Myocardial gene expression of factors of coagulation, inflammation, endothelial activation, and remodeling in cats with hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy (HCM) is the most common form of cardiac disease in domestic cats. One complication is left atrial (LA) thrombus formation, often resulting in euthanasia. Risk of LA thrombus formation is increased by LA dilation and slowed blood flow, however, not all such cats develop thrombi so it is likely that additional factors are involved. We hypothesized that cats with HCM experience higher myocardial gene expression of factors for inflammation, remodeling, coagulation and endothelial activation than cats without cardiac disease, and that those with LA thrombi show a further increase of these markers in their left atria. Real-time reverse transcription polymerase chain reaction was performed using LA and left ventricular (LV) samples from 12 cats with HCM, of which five had an LA thrombus, as well as six young (YC) and six adult (AC) control cats without cardiac disease for the following genes: von Willebrand factor (vWF), a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13, platelet activating factor (PAF), E- and P-selectins, intercellular and vascular adhesion molecules-1, ß2-integrin, vascular endothelial growth factor (VEGF), tumor necrosis factor-, interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), heat shock protein-70, matrix metalloproteinase (MMP) 13, tissue inhibitor of MMP2 (TIMP2), and myocyte-specific enhancer factor 2C. Young control cats showed significantly lower gene expression than AC and cats with HCM. In particular, cats with HCM showed higher IL-6, MCP-1, and vWF and lower VEGF expression in LA samples, and higher MCP-1 and PAF expression in LV samples in comparison to AC cats. The presence of an LA thrombus in cats with HCM was associated with higher LA IL-6 and TIMP2 expression. Results from this study confirm a previously reported influence of age on myocardial gene expression. Factors of inflammation and coagulation might be involved in HCM, while profibrotic TIMP2 and inflammatory IL-6 might be associated with LA thrombus in cats with HCM. Further investigations into the roles of IL-6, MCP-1, VEGF, vWF, and PAF in feline HCM and of IL-6 and TIMP2 in LA thrombus formation appear warranted.