Hemodynamic Modulation of Endocardial Thromboresistance
Key result
Acute elevation of left atrial filling pressure caused a 70% inhibition of atrial endocardial thrombomodulin expression and increased local thrombin generation, mediated by transforming growth factor-beta.
Population
Rats subjected to acute atrial pressure overload caused by aortic banding, and in vitro co-culture models
Comparison
Adenovirus-mediated gene transfer for targeted… vs Acute pressure overload without targeted…
Design
Preclinical
Authors
Discussion
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Implication
Alerts clinicians to hemodynamic drivers of atrial thrombogenicity in HF; leaves open TGF-β modulation for stroke prevention trials.
Structured PICO
P
Population
Rats subjected to acute atrial pressure overload caused by aortic banding, and in vitro co-culture models
I
Intervention
Adenovirus-mediated gene transfer for targeted restoration of atrial thrombomodulin expression, and administration of a neutralizing transforming growth factor-beta antibody
C
Comparator
Acute pressure overload without targeted intervention
O
Outcome
Changes in the expression of thrombomodulin and local thrombin generationsurrogate
Increased hemodynamic load downregulates endocardial thrombomodulin via TGF-beta, suggesting a mechanism for increased thromboembolic risk in heart failure independent of blood stasis.
Cite This Study
Kapur et al. (2006) studied Acute atrial pressure overload / Heart failure. Acute elevation of left atrial filling pressure (aortic banding) vs. Baseline was evaluated on Atrial endocardial thrombomodulin expression and local thrombin generation. Acute elevation of left atrial filling pressure caused a 70% inhibition of atrial endocardial thrombomodulin expression and increased local thrombin generation, mediated by transforming growth factor-beta.