usually occurs first in the sub-endocardial region
occurs due to increased demand or decreased supply that the heart cannot maintain therefore causing areas of oxygen deprevation within the heart
most often it is caused by buildup of plaque, called atherosclerosis
it is caused by foam cell build up and in some cases a fibrous cap forms by smooth muscle cells then which narrows the blood vessel by up to 70% of its lumen which decreases amount of O2 getting through. at rest this is okay and myocardial cells are supplied with enough oxygen. however when O2 demand increases during exertion not enough is able to pass through causing angina (stable angina) due to ischaemia of the myocardial cells
the exact same physiopathological process occurs in each type (build of of atheroma) however in the next 3 i will be discussing the fibrous cap within the lumen is unstable and so is prone to rupture. after the rupture stage many platelets will form and build themselves up forming a thrombus within the blood vessel which acts to stop flow of blood and decrease oxygen saturation allowed thru.
UNSTABLE ANGINA
in stable angina 70% ish of the vessel's lumen can be taken up by atherosclerosis with a fibrous cap, however in unstable angina even up to 90% of the lumen can be taken up.
how/why?
because the fibrous cap in the atherosclerosis is actually not stable/strong so when it comes off many platelets will swarm to the area and form a thrombis which then causes this massive occlusion of the vessel's lumen.
results in chest pain even at rest due to this massive occlusion chest pain in this instance occurs during rest and ischaemia of cells occurs
NSTEMI
same process as unstable angina although less oxygen is allowed through to the myocardium