Maeder Micha T, Thompson Bruce R, Kaye David M
Cardiology Division, Kantonsspital St. Gallen, Switzerland; Heart Failure Research Group, Baker IDI Heart and Diabetes Institute, Melbourne, Vic, Australia; Heart Centre, Alfred Hospital, Melbourne, Vic, Australia.
Allergy, Immunology, and Respiratory Medicine, Alfred Hospital, Melbourne, Vic, Australia.
Heart Lung Circ. 2018 Aug;27(8):995-1003. doi: 10.1016/j.hlc.2017.08.014. Epub 2017 Sep 12.
B-type natriuretic peptide (BNP) has been found to be inversely related to peak oxygen consumption (peak VO) in various patient populations. However, in these studies, circulating plasma BNP, i.e. the net effect of release and elimination, rather than cardiac BNP release has been measured. We assessed the relationship between the transcardiac BNP gradient [ΔBNP, i.e. the difference between BNP in coronary sinus (BNP) and arterial (BNP) plasma] and peak VO in healthy subjects with a view to better understanding the regulation of cardiac BNP release in humans.
We studied 10 asymptomatic subjects (age 64±11 years, two females) with preserved left ventricular function (left ventricular ejection fraction 62±5%, averaged early diastolic mitral annular velocity 9±3cm/s) and low BNP (BNP in venous plasma [BNP] <100ng/l). Subjects underwent measurement of BNP and BNP for the calculation of ΔBNP, maximal cardiopulmonary exercise testing, echocardiography and resting and submaximal exercise right heart catheterisation.
The median (range) BNP, BNP, BNP, and ΔBNP were 62 (14, 82), 60 (13, 79), 110 (25, 157), and 44 (1, 103) ng/l. The median peak VO during cardiopulmonary exercise testing was 21.5 (18, 54) ml/min/kg. There was an inverse correlation between higher ΔBNP and lower peak VO (r=-0.84; p=0.002) and oxygen pulse (r=-0.64, p=0.049). There was a trend towards an inverse correlation between ΔBNP and the exercise arteriovenous oxygen content difference (r=-0.58; p=0.08).
In healthy humans, there is an inverse association between myocardial BNP release and peak VO, which may be due to cardiac and non-cardiac mechanisms.
在不同患者群体中，已发现B型利钠肽（BNP）与峰值耗氧量（峰值VO₂）呈负相关。然而，在这些研究中，所测量的是循环血浆BNP，即释放与消除的净效应，而非心脏BNP的释放。我们评估了经心脏的BNP梯度[ΔBNP，即冠状窦血浆（BNPcs）与动脉血浆（BNPa）中BNP的差值]与健康受试者峰值VO₂之间的关系，以期更好地理解人类心脏BNP释放的调节机制。
我们研究了10名无症状受试者（年龄64±11岁，2名女性），其左心室功能正常（左心室射血分数62±5%，平均舒张早期二尖瓣环速度9±3cm/s）且BNP水平较低（静脉血浆BNP[BNPv]<100ng/l）。受试者接受BNPcs和BNPa测量以计算ΔBNP，进行最大心肺运动试验、超声心动图检查以及静息和次极量运动时的右心导管检查。
BNPcs、BNPa、BNPv和ΔBNP的中位数（范围）分别为62（14，82）、60（13，79）、110（25，157）和44（1，103）ng/l。心肺运动试验期间的峰值VO₂中位数为21.5（18，54）ml/min/kg。较高的ΔBNP与较低的峰值VO₂（r=-0.84；p=0.002）和氧脉搏（r=-?0.64，p=0.049）呈负相关。ΔBNP与运动动静脉氧含量差之间存在负相关趋势（r=-0.58；p=0.08）。
在健康人群中，心肌BNP释放与峰值VO₂之间存在负相关，这可能是由心脏和非心脏机制所致。
