The complex syndrome of heart failure (HF) is characterized by increased left ventricular pressures. Cardiomyocytes increase in size, cardiac fibroblasts transform and make extracellular matrix, and leukocytes infiltrate the cardiac tissue and alter cardiomyocyte and cardiac fibroblast function. Here we review recent advances in our understanding of the cellular composition of the heart during homeostasis and in response to cardiac pressure overload, with an emphasis on immune cell communication with cardiac fibroblasts and its consequences in cardiac remodeling.