The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:
The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.
As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the extracellular matrix, weakening the fibrous cap.
When the fibrous cap ruptures or the plaque erodes, this condition is called unstable angina. The underlying lipid core is exposed to the bloodstream, and reduced blood flow in a coronary artery leads to partial occlusion.
This exposure triggers the activation of platelets and the coagulation cascade, forming a thrombus (blood clot).
A clot begins to form on top of the coronary lesion, but the artery is not completely occluded.
This condition is often referred to as preinfarction angina because, without prompt intervention, the patient is at increased risk of experiencing a myocardial infarction[MI].
In myocardial infarction, the rupture of a plaque results in a more extensive thrombus formation that completely occludes the coronary artery.
Pathophysiologically, an imbalance exists between myocardial oxygen supply and demand, with the infarction area developing over minutes to hours.
This results in ischemia and necrosis of the myocardium supplied by that artery.
As myocardial cells are deprived of oxygen, ischemia develops, leading to cellular injury and, eventually, infarction (death of cells).
Clinical Manifestations of ACD:
Corresponding ECG Findings Based on Pathophysiology:
These ECG changes, along with clinical symptoms and biomarker elevation, guide the diagnosis and management of ACD.
Acute Coronary Syndrome, or ACS, develops due to the buildup of lipid-laden atherosclerotic plaques within the coronary arteries.
As the atherosclerotic plaque grows, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap.
Macrophages within the plaque secrete enzymes such as matrix metalloproteinases, which degrade the extracellular matrix and weaken the fibrous cap.
When the fibrous cap ruptures or the plaque erodes, the lipid core is exposed to the bloodstream, triggering the formation of a thrombus over the coronary lesion.
Initially, the artery may remain partially open, leading to unstable angina.
Although, if the thrombus expands and completely occludes the artery, it results in myocardial infarction. This blockage leads to ischemia, cellular injury, and eventual infarction or cell death.
Patients may present with chest pain, dyspnea, nausea, epigastric discomfort, diaphoresis, lightheadedness, fatigue, and palpitations.
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