Ma. Mclaughlin et V. Fuster, THE 3 MECHANISMS FOR CORONARY-ARTERY DISEASE PROGRESSION - INSIGHTS INTO FUTURE MANAGEMENT, The Mount Sinai journal of medicine, 62(4), 1995, pp. 265-274
The basic mechanisms of atherosclerotic progression have been well elu
cidated during the last few years. Basic experimental and clinical inf
ormation has helped define the three stages of progression. In this re
view we outline the pathologic and clinical differences between slow,
rapid, and intermediate progression. The eight morphologically differe
nt lesions (types I, II, III, IV, Va, Vb, Vc, and VI) in their various
stages are defined. The relationship between specific type of lesion
and chronic endothelial injury, cardiac risk factors, and increased va
scular permeability to lipids is noteworthy. In regard to the acute co
ronary syndromes, the fate of plaque rupture and our understanding of
''passive'' vs. ''active'' rupture are defined. In addition to the phe
nomenon of plaque rupture, the thrombogenicity of atherosclerotic plaq
ues in the genesis of coronary syndromes is described. The combination
of plaque disruption and a high thrombogenic risk profile-including l
ocal and systemic factors-is vital to understanding the genesis of the
acute coronary syndromes. In approaching the use of these new insight
s to arrest or reverse the atherosclerotic process, it is essential to
remember that the disease process starts early in life and takes many
years to progress to the symptomatic stage. The future holds promise
for the development of preventive strategies to halt the progression o
f coronary disease-the number one killer in the United States.