Angina in cold environment. Reactions to exercise.

Abstract

SUMMARY Seventeen male patients with angina pectoris, and a history of increased severity of angina in the cold, performed submaximal bicycle exercise tests in a normal (20°C) and a cold environment (-10°C, 2-2 m/s wind velocity) wearing standardised clothing. Observations were made during and after serial short-term exercise periods each starting at 50 W, with continuous load increase of 10 to 30 W per minute, separated by 30-minute rest intervals.In the group as a whole, maximal work load decreased by 7 per cent during exposure to cold. Heart rate, systolic blood pressure, and rate-pressure product were significantly higher during submaximal exercise in the cold, but at maximal work load there was no difference in heart rate, rate-pressure product, or magnitude of ST segment depression. The decrease in maximal work load exceeded 5 per cent (mean 11%) in 10 patients, who were described as cold-susceptible, while the decrease averaged 1 per cent in the seven non-susceptible patients. The cold-induced reduction in maximal work load showed a significant correlation with the increase in heart rate, blood pressure, and rate-pressure product during submaximal exercise.After exercise, heart rate was significantly lower and blood pressure and rate-pressure product significantly higher in the cold than at normal temperature in all patients. In cold-susceptible patients, blood pressure was significantly higher at two and four minutes after exercise, and rate-pressure product at two minutes after exercise, than in non-susceptible patients, but in spite of this angina disappeared more quickly in cold-susceptible patients.In conclusion, subjective cold intolerance was objectively demonstrated in 10 out of 17 patients with angina pectoris, by exercise in a room at -10°C. Susceptibility to cold was explained by a higher heart rate and blood pressure during exercise in the cold room, than during exercise in the room at normal temperature.Patients with angina pectoris often experience a worsening of their symptoms in cold weather. The physiological explanation of this has been said to be the earlier appearance of myocardial oxygen deficit during exercise in the cold, which may be caused by increased work done by the heart (Epstein et al., 1969), by nervous reflexes to the heart causing coronary vasoconstriction (Freedberg er al., 1944;Mudge et al., 1976), by release of sympatheticoadrenal hormones (Wilkerson et al., 1974), or by cooling of the blood in the heart chambers and coronary arteries (Leon et al., 1970 low exercise tolerance are most affected, because of a relatively greater decrease in work performance. This conclusion was based on studies at rest, and there has been no study of the effects of cold on angina during exercise. We therefore studied the effects of exposure to cold on effort angina during standardised conditions, in order to see whether cold intolerance could be explained by changes which could be measured non-invasively. SubjectsA questionnaire about the relation of their symptoms to cold was given to 50...

Exposure to extreme cold lowers the ischemic threshold in coronary artery disease patients

“…Early studies attributed cold-induced angina to sympathetic activation, resulting in increased peripheral vascular resistance and blood pressure, and leading to a greater cardiac workload (increased rate-pressure product) for any given exercise intensity (1,10). In the present study, we did not find any significant difference in heart rate or rate-pressure product at any time point between the exercise tests performed at +20°C and at -20°C.…”

“…Despite a lowering of the ischemic threshold, exposure to extreme cold was not associated with a decrease in total exercise time, nor was it associated with any deleterious effects on cardiovascular function including serious ventricular arrhythmias. Previous studies have generally reported a lowering of the ischemic threshold on exposure to cold solely in patients suffering from coldinduced angina, suggesting that individual susceptibilities to cold exist (3,(8)(9)(10)(11). Most of these studies, however, used temperatures ranging from +6°C to -10°C.…”

“…The potentially conflicting results regarding hemodynamic responses to cold may be explained by several factors. First, various cold stimuli have been used, including environmental cold (1,3,10,11,13,14), cold air inhalation (9,12,15), regional cutaneous cold exposure (cold pressure test) (2,8,16,17) or a combination of the above (16,17). It is now understood that the cold pressure test cannot be used to simulate hemodynamic responses during exercise in cold weather because exercise abolishes the abnormal increase in coronary resistance induced by the cold pressure test in CAD patients (18).…”

Exercise-induced myocardial ischemia in a cold environment. Effect of antianginal medications.

“…Lassvik et al,2 in 17 patients whose angina was worsened by cold, found that maximal workload with bicycle exercise was reduced by 7% at -10°C compared with 200 C. Heart rate, systolic arterial pressure, and rate-pressure product were significantly higher in the cold at submaximal exercise but at the onset of angina and at peak workload did not differ from the results at normal temperature. Our finding of a lower rate-pressure product at the onset of ischemia in cold-sensitive patients was not observed by Lassvik et al 2 This discrepancy may be due to differences in patient characteristics or methodology; for example, Lassvik et al reported data at the onset of angina, not the onset of ST depression.…”

Comparison of hot and cold spell effects on ­cardiovascular mortality in individual population groups in the Czech Republic

“…An ecological study comparing CVD risk factors of Czech, German and Israeli middle-aged men (Bobak et al 1999) showed an unfavourable risk profile in Czech men that is related to high blood pressure and elevated levels of fibrinogen, triglycerides and D-dimer, a thromboembolic disease marker reflecting an activation of coagulation and predicting subsequent cardiovascular death (Morange et al 2006). Some underlying cardiovascular diseases (such as angina pectoris, I20) may lead to severe deterioration in health conditions after a sudden change of ambient temperature (from heated interior to very cold outdoor conditions) that may ultimately cause myo cardial ischemia, acute myocardial infarction and sudden death (Lassvik & Areskog 1979, Hong et al 2003. The large effects in middle-aged males compared to females may be related to larger prevalence of CVD in middle-aged males (cf.…”