Plasminogen-activator inhibitor type 1 and coronary artery disease
HP Kohler, PJ Grant - New England Journal of Medicine, 2000 - Mass Medical Soc
HP Kohler, PJ Grant
New England Journal of Medicine, 2000•Mass Medical SocThe development of coronary artery disease, and specifically myocardial infarction, involves
hyperplasia of arterial smooth muscle, the development of fatty streaks, atheroma formation,
plaque rupture, and ultimately thrombus formation and vessel occlusion. 1 These changes
are in part genetically determined, as demonstrated by the fact that the risk of myocardial
infarction in persons who have a first-degree relative with myocardial infarction is seven
times the risk in persons who do not. 2, 3 This finding is often used to argue that coronary …
hyperplasia of arterial smooth muscle, the development of fatty streaks, atheroma formation,
plaque rupture, and ultimately thrombus formation and vessel occlusion. 1 These changes
are in part genetically determined, as demonstrated by the fact that the risk of myocardial
infarction in persons who have a first-degree relative with myocardial infarction is seven
times the risk in persons who do not. 2, 3 This finding is often used to argue that coronary …
The development of coronary artery disease, and specifically myocardial infarction, involves hyperplasia of arterial smooth muscle, the development of fatty streaks, atheroma formation, plaque rupture, and ultimately thrombus formation and vessel occlusion.1 These changes are in part genetically determined, as demonstrated by the fact that the risk of myocardial infarction in persons who have a first-degree relative with myocardial infarction is seven times the risk in persons who do not.2,3 This finding is often used to argue that coronary artery disease has a genetic basis, but the extent to which a shared environment contributes to the risk must also . . .
The New England Journal Of Medicine