Key result
Atherosclerosis progresses through three clinical stages over six decades, from fatty streaking to fibrous plaques and local complications like hemorrhage and thrombosis.
The paper provides a conceptual framework for the pathogenesis of atherosclerosis, emphasizing the role of active metabolic work by mesenchymal cells and the progression through three distinct clinical stages.
Does not change clinical practice; leaves open stage-specific interventions in long-term atherosclerosis management.
Efforts should be directed toward detection, concentration, and possible clinical utilization of active principles that govern lipid transportation and local accumulation. The best available evidence makes it seem likely that these active principles are enzyme-hormone complexes and indicates that active metabolic work is performed by the mesenchymal cells in the inner layers of the arterial wall. Much confusion can be avoided by keeping interspecies differences in mind and recognizing the probable stage of atherosclerosis in man at any given age. The three stages leading to clinical disease are fatty streaking in the first two decades, conversion of some fatty streaks to fibrous plaques in the second two decades, and local complications such as hemorrhage and thrombosis about a plaque in the third two decades.
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Russell L. Holman (1959) conducted a review in Atherosclerosis. Atherosclerosis progresses through three clinical stages over six decades, from fatty streaking to fibrous plaques and local complications like hemorrhage and thrombosis.
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