Myocardial Energetics in Heart Failure With Preserved Ejection Fraction
Myocardial Energetics in Heart Failure With Preserved Ejection Fraction
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DOI：
10.1161/circheartfailure.119.006240
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发表时间：
2019-10-01
影响因子：
9.7
通讯作者：
Chareonthaitawee, Panithaya
中科院分区：
文献类型：
--
作者：
AbouEzzeddine, Omar F.;Kemp, Bradley J.;Chareonthaitawee, Panithaya
背景资料：冠状动脉微血管疾病的作用及其对射血分数保留性心力衰竭（HFpEF）功能和能量储备的影响尚不清楚。我们假设HFpEF患者对次最大药物负荷（多巴酚丁胺）的反应是左心室（LV）心肌机械（外功[EW]）、能量（心肌O-2消耗[MVO 2]）和心肌血流（MBF）储备受损。我们进一步评估了HFpEF中MBF与EW的偶联是否受损，以及是否与心肌O-2提取的代偿性增加或病理性减少相关。最后，我们评估了HFpEF中MVO 2与EW（机械效率）的偶联是否受损。方法和结果：在前瞻性入选的HFpEF患者（n=19）和年龄/性别匹配的健康对照组（n=19）中，我们进行了C-11-乙酸正电子发射断层扫描，评估静息和多巴酚丁胺输注期间的MVO 2和MBF。EW计算为每搏输出量（回波）×收缩末期压×心率。静息时，与对照组相比，HFpEF患者的LV EW、MVO 2和MBF较高。使用多巴酚丁胺时，HFpEF和对照组的LV EW、MVO 2和MBF均增加;然而，HFpEF的增加幅度显著较小。在两组中，MBF增加与EW相关，但在HFpEF中，该关系的斜率显著小于对照组。HFpEF组心肌氧摄取增加。HFpEF和对照组的机械效率相似。在事后分析中，与对照组相比，HF pEF伴LV肥大患者（n=10）的LV机械效率显著降低。结论：在次最大多巴酚丁胺应激期间的HFpEF中，存在心肌机械、能量和血流储备功能障碍，血流与需求的耦合受损，心肌O-2提取略有增加。这些发现提供了证据表明，冠状动脉微血管功能障碍存在于HFpEF，限制O-2供应相对于需求，并与储备功能障碍。
Background: The role of coronary microvascular disease and its impact on functional and energetic reserve in heart failure with preserved ejection fraction (HFpEF) remains unclear. We hypothesized that in response to submaximal pharmacologic stress (dobutamine), patients with HFpEF have impairment in left ventricular (LV) myocardial mechanical (external work [EW]), energetic (myocardial O-2 consumption [MVO2]), and myocardial blood flow (MBF) reserve. We further assessed whether coupling of MBF to EW is impaired in HFpEF and associated with compensatory increases or pathological decreases in myocardial O-2 extraction. Lastly, we assessed whether coupling of MVO2 to EW (mechanical efficiency) was impaired in HFpEF. Methods and Results: In prospectively enrolled patients with HFpEF (n=19) and age/sex-matched healthy controls (n=19), we performed C-11-acetate positron emission tomography assessing MVO2 and MBF at rest and during dobutamine infusion. EW was calculated as stroke volume (echo)xend-systolic pressurexheart rate. At rest, compared with controls, patients with HFpEF had higher LV EW, MVO2, and MBF. With dobutamine, LV EW, MVO2, and MBF increased in both HFpEF and controls; however, the magnitude of increases was significantly smaller in HFpEF. In both groups, MBF increased in relation to EW, but in HFpEF, the slope of the relationship was significantly smaller than in controls. Myocardial O-2 extraction was increased in HFpEF. Mechanical efficiency was similar in HFpEF and controls. In a post hoc analysis, HFpEF patients with LV hypertrophy (n=10) had significant reductions in LV mechanical efficiency relative to controls. Conclusions: In HFpEF during submaximal dobutamine stress, there is myocardial mechanical-, energetic- and flow-reserve dysfunction with impaired coupling of blood flow to demand and slight increases in myocardial O-2 extraction. These findings provide evidence that coronary microvascular dysfunction is present in HFpEF, limits O-2 supply relative to demand, and is associated with reserve dysfunction.