Marchant B, Donaldson G, Mridha K, Scarborough M, Timmis A D
Department of Cardiology, London Chest Hospital, England, United Kingdom.
J Am Coll Cardiol. 1994 Mar 1;23(3):630-6. doi: 10.1016/0735-1097(94)90747-1.
Patients with angina often report that symptoms are worse in cold weather. This study was designed to determine differences between cold-tolerant and cold-intolerant patients in the hemodynamic and ischemic response to exercise at cold temperatures and to assess the role of catecholamines and baroreceptor function.
Studies have suggested that the heart rate response may differ at cold temperatures, but the mechanism and role of this variation have not been examined.
Seven cold-intolerant and seven cold-tolerant patients with angina underwent exercise treadmill testing at 6 and 25 degrees C with measurement of catecholamines. Baroreceptor function was assessed by the decrease in systolic blood pressure after patients stood up from the supine position.
Norepinephrine levels increased by 139% in the cold environment, but there were no differences between cold-intolerant and cold-tolerant patients. Consequently, blood pressure was higher in the cold environment in all patients, but the heart rate response was similar. However, cold-intolerant patients had a steeper heart rate response in the cold and developed ischemia (mean [+/- SEM] 201 +/- 58 vs. 242 +/- 50 s, p = 0.05) and angina (348 +/- 87 vs. 449 +/- 60 s, p = 0.04) earlier in the cold environment, a difference not seen in the cold-tolerant patients. Baroreceptor function was impaired in cold-intolerant patients (decrease in systolic blood pressure after patients stood up from the supine position 19 +/- 7 vs. 0 +/- 4 mm Hg, p = 0.04).
Exposure to cold causes an increase in blood pressure with an associated increase in myocardial oxygen demand in all patients. In cold-tolerant patients, this increase may be offset by a reduction in heart rate if baroreceptor function is normal. If baroreceptor function is abnormal, heart rate may not decrease in response to a cold-induced increase in blood pressure. This mechanism may account for some of the variability in tolerance to cold exposure that affects patients with exertional angina.
心绞痛患者常报告症状在寒冷天气时加重。本研究旨在确定耐寒和不耐寒患者在寒冷温度下运动时的血流动力学和缺血反应差异,并评估儿茶酚胺和压力感受器功能的作用。
研究表明,心率反应在寒冷温度下可能有所不同,但这种变化的机制和作用尚未得到研究。
7名不耐寒和7名耐寒的心绞痛患者在6℃和25℃下进行运动平板试验,并测量儿茶酚胺。通过患者从仰卧位站立后收缩压的下降来评估压力感受器功能。
在寒冷环境中,去甲肾上腺素水平升高了139%,但不耐寒和耐寒患者之间没有差异。因此,所有患者在寒冷环境中的血压都较高,但心率反应相似。然而,不耐寒患者在寒冷环境中心率反应更陡峭,更早出现缺血(平均[±标准误]201±58秒对242±50秒,p = 0.05)和心绞痛(348±87秒对449±60秒,p = 0.04),耐寒患者未出现这种差异。不耐寒患者的压力感受器功能受损(患者从仰卧位站立后收缩压下降19±7毫米汞柱对0±4毫米汞柱,p = 0.04)。
暴露于寒冷会导致所有患者血压升高,同时心肌需氧量增加。在耐寒患者中,如果压力感受器功能正常,这种升高可能会被心率降低所抵消。如果压力感受器功能异常,心率可能不会因寒冷引起的血压升高而降低。这种机制可能解释了影响劳力性心绞痛患者对寒冷暴露耐受性差异的部分原因。