Acute Coronary Syndrome (ACS) describes a sudden and serious medical emergency where blood flow to the heart muscle is abruptly reduced or blocked. This condition requires immediate medical attention to restore blood flow. ACS is time-sensitive, with symptoms like chest pain or discomfort often signaling an issue.
The Foundation: Atherosclerosis
The underlying condition for ACS is atherosclerosis, a chronic disease affecting the arteries. This process begins with injury to the inner lining of the arteries, the endothelium. Over time, cholesterol, fats, and other substances accumulate within artery walls, forming deposits called plaques. These plaques are composed of lipids, inflammatory cells, smooth muscle cells, and connective tissue.
As plaques grow, they harden and narrow the arteries, restricting blood flow to the heart and other organs. This narrowing can lead to symptoms like chest pain during exertion, known as stable angina. Not all plaques are stable; some are “vulnerable” due to their unstable nature.
Vulnerable plaques possess a thin fibrous cap, a large lipid-rich core, and increased inflammation. These characteristics make them more prone to rupture or erosion compared to stable plaques, which have a thicker fibrous cap and less lipid content.
The Acute Trigger: Plaque Rupture and Blood Clot Formation
The sudden onset of ACS is triggered by the disruption of a vulnerable atherosclerotic plaque within a coronary artery. This disruption can occur as a rupture of the thin fibrous cap or an erosion of the plaque surface. When the plaque ruptures, the highly thrombogenic contents of its lipid-rich core are exposed to the bloodstream.
Exposure triggers a rapid clotting process at the injury site. Platelets quickly adhere to the exposed plaque material and become activated. This activation leads to the aggregation of more platelets, forming a platelet plug.
Concurrently, the coagulation cascade is activated, leading to fibrin formation. This fibrin mesh traps red blood cells and platelets, creating a stable blood clot (thrombus) at the site of plaque disruption. This thrombus can partially or completely block blood flow through the coronary artery, leading to acute ACS symptoms.
Differentiating Acute Coronary Syndrome Types
The degree and duration of coronary artery occlusion by the newly formed blood clot determine the specific type of Acute Coronary Syndrome (ACS) a patient experiences. Unstable Angina (UA) and Non-ST-Elevation Myocardial Infarction (NSTEMI) involve partial or transient blockages of the coronary artery.
In Unstable Angina, there is a reduction in blood flow to the heart muscle, causing ischemia, but no detectable heart muscle cell death. Patients experience chest pain at rest or with minimal exertion, which may be new in onset or worsening from previous angina. The lack of elevated cardiac biomarkers, such as troponin, differentiates UA from NSTEMI.
NSTEMI involves a partial or temporary coronary artery blockage severe enough to cause heart muscle cell injury and death. This myocardial damage is indicated by elevated levels of cardiac biomarkers, like troponin, in the blood.
ST-Elevation Myocardial Infarction (STEMI) represents the most severe form of ACS, characterized by a complete and sustained blockage of a coronary artery. This total occlusion leads to extensive myocardial damage, affecting the full thickness of the heart muscle wall. The complete blockage results in distinct changes on an electrocardiogram (ECG), specifically ST-segment elevation.
Consequences for Heart Tissue
The reduction or complete cessation of blood flow to the heart muscle (myocardial ischemia) has severe consequences. This initial lack of oxygen can lead to myocardial injury, where heart muscle cells are damaged but may still be salvageable if blood flow is quickly restored.
If the deprivation of oxygenated blood persists for an extended period, myocardial necrosis (heart muscle cell death) occurs. This irreversible damage is a myocardial infarction, or heart attack. The extent of this cell death directly correlates with the duration and severity of the coronary artery blockage.
The dead heart muscle tissue is eventually replaced by fibrotic scar tissue, which lacks the contractile properties of healthy heart muscle. This scarring can impair the heart’s ability to pump blood effectively throughout the body, potentially leading to weakened heart function or heart failure over time. The larger the area of necrosis, the greater the impact on the heart’s overall pumping capacity and the higher the risk of adverse outcomes.