What is the initial pathological process in myocardial infarction (MI) with a history of hypertension: activation of factor VII, adhesion of platelets, or conversion of fibrinogen?

From the Guidelines

The initial pathological process in myocardial infarction (MI) with a history of hypertension is adhesion of platelets.

Pathogenesis of Myocardial Infarction

• The pathogenesis of ST-segment elevation acute myocardial infarction is caused by an occlusion of a major coronary artery, usually due to physical disruption of an atherosclerotic plaque with subsequent formation of an occluding thrombus 1.
• The risk of plaque disruption depends on plaque composition and vulnerability, and degree of stenosis, with inflammation playing an important role in plaque instability 1.
• The circadian variation of STEMI, with a higher incidence in the early morning hours, can be explained by the combination of β-adrenergic stimulation, hypercoagulability of the blood, and hyper-reactivity of platelets 1.

Role of Platelets and Fibrin

• Both platelets and fibrin are involved in the evolution of a persisting coronary thrombus, with platelet adhesion and aggregation initiating mural thrombus formation, and fibrin important for the subsequent stabilization of the early and fragile platelet thrombus 1.
• The thrombotic response to plaque disruption is dynamic, with thrombosis and clot lysis, often associated with vasospasm, occurring simultaneously, and may cause intermittent flow obstruction and distal embolization 1.

From the Research

Initial Pathological Process in Myocardial Infarction (MI)

The initial pathological process in myocardial infarction (MI) with a history of hypertension involves several factors. The key steps include:

• Adhesion of platelets: Platelets play a crucial role in the pathogenesis of myocardial infarction by adhering to the site of a ruptured atherosclerotic plaque 2.
• Activation of coagulation cascade: The coagulation cascade is activated, leading to the formation of thrombin and fibrin 3, 4.
• Conversion of fibrinogen: Fibrinogen is converted to fibrin, which forms the clot 4.

Role of Factor VII

The role of factor VII in the initial pathological process of MI is not entirely clear. Some studies suggest that activated factor VII levels are not increased in patients with acute coronary syndromes, including MI 3. However, other studies have found increased levels of factor VII activity in patients with a history of MI 4.

Adhesion of Platelets

The adhesion of platelets to the site of a ruptured atherosclerotic plaque is a critical step in the development of MI. Platelets release microRNAs, which can regulate endothelial cell gene expression 2. The adhesion of platelets is also influenced by various factors, including hypertension, which can increase the risk of MI.

Conversion of Fibrinogen

The conversion of fibrinogen to fibrin is an important step in the coagulation cascade. Studies have found increased levels of fibrinogen in patients with a history of MI 4. The conversion of fibrinogen to fibrin is influenced by various factors, including thrombin, which is formed during the coagulation cascade 3, 4.