Evidence for a Role of Mast Cells in the Evolution to Congestive Heart Failure
Key result
Mast cell deficiency or treatment with the mast cell-stabilizing agent tranilast prevented the evolution from compensated hypertrophy to decompensated heart failure in mice.
Why the study?
Does mast cell deficiency or stabilization prevent the evolution to congestive heart failure in a mouse model of pressure overload?
Population
Mast cell-deficient (WBB6F1-W/W) mice and congenic wild-type mice subjected to systolic pressure overload…
Comparison
Mast cell deficiency or treatment with tranilast. vs Wild-type mice subjected to the same aortic…
Design
Preclinical
Follow-up
15 weeks
Authors
Discussion
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Implication
Mast cell stabilization merits preclinical follow-up but should not alter care; leaves open its efficacy in human HF.
Structured PICO
Does mast cell deficiency or stabilization prevent the evolution to congestive heart failure in a mouse model of pressure overload?
P
Population
Mast cell-deficient (WBB6F1-W/W(v)) mice and congenic wild-type (WT) mice subjected to systolic pressure overload via abdominal aorta banding.
I
Intervention
Mast cell deficiency (genetic) or treatment with tranilast (a mast cell-stabilizing agent).
C
Comparator
Wild-type (WT) mice subjected to the same aortic banding.
O
Outcome
Cardiac function (left ventricular performance) and development of pulmonary congestion over 15 weeks.surrogate
Mast cells play a critical role in the progression to heart failure, and their stabilization may represent a novel therapeutic approach.
Cite This Study
Hara et al. (2002) studied Congestive Heart Failure. Mast cell deficiency or tranilast vs. Wild-type controls was evaluated on Cardiac function and pulmonary congestion. Mast cell deficiency or treatment with the mast cell-stabilizing agent tranilast prevented the evolution from compensated hypertrophy to decompensated heart failure in mice.