In contrast, “dysfunctional” ECs favored spontaneous metastasis in adjacent tumors through an aberrant expression of pro-inflammatory cytokines, extracellular matrix, alterations in the leukocyte adhesion process, increasing the expression of vascular cell adhesion molecule-1 (VCAM-1) and abnormal responses to oxidative stress, which are pathological stimuli present both in atherosclerotic lesions, precursors of MI and HF, as well as in the tumor environment (Figure 3) [66,70]. Here, VCAM1 is linked to neoplasm.