I am truly confused about the term 'heart attack'. The definition used in cardiology seems to be that it refers to heart muscle being zero supplied by oxygen and necrosis is a result. Yet, we hear so many times of people having a heart attack, going into the angio suite, having no procedure and being sent home with no damage. This cannot be a heart attack then? In march, my troponin was elevated and I was told by the cardiologist that I had a heart attack. I had no tissue damage and that was because the paramedics gave me nitrates which relieved things. However, in rehab last week, the senior cardiac nurse said "oh, if nitrates eased the pain, then it wasn't a heart attack, nitrates won't help because it's a total blockage". I can see his point on this, but can't nitrates open the artery enough just to get a trickle of blood through? enough for the heart at rest? even 5% would make a huge difference.
So when does the term get used? If for example a patient had a thrombus form at a plaque rupture site, and it caused the start of a heart attack, would it still be classed as such if the thrombus broke down sufficiently after a few minutes? What if a stent is inserted before necrosis, does this remove the term heart attack from the equation?
Isn't it amazing how words can cause so much confusion lol.
I even asked a Cardiologist when I was in hospital in March, "when does angina actually become a heart attack? surely pain means damage, so how do we know if it's a heart attack or not? is severe angina a heart attack in reality?" I felt an idiot when he said "I know what you are trying to say, but angina is the symptom, not the actual physical event". It still left me wondering though. If I had a 90% blockage and exercised, then I would get pain. This pain is telling me that damage is occurring. So, if I carry on with pain, exercising even harder for hours, then would I cause irreversible damage to some cells? if so, did I cause a heart attack?
Surely it's much simpler than this?