A theory concerning the course of events in angina and myocardial infarction.
Evidence is discussed which suggests that coronary arterial thrombosis need not be the primary event in myocardial infarction. If this is so, it is necessary to consider the initial changes which might occur in the myocardium rather than the effects of experiments in which the coronary arterial supply has been suddenly cut off. Results of recent investigations on patients suggest that, during the anginal attack, there is an inability of the affected myocardium to relax and a diminution in the flow of blood to the region. The former implies an increased myofibrillar concentration of calcium ions, the latter may be explained by the mechanical compression of small intramyocardial blood vessels. It is argued that these two factors may initiate vicious circles which could lead to the death of myocardial cells and thus to myocardial infarction.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000787:Angina Pectoris / Q000209:etiology* / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D003327:Coronary Disease / Q000150:complications; D006801:Humans; D006868:Hydrolysis; D009203:Myocardial Infarction / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D009206:Myocardium / Q000378:metabolism; D009210:Myofibrils / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
D000255:Adenosine Triphosphate; D012964:Sodium; D000251:Adenosine Triphosphatases; D011188:Potassium; D002118:Calcium