Non-Ischemic Dilated Cardiomyopathy: Biopsy Proved Markers of Disease Sub-Entities

s S273 Results: CMC p65 NF-κ B deletion promoted maladaptive LVH and accelerated progression towards heart failure, as measured by ejection fraction, LV mass, and lung congestion. Left main coronary artery flow was significantly lower in the knockout mice, but the coronary flow to cardiac output and LV mass ratio was not different between groups. Transgenic mice have higher levels of fibrosis despite similar CMC size. Compared to WT mice, knockouts expressed less HIF-1a, VEGFr2, and more periostin. Whole-field digital microscopy with endothelial-specific immunohistochemistry revealed increased capillary domain areas in KO mice while concurrently demonstrating decreased microvessel density compared to WT. Conclusion: Whereas acute pressure overload promoted compensatory LVH in WT mice, CMC NF-κ B deletion resulted in immediate functional deterioration that was associated with increased fibrosis, decreased HIF expression, and decreased microvessel density. These observations mechanistically implicate NF-κ B and its regulation of hypoxic stress and angiogenesis as an important factor that determines the path, to and between, compensatory hypertrophy and maladaptive HF.