Cardiovascular diseases (CVD) account for the majority of morbidity and mortality in Western countries, and are often clinically manifest as acute coronary syndromes (ACS), including myocardial infarction (MI). The underlying mechanism of ACS is atherosclerotic plaque rupture, in which vascular immune-mediated inflammation has been recognized of major importance, and atherosclerosis-related inflammation even fulfils the required “Koch’s postulates” to be considered as an autoimmune disease. Consistent with this hypothesis, there is a growing body of biological evidences demonstrating that auto-antibodies could modulate inflammation through innate immune receptor signalling which can either stimulate or inhibit atherogenesis-related processes, as reviewed elsewhere. Accordingly, different clinical trials have demonstrated that high levels of anti-cardiolipin, anti-β2 glycoprotein-I (anti-β2 GPI), anti-heat shock protein 60 (anti-HSP-60), anti-apolipoproteinA-1 (apoA-1) auto-antibodies were associated with an increased CV risk, whereas other studies demonstrated that high levels of autoantibodies of IgM subtype against phosphorylcholine (anti-PC IgM), the immunodominant epitope of oxidised Low-Density Lipoprotein (oxLDL), protected against CVD. Given their relative independence toward classical cardiovascular risk factors, those autoantibodies have been proposed as emergent tools for cardiovascular risk stratification.