Santos Mário, Opotowsky Alexander R, Shah Amil M, Tracy Julie, Waxman Aaron B, Systrom David M
From the Department of Physiology and Cardiothoracic Surgery, Cardiovascular R&D Unit, Faculty of Medicine, University of Porto, Porto, Portugal (M.S.); Pulmonary and Critical Care Medicine (J.T., A.B.W., D.M.S.) and Division of Cardiovascular Medicine (A.R.O., A.M.S.), Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA; Department of Cardiology, Boston Children's Hospital, MA (A.R.O.).
Circ Heart Fail. 2015 Mar;8(2):278-85. doi: 10.1161/CIRCHEARTFAILURE.114.001551. Epub 2014 Dec 30.
The mechanism of functional limitation in heart failure with preserved ejection fraction remains controversial. We examined the contributions of central cardiac and peripheral mechanisms and hypothesized that the pulmonary vascular response to exercise is an important determinant of aerobic capacity among patients with exertional pulmonary venous hypertension (ePVH).
We compared 31 ePVH patients (peak VO2<80% of predicted and peak pulmonary arterial wedge pressure≥20 mm Hg) with 31 age- and sex-matched controls (peak VO2>80% predicted) who underwent invasive cardiopulmonary exercise testing for unexplained exertional intolerance. ePVH patients had lower peak cardiac output (73±14% versus 103±18% predicted; P<0.001) compared with controls, related both to impaired chronotropic response (peak heart rate 111±25 beats per minute versus 136±24 beats per minute; P<0.001) and to reduced peak stroke volume index (47±10 mL/min per m(2) versus 54±15 mL/min per m(2); P=0.03). Peak systemic O2 extraction was not different between groups (arterial-mixed venous oxygen content difference: 13.0±2.1 mL/dL versus 13.4±2.4 mL/dL; P=0.46). ePVH patients had higher resting (150±74 versus 106±50 dyne/s per cm(-5); P=0.009), peak (124±74 dyne/s per cm(-5) versus 70±41 dyne/s per cm(-5); P<0.001), and isoflow pulmonary vascular resistance (124±74 dyne/s per cm(-5) versus 91±33 dyne/s per cm(-5) at cardiac output≈10.6 L/min; P=0.04). Pulmonary vascular resistance decreased with exercise in all control subjects but increased in 36% (n=11) of ePVH patients. Abnormal pulmonary vascular response was not associated with peak VO2.
Reduced cardiac output response, rather than impaired peripheral O2 extraction, constrains oxygen delivery and aerobic capacity in ePVH. Pulmonary vascular dysfunction is common in patients with ePVH at rest and during exercise.
射血分数保留的心力衰竭患者功能受限的机制仍存在争议。我们研究了心脏中枢和外周机制的作用,并假设运动时肺血管反应是运动性肺静脉高压(ePVH)患者有氧运动能力的重要决定因素。
我们将31例ePVH患者(峰值摄氧量<预测值的80%且峰值肺动脉楔压≥20 mmHg)与31例年龄和性别匹配的对照者(峰值摄氧量>预测值的80%)进行比较,这些对照者因不明原因的运动不耐受接受了有创心肺运动试验。与对照组相比,ePVH患者的峰值心输出量较低(分别为预测值的73±14%和103±18%;P<0.001),这与变时反应受损(峰值心率分别为每分钟111±25次和136±24次;P<0.001)和峰值每搏量指数降低(分别为47±10 mL/min per m²和54±15 mL/min per m²;P=0.03)有关。两组间的峰值全身氧摄取无差异(动脉-混合静脉血氧含量差:分别为13.0±2.1 mL/dL和13.4±2.4 mL/dL;P=0.46)。ePVH患者静息时(分别为150±74和106±50达因/秒每厘米⁻⁵;P=0.009)、峰值时(分别为124±74达因/秒每厘米⁻⁵和70±41达因/秒每厘米⁻⁵;P<0.001)以及等流量肺血管阻力更高(心输出量≈10.6 L/min时分别为124±74达因/秒每厘米⁻⁵和91±33达因/秒每厘米⁻⁵;P=0.04)。所有对照者运动时肺血管阻力降低,但36%(n=11)的ePVH患者运动时肺血管阻力增加。异常的肺血管反应与峰值摄氧量无关。
心输出量反应降低而非外周氧摄取受损限制了ePVH患者的氧输送和有氧运动能力。肺血管功能障碍在静息和运动时的ePVH患者中很常见。