitive to temperature. An earlier benchmark study funded by the National Institutes of Health and the Maine Heart Association demonstrated that when the temperature of blood is decreased from 37°C to 22°C, blood viscosity increases as a direct result by 50 to 300%.8 It is helpful to remember that while each 1°C reduction in temperature causes the viscosity of blood to increase by about 2 percent, this is just a rule of thumb that applies to normal high-shear blood viscosity. At vulnerable low-shear flow regimes, as experienced at the tissue and organ level of the microvasculature, blood viscosity increases exponentially with colder temperatures.
In addition to the direct modulation of blood viscosity by temperature, cold-induced shunting of blood further increases blood viscosity, amplifying the hyperviscosity surge caused by cold temperature. When the body is exposed to temperatures cold enough to induce shivering, blood supply is shunted from the skin to internal organs. In doing so, heat loss from the skin is minimized while essential physiological functions are initially preserved. This process causes about 1 liter of blood to shunt towards central organs, overloading them with volume.9
The kidneys respond by removing water and salt from the blood via urine. Other excess volume is distributed to intercellular fluids. As a result of these fluid shifts alone, blood concentration increases by about 10%. Consequently, blood viscosity increases by about 20% with mild surface-cooling, enough to reduce core body temperature by about 0.4°C.9,10 Platelets have also shown increased activity, paralleling blood viscosity surges, when temperature decreases below normothermic levels.11 These blood viscosity changes are cumulative.
Increased blood pressure, respiratory infections, indoor temperature changes, age-related decline in health, dietary shifts, sedentary behaviors, indoor living conditions, socioeconomic factors, and changes in blood composition have all been researched as potential explanations and as co-variates for increased cardiovascular risk in colder climates. The highest cold-induced cardiovascular risk exists just hours or days after exposure to cold. 11
Cold temperatures induce vasoconstriction of the myocardium and peripheral vessels, resulting in increased blood flow velocities, however these narrower vessels also become more prone to frictional forces and vascular resistance.12 Healthy individuals are capable of adapting to these changes while many people with underlying health conditions as well as the elderly are less capable.
Case Scenario: Risk of Sudden Cardiac Death in Triathlons
Cold-induced blood viscosity surges help to explain the elevated risk of sudden heart attacks during the swimming portion of triathlons. According to an investigation published by USA Triathlon, the governing body for triathlon competitions in the U.S., 31 of 45 total triathlon deaths between 2003 and 2011 occurred during the swimming segment.13 These deaths were all due to cardiac failure.
Despite the fact that these deaths are relatively rare, clinical scientists, athletes, and sports enthusiasts alike are becoming increasingly concerned about the potential for increased risk of death during this portion of triathlon events. Why would athletes who have trained so long and hard for such an event experience a life-threatening problem only during one specific portion of the event?
A perfect storm of cold-shock, constricted blood vessels, shunting of blood, increased myocardial demand, tight wetsuits placing burden on arteries of the chest, and stress-induced release of catecholamines all contribute to this phenomenon. Blood viscosity levels are very sensitive to changes in temperature, and blood viscosity surges can explain how all of these contributing factors translate into increased risk for sudden cardiac death in triathlon swims.
In addition, increased red blood cell count, cholesterol, and fibrinogen have all been shown to elevate in the cold.9 These factors also contribute directly to blood viscosity. When the body is exposed to colder temperatures than it is acutely adapted to deal with, normal homeostatic mechanisms are initiated to protect the body from excessive stress. Healthy individuals are able to adapt to the cold, however the risk of a cold-induced hyperviscosity surge in the blood is higher in the elderly.
Certain athletes, such as those who compete in triathlons, provide unique opportunity to deepen our understanding of the cardiac risks of temperature. Blood viscosity screening and monitoring may provide additional clinical insight for identifying individuals who are predisposed to higher risk of cold-induced cardiac death.
1. Huffington Post. Cold Weather Linked with Heart Risk Factors, Heart Attack, in New Studies. 2013. http://www.huffingtonpost.com/2013/09/07/cold-weather-heart-attack-risk-factors_n_3861519.html. Accessed September 8, 2013.
3. Spencer FA, Goldberg RJ, Becker RC, Gore JM. Seasonal Distribution of Acute Myocardial Infarction in the Second National Registry of Myocardial Infarction 1. Journal of the American College of Cardiology. 1998;31(6):1226-1233.
5. Medina-Ramón M, Zanobetti A, Cavanagh DP, Schwartz J. Extreme temperatures and mortality: assessing effect modification by personal characteristics and specific cause of death in a multi-city case-only analysis. Environmental Health Perspectives.2006;114(9):1331.
6. Arntz H-R, Willich S, Schreiber C, Brüggemann T, Stern R, Schultheiß H-P. Diurnal, weekly and seasonal variation of sudden death. Population-based analysis of 24061 consecutive cases. European heart journal. 2000;21(4):315-320.
9. Keatinge WR, Coleshaw SR, Easton JC, Cotter F, Mattock MB, Chelliah R. Increased platelet and red cell counts, blood viscosity, and plasma cholesterol levels during heat stress, and mortality from coronary and cerebral thrombosis. The American journal of medicine. Nov 1986;81(5):795-800.
10. Keatinge WR, Coleshaw SR, Cotter F, Mattock M, Murphy M, Chelliah R. 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. Br Med J (Clin Res Ed). Nov 24 1984;289(6456):1405-1408.
13. USA Triathlon. USA Triathlon Fatal Incidents Study, 2012. Colorado Springs, CO. Retrieved from:http://www.usatriathlon.org/~/media/d0cc25327b574798934fca3366270f12.ashx.