Right ventriculo-arterial uncoupling and impaired contractile reserve in obese patients with unexplained exercise intolerance.
Right ventriculo-arterial uncoupling and impaired contractile reserve in obese patients with unexplained exercise intolerance.
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DOI：
10.1007/s00421-018-3873-4
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发表时间：
2018-07
影响因子：
3
通讯作者：
Systrom DM
中科院分区：
文献类型：
--
作者：
McCabe C;Oliveira RKF;Rahaghi F;Faria-Urbina M;Howard L;Axell RG;Priest AN;Waxman AB;Systrom DM
右室功能障碍和射血分数保留的心力衰竭可能导致肥胖患者的运动不耐受。为了进一步确定右室运动反应，我们研究了肥胖伴和不伴运动性肺静脉高压(EPVH)的右室-动脉偶联。根据有创心肺运动试验数据计算6例正常对照组、8例肥胖组(肥胖组)和8例肥胖组(肥胖组+肥胖组)的右室-动脉偶联，定义为右室收缩末期弹性/肺动脉弹性(Ees/Ea)。其中6例正常对照组、8例肥胖组(肥胖组)和8例肥胖组(肥胖组+−组)的右室-动脉-动脉偶联。EPVH定义为静息状态下的肺动脉楔压 <； 为15 mm Hg，而运动时≥ 为20 mm Hg。对18名对照组、20名肥胖的−患者和17名肥胖+EPVH患者的运动血流动力学进行了进一步的评估。肥胖−组和肥胖+EPVH组均出现运动性右室动脉不偶联(Ees/Ea = 峰值1.45 ± 0.26 vs 0.67 ± 0.18 vs 0.56 ± 0.11，p <； 0.001，对照组、肥胖组和肥胖+−组)峰值后负荷较高(Ea = 峰值分别为0.31 ± 0.07vs0.75 ± 0.32vs0.88 ± 0.62毫升/毫米汞柱，p = 0.043)，而峰值收缩能力相似(峰值EES = 0.50 ± 0.16vs0.45 ± 0.22vs 0.48 ± 0.17毫升/毫米汞柱，p = 0.89)。对照组右室收缩储备最高(ΔEes = 224 ± 80 vs 154 ± 39 vs 141 ± 34%，p <； 0.001)。Ees/Ea峰值与最大肺血管顺应性(Pvc，r = 0.5 3，p = 0.0 2)相关，与最大肺血管阻力(Pvr，r = − 0.2 0，p = 0.46)无关。在较大的队列中，肥胖+ePVH患者在运动中表现出更高的右房压、更低的心输出量和更陡峭的压力-流量反应。体重指数与峰值PVR值相关(r = − 0.35，p = 0.0 4)，与峰值PVR值无关(r = 0.2 4，p = 0.2 5)。运动RV-动脉解偶联和RV收缩储备减少进一步表现了肥胖相关的运动耐受性。肥胖患者的右室功能障碍可能不受运动左心室充盈压力的影响。
Right ventricular (RV) dysfunction and heart failure with preserved ejection fraction may contribute to exercise intolerance in obesity. To further define RV exercise responses, we investigated RV–arterial coupling in obesity with and without development of exercise pulmonary venous hypertension (ePVH). RV–arterial coupling defined as RV end-systolic elastance/pulmonary artery elastance (Ees/Ea) was calculated from invasive cardiopulmonary exercise test data in 6 controls, 8 obese patients without ePVH (Obese−ePVH) and 8 obese patients with ePVH (Obese+ePVH) within a larger series. ePVH was defined as a resting pulmonary arterial wedge pressure < 15 mmHg but ≥ 20 mmHg on exercise. Exercise haemodynamics were further evaluated in 18 controls, 20 Obese−ePVH and 17 Obese+ePVH patients. Both Obese−ePVH and Obese+ePVH groups developed exercise RV–arterial uncoupling (peak Ees/Ea = 1.45 ± 0.26 vs 0.67 ± 0.18 vs 0.56 ± 0.11, p < 0.001, controls vs Obese−ePVH vs Obese+ePVH respectively) with higher peak afterload (peak Ea = 0.31 ± 0.07 vs 0.75 ± 0.32 vs 0.88 ± 0.62 mL/mmHg, p = 0.043) and similar peak contractility (peak Ees = 0.50 ± 0.16 vs 0.45 ± 0.22 vs 0.48 ± 0.17 mL/mmHg, p = 0.89). RV contractile reserve was highest in controls (ΔEes = 224 ± 80 vs 154 ± 39 vs 141 ± 34% of baseline respectively, p < 0.001). Peak Ees/Ea correlated with peak pulmonary vascular compliance (PVC, r = 0.53, p = 0.02) but not peak pulmonary vascular resistance (PVR, r = − 0.20, p = 0.46). In the larger cohort, Obese+ePVH patients on exercise demonstrated higher right atrial pressure, lower cardiac output and steeper pressure-flow responses. BMI correlated with peak PVC (r = − 0.35, p = 0.04) but not with peak PVR (r = 0.24, p = 0.25). Exercise RV–arterial uncoupling and reduced RV contractile reserve further characterise obesity-related exercise intolerance. RV dysfunction in obesity may develop independent of exercise LV filling pressures.
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影响因子：
37.8
作者：
Lai YC;Tabima DM;Dube JJ;Hughan KS;Vanderpool RR;Goncharov DA;St Croix CM;Garcia-Ocaña A;Goncharova EA;Tofovic SP;Mora AL;Gladwin MT
通讯作者：
Gladwin MT
影响因子：
3.7
作者：
Metkus, Thomas S.;Mullin, Christopher J.;Tedford, Ryan J.
通讯作者：
Tedford, Ryan J.
DOI：
10.1186/s13054-016-1440-0
发表时间：
2016-09-10
期刊：
Critical care (London, England)
影响因子：
--
作者：
Pinsky MR
通讯作者：
Pinsky MR
影响因子：
5.5
作者：
BARER, GR;SHAW, JW
通讯作者：
SHAW, JW
DOI：
10.1152/ajpheart.01023.2002
发表时间：
2003-05-01
影响因子：
4.8
作者：
Brimioulle, S;Wauthy, P;Naeije, R
通讯作者：
Naeije, R