Changes in the Monocytic Subsets CD14dimCD16+and CD14++CD16−in Chronic Systolic Heart Failure Patients
Key result
Chronic systolic heart failure was associated with an 11% decrease in the classical CD14(++)CD16(-) monocytic subset and a 4% expansion in the nonclassical CD14(dim)CD16(+) subset (P<0.001).
Population
59 chronic systolic heart failure patients and 29 age-matched controls with no previous heart disease.
Design
Case-control
Authors
Discussion
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Implication
Monocyte shifts in systolic HF may influence remodeling; hypothesis-generating for immunomodulatory targets in prospective studies.
Study Design
Type
Case-Control (n=88)
Structured PICO
P
Population
88 participants comprising 59 patients with chronic systolic heart failure and 29 age-matched healthy controls.
C
Comparator
Age-matched controls with no previous heart disease
O
Outcome
Distribution of monocytic subsets (CD14(+)CD16(+), CD14(++)CD16(-), CD14(dim)CD16(+)) and serum cytokine levels (TNFα, IL-1β, IL-10, IL-13)surrogate
Main Result
p-value: p=<0.001
Chronic systolic heart failure is associated with a shift in monocytic subsets, specifically an expansion of the nonclassical CD14(dim)CD16(+) subset that produces IL-13, which may counterbalance adverse remodeling.
Cite This Study
Amir et al. (2012) conducted a case-control in Chronic systolic heart failure (n=88). Chronic systolic heart failure vs. Age-matched controls with no previous heart disease was evaluated on Distribution of monocytic subsets (p=<0.001). Chronic systolic heart failure was associated with an 11% decrease in the classical CD14(++)CD16(-) monocytic subset and a 4% expansion in the nonclassical CD14(dim)CD16(+) subset (P<0.001).