Canada Justin McNair, Fronk Daniel Taylor, Cei Laura Freeman, Carbone Salvatore, Erdle Claudia Oddi, Abouzaki Nayef Antar, Melchior Ryan David, Thomas Christopher Scott, Christopher Sanah, Turlington Jeremy Shane, Trankle Cory Ross, Thurber Clinton Joseph, Evans Ronald Kenneth, Dixon Dave L, Van Tassell Benjamin Wallace, Arena Ross, Abbate Antonio
VCU Pauley Heart Center, Virginia Commonwealth University, Richmond, Virginia; Department of Kinesiology and Health Sciences, Virginia Commonwealth University, Richmond, Virginia.
VCU Pauley Heart Center, Virginia Commonwealth University, Richmond, Virginia.
Am J Cardiol. 2016 Jan 1;117(1):116-20. doi: 10.1016/j.amjcard.2015.10.020. Epub 2015 Oct 19.
Patients with heart failure (HF) have evidence of chronic systemic inflammation. Whether inflammation contributes to the exercise intolerance in patients with HF is, however, not well established. We hypothesized that the levels of C-reactive protein (CRP), an established inflammatory biomarker, predict impaired cardiopulmonary exercise performance, in patients with chronic systolic HF. We measured CRP using high-sensitivity particle-enhanced immunonephelometry in 16 patients with ischemic heart disease (previous myocardial infarction) and chronic systolic HF, defined as a left ventricular ejection fraction ≤ 50% and New York Heart Association class II-III symptoms. All subjects with CRP >2 mg/L, reflecting systemic inflammation, underwent cardiopulmonary exercise testing using a symptom-limited ramp protocol. CRP levels predicted shorter exercise times (R = -0.65, p = 0.006), lower oxygen consumption (VO2) at the anaerobic threshold (R = -0.66, p = 0.005), and lower peak VO2 (R = -0.70, p = 0.002), reflecting worse cardiovascular performance. CRP levels also significantly correlated with an elevated ventilation/carbon dioxide production slope (R = +0.64, p = 0.008), a reduced oxygen uptake efficiency slope (R = -0.55, p = 0.026), and reduced end-tidal CO2 level at rest and with exercise (R = -0.759, p = 0.001 and R = -0.739, p = 0.001, respectively), reflecting impaired gas exchange. In conclusion, the intensity of systemic inflammation, measured as CRP plasma levels, is associated with cardiopulmonary exercise performance, in patients with ischemic heart disease and chronic systolic HF. These data provide the rationale for targeted anti-inflammatory treatments in HF.
心力衰竭(HF)患者存在慢性全身炎症的证据。然而,炎症是否导致HF患者运动耐量下降尚未明确。我们假设,作为一种已确定的炎症生物标志物,C反应蛋白(CRP)水平可预测慢性收缩性HF患者心肺运动表现受损。我们使用高灵敏度颗粒增强免疫比浊法测量了16例缺血性心脏病(既往心肌梗死)和慢性收缩性HF患者的CRP,慢性收缩性HF定义为左心室射血分数≤50%且有纽约心脏协会II-III级症状。所有CRP>2 mg/L(反映全身炎症)的受试者均采用症状限制递增方案进行心肺运动测试。CRP水平可预测运动时间缩短(R = -0.65,p = 0.006)、无氧阈值时较低的耗氧量(VO2)(R = -0.66,p = 0.005)以及较低的峰值VO2(R = -0.70,p = 0.002),反映出心血管功能较差。CRP水平还与通气/二氧化碳产生斜率升高(R = +0.64,p = 0.008)、氧摄取效率斜率降低(R = -0.55,p = 0.026)以及静息和运动时呼气末二氧化碳水平降低(分别为R = -0.759,p = 0.001和R = -0.739,p = 0.001)显著相关,反映气体交换受损。总之,以CRP血浆水平衡量的全身炎症强度与缺血性心脏病和慢性收缩性HF患者的心 肺运动表现相关。这些数据为HF的靶向抗炎治疗提供了理论依据。