An explanation of the progression of stenotic lesions was sought in animal experiments. After surgical decrease of the lumen of arteries, progressive ingrowth of fibrous connective tissue led to the development of stenosis with changes in the artery that resembled those of coaretation. These changes are explained by the action of local blood pressures. Phenomena such as progressive stenosis, valvulogenesis, patterns of lipid infiltration, medial hypertrophy, thinning, and cystic change are discussed in terms of the concepts derived from these studies.T IHE high pressure cardiad to stenotic arterial lesions, as for example in coaretation of the aorta and in closure of vital vessels such as the coronary arteries, is often sufficient to cause vascular injury with the production of aneurysms and rupture of the vessel wall.' Paradoxically, these continuously high arterial pressures never dilate the constricted a-terial ring and relieve the stenosis.The same paradox holds for stenotic lesions of the cardiac valves. Thus, in aortic or pulmonic valvular stenosis, the hypertrophied ventricle generates high pressures that beat recurrently against the contracted outlet; yet the stenosis is inexorably progressive, leading ultimately to cardiac failure.2 3 These anomalous situations have been highlighte(l recently by repeated demonstrations that gentle digital dilation of stenotic mitral valves is sometimes sufficient to free the ag-