This is a discussion I had with a lot of people. My questions are put in inverted commas.
"I don't understand the next best step in the management in acute coronary syndromes. If there's ST elevation MI, you do angioplasty. But when there was a ST depression, they preferred heparin after aspirin even when angioplasty was in the options. Why is that? Why does the management change depending on elevation or depression?"
ST elevation means transmural ischemia so maybe angioplasty is the only way to restore flow. ST depression means subendocardial ischemia so occlusion isn't complete. Heparin and blood thinners might work.
"But then if you can do angioplasty (Catherization lab available), why give heparin?"
They do send for angioplasty later. Heparin can be given immediately to prevent the situation from getting worse.
"But then again, why wouldn't you do that with ST elevation too?"
ST elevation means the occlusion is complete. Heparin wouldnt be effective. In NSTEMI and unstable angina, there's still some lumen viable.
"Patients with MI with ST-segment depression should not be treated with fibrinolysis. Why isn't fibrinolysis done in ST depression angina?
We say that the occlusion isn't complete because there is subendocardial ischemia in ST depression and we give heparin to prevent further occlusion. But why not give streptokinase? Why not eradicate what is already formed instead of trying to prevent progression of clot?"
Because fibrinolysis treatment has it's own side effects and it's not effective in all the cases. It's contraindicated because studies have shown it does more harm than good in only ST depression.
Like, for example, there is reperfusion injury which would might make the only subendocardial infarct into a transmural one. 3 in ten patients end up with cerebral haemorrhage. There are so many other clauses.
Hence it's only indication is a transmural infarction.. The damage is already great. Irrespective of using t-PA the patient condition is critical.
Thank you everyone who helped me out on this one.