Acute myocardial infarction is a disease or a clinical syndrome accompanying other diseases. All that occurs simultaneously with infarction is highly pathologic but not physiologic. But it corresponds to current requirements and, therefore, is normal. More read here.
Inflammation, the typical pathologic process underlying the disease, is just that by definition. Let us remember transitional atrial flutter accompanying large acute myocardial infarction. Whatever they say, a decrease in heart preload is an extremely precise mechanism. Of course, if this arrhythmia is normosystolic, and what is more, at a rate within upper limits of the norm. Try to restore sinus rhythm in such a patient, and his heart would start to ‘choke’. Have you ever met such a situation?
We have already discussed compensatory functions of naturally formed thromboendocarditis. But if this process is disturbed? Of course, when we actively intervene in blood coagulability with the purpose of treatment. Or let us remember coronaroactive drugs for improving the blood supply in the peri-infarction zone. It appeared that they robbed it. Simply, because Nature did it the
way that in the case of infarction, the vessels of the infarction zone are dilated as much as possible. There is nowhere to dilate them anymore. We administer coronaroactive drugs and dilate the vessels of an intact myocardium. Blood flows out of the peri-infarction zone. It is an old story.
The conclusion is simple. Before improving something, one should first think for a while. And no more than that.
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