This study demonstrates that treated with trastuzumab induces an inflammatory response that contributes to myocardial tissue TLR4 as mediates chemokine expression (TNF-α, MCP-1and ICAM-1), so in experimental animals TLR4 deficiency improves left ventricular function and attenuates pathophysiological key mechanisms in herciptin-induced cardiomyopathy. This evidence concerns the gene ICAM1 and cardiomyopathy.