From plaque biology to clinical setting

Coronary atherosclerosis may cause acute and chronic ischemic syndromes; th e former are caused by "acute plaque events," mostly thrombosis complicatin g 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 comp licated by thrombosis. Furthermore, plaque rupture is not the only thrombus substrate in acute ischemic syndromes: Superficial erosion of Fibrous plaq ues is found in 44% of acute thrombi in sudden coronary deaths and in 25% o f those in acute myocardial infarctions. Coronary thrombosis appears to be triggered by superficial intimal inflammation in plaque ulceration and by n eointimal hyperplasia in plaque erosion. "Endogenous" and, recently, exogen ous factors, particularly infective intracellular organisms, have been prop osed as major contributors to plaque inflammation, activation, and vulnerab ility. Possible exogenous triggers are DNA and RNA viruses and intracellula r bacteria such as Chlamydia pneumoniae, which has been identified with mic robiological, ultrastructural, immunohistochemical, and molecular tools in a consistent proportion of human plaque samples. Chlamydia increases local thrombogenicity and is associated with on atherogenic lipid profile. System ic indexes of inflammation, such as PCR, SAA, and fibrinogen, are also incr eased 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: Wh ite cells infected in its target tissue could circulate into the flow and b e captured, on a specific local trigger, into vessel walls thus stimulating local inflammation.