Cold Exposure and Ischemic Heart Disease

Abstract

Exposure to cold causes a vasoconstriction and a tachycardia, both resulting in a rise of blood pressure and cardiac work. This last effect may have a deleterious influence on people suffering from ischaemic heart disease (IHD). Moreover, coronary artery spasm could occur if vasoconstriction extends to the heart vessels. Epidemiologic studies have shown that mortality from IHD was correlated to the ambient temperature. There will be more deaths per day in the winter, and fewer in the summer. However, the daily number of deaths also increases during the heat waves. During a cold test, the coronary blood flow remains normal or slightly increased in normal subject. There is never a coronary artery spasm. Subjects who suffer from angina but have normal coronary arteries behave in the same way as normal subjects. Patients with IHD show a decrease in coronary blood flow. In a few cases, those patients may exhibit a coronary spasm with chest pain and even myocardial infarction. It is concluded that people with normal cardiovascular function are unaffected by cold stress whereas those with IHD may be crippled, although rarely, by exposure to cold, especially if they perform a physical work.

Influence of climatic variables on acute myocardial infarction hospital admissions

“…In cold conditions both increased sympathetic nervous activity and greater sodium intake lead to an increase in blood pressure, heart rate, and left ventricular end-diastolic pressure and volume [27][28][29] with, in turn, greater heart oxygen requirement and reduction of ischemic threshold [29] that may be clinically relevant in patients whose coronary circulation is already compromised. There may be also more dramatic events, such as sudden death, due to the increased frequency of cardiac arrhythmias, or, perhaps through rises in blood pressure, abrupt rupture of atherosclerotic plaques [29]. Air temperature, besides, exerts other biological negative effects on haemostasis, rheological factors, lipids, salt intake, alcohol consumption, and body weight gain [30,31].…”

Effects of ambient temperature, humidity, and other meteorological variables on hospital admissions for angina pectoris

“…Different heart and circulation adjustments occur when humans are acutely exposed to low temperatures. The increase in the circulating levels of catecholamines, secondary to thermoreceptor activation, 27 leads to an increase in blood pressure, heart rate, and left ventricular end-diastolic pressure and volume. [27][28][29][30] The increased cardiac work and peripheral resistance contributes to greater heart oxygen consumption and hence a reduction of ischemic threshold, clinically relevant when the coronary circulation is already compromised.…”

“…The increase in the circulating levels of catecholamines, secondary to thermoreceptor activation, 27 leads to an increase in blood pressure, heart rate, and left ventricular end-diastolic pressure and volume. [27][28][29][30] The increased cardiac work and peripheral resistance contributes to greater heart oxygen consumption and hence a reduction of ischemic threshold, clinically relevant when the coronary circulation is already compromised. 28 Finally, cold exerts other biological negative effects on hemostasis, rheological factors, lipids (probably related to hemoconcentration), salt intake, alcohol consumption, and body weight gain.…”

Effects of meteorological parameters on hospital admission for respiratory and cardiovascular diseases

“…Cold temperature causes peripheral vasoconstriction secondary to the activation of cutaneous thermoceptors, which in turn increases blood pressure (Hiramatsu et al 1984). Sympathetic nervous activity is also stimulated under cold conditions, resulting in elevation of blood pressure, heart rate, as well as left ventricular end-diastolic pressure and volume, which leads to greater heart oxygen requirement and reduction of ischemic threshold in patients whose coronary circulation is already compromised (Hiramatsu et al 1984;Houdas et al 1992;Modesti et al 2006).…”