Chua T P, Ponikowski P, Webb-Peploe K, Harrington D, Anker S D, Piepoli M, Coats A J
Royal Brompton Hospital, London, U.K.
Eur Heart J. 1997 Mar;18(3):480-6. doi: 10.1093/oxfordjournals.eurheartj.a015269.
The peripheral chemoreflex may be augmented in chronic heart failure and may play a role in its pathophysiology including the mediation of exercise hyperpnoea and sympathetic activation. The objective of this study was to characterize the patients with an augmented peripheral chemoreflex.
Peripheral chemoreflex sensitivity was assessed by measuring the ventilatory response to hypoxia using transient inhalations of pure nitrogen in 50 patients with chronic heart failure (age 58.7 +/- 12.1 (SD) years; radionuclide left ventricular ejection fraction 26.5 +/- 13.0%). The peripheral chemoreflex of 12 healthy controls with similar demographic characteristics was 0.272 +/- 0.201l.min-1.%Sao(2)-1 compared with 0.673 +/- 0.410l. min-1.%Sao(2)-1 (P < 0.0001) in the chronic heart failure patients. Using 2 standard deviations above the mean level of the controls peripheral chemoreflex sensitivity as the upper limit of normal, we defined an augmented chemoreflex as greater than 0.6751.min-1.%Sao(2)-1. Twenty of the chronic heart failure patients (40%) demonstrated such an augmented peripheral chemoreflex. Compared with patients with peripheral chemoreflex sensitivity within the normal range, they had a reduced peak oxygen consumption during cardiopulmonary exercise (15.1 +/- 4.4 vs 18.5 +/- 5.8 ml.kg-1.min-1, P = 0.02), reduced radionuclide left ventricular ejection fraction (21.8 +/- 11.8 vs 29.4 +/- 13.1%, P = 0.046) and were in a worse New York Heart Association functional class (2.8 vs 2.4, P = 0.05). The ventilatory response to exercise, as characterized by the regression slope relating minute ventilation to carbon dioxide output during exercise, was also higher (40.48 +/- 9.32 vs 34.54 +/- 7.19, P = 0.02), consistent with the role of the peripheral chemoreflex in mediating exercise hyperpnoea. There was also an increased proportion of patients with non-sustained ventricular tachycardia in the group with an augmented peripheral chemoreflex (61% vs 21%, chi-squared 7.08, P < 0.01). No difference was seen in the age, height, weight and lung function measurements of these patients compared with the normal chemoreflex group.
An augmented peripheral chemoreflex is a common finding in chronic heart failure patients, one associated with increasing severity and with the exercise hyperpnoea seen in the condition. That there was an excess of patients with non-sustained ventricular tachycardia in the group with an augmented peripheral chemoreflex may be related to the chemoreflex-driven sympathetic stimulation. The peripheral chemoreflex may be important in the pathophysiology of chronic heart failure, both in terms of symptoms and exercise limitation.
慢性心力衰竭时外周化学反射可能增强,且可能在其病理生理过程中发挥作用,包括介导运动性通气过度和交感神经激活。本研究的目的是对具有增强外周化学反射的患者进行特征描述。
通过在50例慢性心力衰竭患者(年龄58.7±12.1(标准差)岁;放射性核素左心室射血分数26.5±13.0%)中使用纯氮短暂吸入测量对低氧的通气反应来评估外周化学反射敏感性。12例具有相似人口统计学特征的健康对照者的外周化学反射为0.272±0.201l·min⁻¹·%Sao₂⁻¹,而慢性心力衰竭患者为0.673±0.410l·min⁻¹·%Sao₂⁻¹(P<0.0001)。以对照者外周化学反射敏感性均值以上2个标准差作为正常上限,我们将增强的化学反射定义为大于0.675l·min⁻¹·%Sao₂⁻¹。20例(40%)慢性心力衰竭患者表现出这种增强的外周化学反射。与外周化学反射敏感性在正常范围内的患者相比,他们在心肺运动期间的峰值耗氧量降低(15.1±4.4 vs 18.5±5.8 ml·kg⁻¹·min⁻¹,P = 0.02),放射性核素左心室射血分数降低(21.8±11.8 vs 29.4±13.1%,P = 0.046),且纽约心脏协会功能分级更差(2.8 vs 2.4,P = 0.05)。运动时的通气反应,以运动期间分钟通气量与二氧化碳排出量的回归斜率表示,也更高(40.48±9.32 vs 34.54±7.19,P = 0.02),这与外周化学反射在介导运动性通气过度中的作用一致。在外周化学反射增强组中,非持续性室性心动过速患者的比例也增加(61% vs 21%,卡方值7.08,P<0.01)。与正常化学反射组相比,这些患者的年龄、身高、体重和肺功能测量值无差异。
增强的外周化学反射在慢性心力衰竭患者中很常见,与病情严重程度增加以及该疾病中出现的运动性通气过度有关。外周化学反射增强组中非持续性室性心动过速患者过多可能与化学反射驱动的交感神经刺激有关。外周化学反射在慢性心力衰竭的病理生理过程中可能很重要,无论是在症状方面还是运动受限方面。