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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:
- Chest Pain (Angina): Typically described as a crushing, pressure-like pain in the chest that may radiate to the jaw, left arm, shoulder, or back.
- Shortness of Breath or Dyspnea: Due to impaired oxygen delivery to the myocardium.
- Diaphoresis: Excessive sweating caused by sympathetic nervous system activation.
- Nausea and Vomiting: Due to vagal stimulation.
- Palpitations: Resulting from arrhythmias triggered by ischemic myocardial tissue.
- Fatigue and Weakness: Due to inadequate cardiac output.
- Syncope (Fainting): Caused by reduced cerebral perfusion.
Corresponding ECG Findings Based on Pathophysiology:
- Unstable Angina: May show ST-segment depression or T-wave inversions but no ST-segment elevation or Q waves.
- Non-ST Elevation Myocardial Infarction (NSTEMI): ST-segment depression and/or T-wave inversions, often with elevated cardiac biomarkers.
- ST Elevation Myocardial Infarction (STEMI): Characterized by ST-segment elevation in at least two contiguous leads, new-onset left bundle branch block (LBBB), and the eventual development of Q waves, indicative of myocardial necrosis.
These ECG changes, along with clinical symptoms and biomarker elevation, guide the diagnosis and management of ACD.
