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.

The American Journal of Cardiology, January
2016, Vol. 117 Issue: Number 1 p116-120, 5p;

Abstract: 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 CO2level 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.