August 19, 2003Circulation
Regional Alterations in Protein Expression in the Dyssynchronous Failing Heart
Key result
In dyssynchronous failing hearts, the lateral LV endocardium exhibited a 2-fold increase in phosphorylated erk and significant declines in key calcium handling proteins.
Why the study?
Does right ventricular pacing-induced dyssynchrony alter regional protein expression in the failing canine heart?
Population
Dogs with tachycardia-induced heart failure and noninstrumented controls
Comparison
Right ventricular free wall pacing vs Right atrial pacing and noninstrumented controls
Design
Preclinical
Authors
Discussion
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Implication
Regional molecular remodeling in dyssynchronous canine HF may worsen function and arrhythmias; leaves open whether targeting ERK or calcium proteins benefits patients.
Structured PICO
Does right ventricular pacing-induced dyssynchrony alter regional protein expression in the failing canine heart?
P
Population
Dogs with tachycardia-induced heart failure and noninstrumented controls
I
Intervention
Right ventricular free wall pacing (inducing dyssynchronous heart failure)
C
Comparator
Right atrial pacing (synchronous heart failure) and noninstrumented controls
O
Outcome
Regional alterations in protein expression (phosphorylated erk MAPK, SERCA, phospholamban, connexin43)surrogate
Left ventricular dyssynchrony in failing hearts causes regional downregulation of calcium handling and gap junction proteins in the lateral endocardium, potentially worsening function and arrhythmia risk.
Cite This Study
Spragg et al. (2003) studied this question. In dyssynchronous failing hearts, the lateral LV endocardium exhibited a 2-fold increase in phosphorylated erk and significant declines in key calcium handling proteins.