LAUSR

A good number of us have forgotten Jean Georges Chretien Frederic Martin Lobstein, but the observations of this 19th-century surgeon-pathologist are codified in disease nomenclature used today. As an amateur archeologist, he had a particular interest in mineralized tissues, including bones, and Lobstein’s detailed autopsies led him to coin the word “osteoporosis” to denote the skeletal frailty afflicting older individuals. In many of these aged subjects, Lobstein also noted a vascular disease process that, in 1829, he called “arteriosclerosis”: the hardening of normally compliant conduit arteries.1 As such, Lobstein was among the first to embrace an osseocentric view of arterial disease. Virchow1 expanded on this idea in 1860, recounted in his lecture series, Cellular Pathology . He highlighted the inflammatory nature of lipid-laden atherosclerotic lesions and noted that beyond calcification, 1 outcome of arteriosclerotic disease was true focal vascular ossification. With recognition that oxidized low-density lipoprotein cholesterol is proinflammatory and pathogenic in vascular disease leading to acute ischemia—and the advent of successful cholesterol-lowering therapies—atherosclerosis looms large in the awareness of modern medicine as 1 type of arteriosclerosis. However, the broader concepts and consequences of Lobstein’s arteriosclerosis—be it from atherosclerosis or fibrosis and medial thickening of conduit arteries with or without calcific sclerosis—are frequently dismissed. This has led to terminology and experimental design that treat atherosclerosis and arteriosclerosis as interchangeable without consideration of the impact of chronic vascular stiffening. Arteriosclerosis impairs Windkessel physiology—the rubbery elasticity of conduit vessels that ensures smooth distal tissue perfusion throughout the cardiac cycle2—and is …