From the Guidelines
Unstable angina, a form of acute coronary syndrome (ACS), is primarily caused by the rupture or erosion of atherosclerotic plaques in the coronary arteries, leading to partial obstruction of blood flow to the heart muscle, as supported by the most recent guidelines from the European Society of Cardiology in 2021 1. The process begins with atherosclerosis, where lipid-rich plaques develop in the arterial walls over time due to factors like hyperlipidemia, hypertension, diabetes, smoking, and genetic predisposition. When these plaques become unstable, they can rupture, exposing thrombogenic material to the bloodstream and triggering platelet aggregation and thrombus formation. Unlike myocardial infarction, in unstable angina, the thrombus does not completely occlude the artery or the occlusion is transient, resulting in myocardial ischemia without permanent damage.
Some key points to consider in the etiology of unstable angina include:
- The role of inflammation in plaque instability, with inflammatory cells like macrophages releasing enzymes that weaken the fibrous cap of plaques 1.
- Secondary causes can include coronary vasospasm (Prinzmetal's angina), severe anemia, hyperthyroidism, tachyarrhythmias, or cocaine use, which increase myocardial oxygen demand or decrease oxygen supply.
- The importance of identifying patients with suspected ACS, including those with unstable angina, and initiating appropriate management, which typically includes antiplatelet therapy, anticoagulation, statins, and often early invasive strategies to restore coronary blood flow 1.
Understanding the pathophysiology of unstable angina is essential for appropriate management, and the most recent guidelines from the European Society of Cardiology in 2021 provide the foundation for evidence-based practice in this area 1.
From the FDA Drug Label
Eptifibatide injection is indicated to decrease the rate of a combined endpoint of death or new myocardial infarction (MI) in patients with ACS (unstable angina [UA]/non-ST- elevation myocardial infarction [NSTEMI]), including patients who are to be managed medically and those undergoing percutaneous coronary intervention (PCI).
The FDA drug label does not answer the question.
From the Research
Etiology of Acute Coronary Syndrome (ACS) - Unstable Angina
The etiology of Acute Coronary Syndrome (ACS), specifically unstable angina, can be attributed to several factors, including:
- Disturbance of the integrity of atherosclerotic plaque by a fissure, rupture, or ulceration, leading to the formation of unstable atherosclerotic plaque and thrombi 2
- Partial or intermittent occlusion of the coronary artery, causing a reduction in blood supply to the heart 3
- Plaque composition and vulnerability to rupture, with lipid-rich and soft plaques being more prone to rupture than collagen-rich and hard plaques 4
- Ongoing inflammation and repair processes within the fibrous cap of the plaque, which can destabilize the plaque and make it more vulnerable to rupture 4
Pathophysiological Mechanisms
The pathophysiological mechanisms underlying ACS, including unstable angina, involve:
- Thrombogenesis, which occurs in coincidence with factors such as vascular wall, rheologic, thrombotic, and antithrombotic factors 2
- Activation of platelets, which play a key role in the pathophysiology of cardiovascular acute events 5
- Dynamic obstruction of the coronary artery, caused by the formation of thrombi and vasoconstriction 2
Clinical Presentation
The clinical presentation of ACS, including unstable angina, can vary, but common symptoms include: