What happens to the body when there is an acute myocardial infarction (MI)?

From the Guidelines

When an acute myocardial infarction (MI) occurs, the body experiences an acute imbalance in myocardial oxygen demand and supply, leading to myocardial cell necrosis and infarction due to the occlusion of the coronary artery by a "plaque + superimposed thrombus complex". This imbalance is caused by coronary heart disease with atherosclerotic plaque disruption and superimposed platelet-rich thrombus formation, as described in the 2017 AHA/ACC clinical performance and quality measures for adults with ST-elevation and non-ST-elevation myocardial infarction 1.

The pathophysiological mechanisms causing MI can result in either ST-elevation myocardial infarction (STEMI) or non-ST-elevation myocardial infarction (NSTEMI), depending on the degree of occlusion of the coronary artery. STEMI usually presents with persistent ST-elevation on the ECG, while NSTEMI is characterized by the absence of persistent ST elevation on ECG, but rather the presence of ST depression, T-wave inversion, or other nonspecific changes.

Key points to consider in the management of acute MI include:

• The importance of prompt administration of aspirin to inhibit platelet aggregation, with a loading dose of 162 to 325 mg of non–enteric-coated aspirin formulation, followed by an 81-mg daily dose to minimize bleeding risk 1
• The need for timely restoration of blood flow to limit the extent of tissue damage, which can be achieved through treatments like thrombolytics or percutaneous interventions
• The potential consequences of acute MI, including heart failure and neurological deficits, depending on the severity and location of the infarct.

In terms of treatment, aspirin therapy administered within the first 24 h after acute STEMI has been shown to result in a 23% relative risk reduction in 5-week vascular mortality, as well as significant reductions in the incidence of non-fatal reinfarction and stroke 1. Overall, the management of acute MI requires a comprehensive approach that takes into account the underlying pathophysiological mechanisms, as well as the need for prompt and effective treatment to minimize morbidity and mortality.

From the FDA Drug Label

Alteplase is an enzyme (serine protease) that has the property of fibrin-enhanced conversion of plasminogen to plasmin. It produces limited conversion of plasminogen in the absence of fibrin. Alteplase binds to fibrin in a thrombus and converts the entrapped plasminogen to plasmin, thereby initiating local fibrinolysis (1) In patients with acute myocardial infarction administered 100 mg of Activase as an accelerated intravenous infusion over 90 minutes, plasma clearance occurred with an initial half‑life of less than 5 minutes and a terminal half‑life of 72 minutes.

The body experiences local fibrinolysis when there is an acute myocardial infarction (MI) and alteplase is administered, as it binds to fibrin in the thrombus and converts plasminogen to plasmin.

• The plasma clearance of alteplase occurs with an initial half-life of less than 5 minutes and a terminal half-life of 72 minutes in patients with acute MI 2.
• The mechanism of action of alteplase involves the conversion of plasminogen to plasmin, thereby initiating local fibrinolysis.

From the Research

Pathophysiology of Acute Myocardial Infarction (MI)

When there is an acute myocardial infarction (MI), the body's response is complex and involves multiple systems.

• The heart muscle is damaged due to a lack of blood flow, leading to cell death and tissue damage 3.
• The damage to the heart muscle can lead to a range of complications, including arrhythmias, heart failure, and even death.

Treatment and Management of Acute MI

The treatment and management of acute MI typically involve a combination of medications and interventions, including:

• Antiplatelet agents, such as aspirin and clopidogrel, to prevent further clotting 4, 5, 6.
• Beta-blockers to reduce the workload on the heart and prevent arrhythmias 4, 5, 6.
• Statins to lower cholesterol levels and reduce the risk of further heart disease 4, 5, 7, 6.
• Angiotensin-converting enzyme (ACE) inhibitors to reduce blood pressure and prevent further damage to the heart 4, 5, 7, 6.
• Reperfusion strategies, such as percutaneous coronary intervention (PCI) or fibrinolysis, to restore blood flow to the affected area of the heart 3.

Importance of Secondary Prevention

Secondary prevention is critical in reducing the risk of further heart disease and improving outcomes after an acute MI.

• Studies have shown that combination therapy with aspirin, an ACE inhibitor, and a statin can reduce 1-year mortality after acute MI 7.
• Patient education and adherence to medication regimens are essential in improving treatment persistence and reducing the risk of further complications 4.