Coronary atherosclerosis may cause acute and chronic ischemic syndromes; the former are caused by "acute plaque events," mostly thrombosis complicating vulnerable ruptured plaques, namely severe lesions with large core, thin cap, and weak shoulder infiltrated by activated inflammatory cells. Plaque rupture may also occur in nonischemic settings and is not obligatorily complicated by thrombosis. Furthermore, plaque rupture is not the only thrombus substrate in acute ischemic syndromes: Superficial erosion of fibrous plaques is found in 44% of acute thrombi in sudden coronary deaths and in 25% of those in acute myocardial infarctions. Coronary thrombosis appears to be triggered by superficial intimal inflammation in plaque ulceration and by neointimal hyperplasia in plaque erosion. "Endogenous" and, recently, exogenous factors, particularly infective intracellular organisms, have been proposed as major contributors to plaque inflammation, activation, and vulnerability. Possible exogenous triggers are DNA and RNA viruses and intracellular bacteria such as Chlamydia pneumoniae, which has been identified with microbiological, ultrastructural, immunohistochemical, and molecular tools in a consistent proportion of human plaque samples. Chlamydia increases local thrombogenicity and is associated with an atherogenic lipid profile. Systemic indexes of inflammation, such as PCR, SAA, and fibrinogen, are also increased in acute syndromes and common infectious diseases with high morbidity and minimal clinical impact are good candidates; Helicobacter pylori is a major one. Infectious agents could link local and systemic inflammation: White cells infected in its target tissue could circulate into the flow and be captured, on a specific local trigger, into vessel walls thus stimulating local inflammation.