Mezzani Alessandro, Giordano Andrea, Komici Klara, Corrà Ugo
Exercise Pathophysiology Laboratory, Cardiac Rehabilitation Division, Istituti Clinici Scientifici Maugeri Spa SB-Scientific Institute of Veruno IRCCS, Veruno (NO), Italy
Bioengineering Service, Istituti Clinici Scientifici Maugeri Spa SB-Scientific Institute of Veruno IRCCS, Veruno (NO), Italy.
J Am Heart Assoc. 2017 May 9;6(5):e005278. doi: 10.1161/JAHA.116.005278.
It is not known whether determinants of ventilation (VE)/volume of exhaled carbon dioxide (VCO) slope during incremental exercise may differ at different stages of reduced ejection fraction chronic heart failure natural history.
VE/VCO slope was fitted up to lowest VE/VCO ratio, that is, a proxy of the VE/perfusion ratio devoid of nonmetabolic stimuli to ventilatory drive. VE/VCO slope tertiles were generated from our database (<27.5 [tertile 1], ≥27.5 to <32.0 [tertile 2], and ≥32.0 [tertile 3]), and 147 chronic heart failure patients with repeated tests yielding VE/VCO slopes in 2 different tertiles were selected. Determinants of VE/VCO slope changes across tertile pairs 1 versus 2, 2 versus 3, and 1 versus 3 were assessed by exploring changes in VE and VCO at lowest VE/VCO and those in VE/work rate (W) and VCO/W slope. Resting and peak cardiac output (CO) were calculated as VO/estimated arteriovenous O difference and the CO/W slope analyzed. Notwithstanding a progressively lower W with increasing tertile, VE at lowest VE/VCO and VE/W slope were significantly higher in tertiles 2 and 3 versus tertile 1. Conversely, VCO at lowest VE/VCO and CO/W slope significantly decreased across tertiles, whereas VCO/W slope did not. Difference (Δ) in VE/W slope between tertiles accounted for 71% of ΔVE/VCO slope variance, with ΔVCO/W slope explaining an additional 26% (model =0.99; =0.97; <0.0001). Similar results were obtained substituting ΔVCO/W slope with ΔCO/W slope.
Ventilatory overactivation is the predominant cause of VE/VCO slope increase at initial stages of chronic heart failure, whereas hemodynamic impairment plays an additional role at more-advanced pathophysiological stages.
射血分数降低的慢性心力衰竭自然病程不同阶段，递增运动期间通气量（VE）/呼出二氧化碳量（VCO）斜率的决定因素是否存在差异尚不清楚。
将VE/VCO斜率拟合至最低VE/VCO比值，即排除对通气驱动的非代谢性刺激后的VE/灌注比值指标。根据我们的数据库生成VE/VCO斜率三分位数（<27.5[三分位数1]，≥27.5至<32.0[三分位数2]，以及≥32.0[三分位数3]），并选取147例慢性心力衰竭患者，其重复检测结果得出的VE/VCO斜率处于2个不同三分位数。通过探究最低VE/VCO时VE和VCO的变化以及VE/工作率（W）和VCO/W斜率的变化，评估三分位数对1与2、2与3以及1与3之间VE/VCO斜率变化的决定因素。静息和峰值心输出量（CO）分别计算为VO/估计动静脉氧分压差，并分析CO/W斜率。尽管随着三分位数增加W逐渐降低，但三分位数2和3中最低VE/VCO时的VE以及VE/W斜率显著高于三分位数1。相反，最低VE/VCO时的VCO以及CO/W斜率在各三分位数间显著降低，而VCO/W斜率则无变化。三分位数间VE/W斜率的差异（Δ）占ΔVE/VCO斜率方差的71%，ΔVCO/W斜率额外解释了26%（模型=0.99；=0.97；<0.0001）。用ΔCO/W斜率替代ΔVCO/W斜率得到了相似结果。
通气过度激活是慢性心力衰竭初始阶段VE/VCO斜率增加的主要原因，而血流动力学损害在更晚期的病理生理阶段起额外作用。
