Hi Tom, Just a comment on your pathophysiology of an MI. You talk about plaque rupture leading to embolus and then clotting, this isn't what happens. The reason that your explanation doesn't work (and I keep hearing it, I don't know where it comes from) is that atheromatous plaques generally occur in arteries. If we say that an aortic plaque ruptures, to get to the coronary arteries, it would have to pass through the arteries -> arterioles -> capillaries -> venules -> veins -> IVC -> Right Atrium -> Right Ventricle -> Pulmonary Artery -> Pulmonary Capillary Bed -> Pulmonary Vein -> Left Atrium -> Left Ventricle -> Coronary Arteries. There are two "filters" there which atheromatous would lodge in, the systemic capillary beds and pulmonary capillary beds, and would stop the plaque reaching the coronary arteries. Far and away, the most common pathology is that an atheromatous plaque ruptures in a coronary artery. This causes exposure of various tissue factors leading to a clotting cascade, and forming an occlusive thrombus at the site in the coronary artery, thus stopping blood flow. For more info, you can read This sample chapter of a text book. RS Final Year Medical Student