A heart attack happens when blood flow to part of the heart muscle gets blocked, usually by a blood clot that forms inside a narrowed coronary artery. Without blood, heart muscle cells start dying within minutes. About 805,000 people in the United States have a heart attack every year, which works out to one every 40 seconds.
But the blockage itself is just the final event. The process that sets the stage typically takes years or even decades, and understanding it can help you recognize what puts you at risk.
How Arteries Narrow Over Time
The underlying process behind most heart attacks is atherosclerosis, a slow buildup of fats, cholesterol, and other substances inside artery walls. It starts when cholesterol particles (particularly LDL, often called “bad” cholesterol) get trapped in the inner lining of a coronary artery. Your immune system treats these deposits as a threat and sends white blood cells to clean them up. Those cells absorb the fat, swell into what scientists call foam cells, and eventually die, leaving behind a growing core of debris.
Over time, smooth muscle cells in the artery wall build a fibrous cap of collagen and other structural proteins over this fatty core. Think of it as a scab forming over an internal wound. The result is a plaque: a bump on the inside of the artery that narrows the channel blood flows through. This process can begin as early as your twenties and progress silently for decades before causing any symptoms.
What Triggers the Actual Heart Attack
A narrowed artery alone doesn’t usually cause a heart attack. The danger comes when a plaque becomes unstable and breaks open. The most common scenario is plaque rupture: the fibrous cap covering the fatty core becomes extremely thin, then tears. This exposes the material inside, which is highly thrombogenic, meaning it causes blood to clot on contact. Within moments, a clot can grow large enough to completely block the artery.
Not all heart attacks follow this pattern. In roughly a third of cases, a clot forms on the surface of a plaque that hasn’t actually ruptured, a process called plaque erosion. The end result is the same: a blocked artery and starving heart muscle.
Once blood flow stops, the damage clock starts immediately. If the blockage is severe and lasts more than a few minutes, heart muscle cells begin to die. The longer the artery stays blocked, the more muscle is lost permanently. This is why rapid treatment matters so much.
The Role of Inflammation
Inflammation is the thread that runs through every stage of heart attack risk. It helps plaques form, makes them unstable, and can ultimately trigger the clot that causes a heart attack. Inflammatory signaling molecules break down collagen in the fibrous cap, weakening it. White blood cells called neutrophils, when activated in large numbers, further destabilize plaques and promote clot formation.
This matters practically because inflammation can be a better predictor of danger than cholesterol levels alone. Among people already taking cholesterol-lowering medication, a blood marker of inflammation called high-sensitivity C-reactive protein (hsCRP) is a stronger predictor of future heart attacks than LDL cholesterol itself. In other words, someone with well-controlled cholesterol but high inflammation may still be at significant risk.
Major Risk Factors
Several conditions accelerate the process of plaque buildup and instability:
- High blood pressure damages artery walls, making them more vulnerable to cholesterol deposits. Current guidelines classify blood pressure of 130/80 or above as stage 1 hypertension. At 140/90 or higher, medication is typically recommended alongside lifestyle changes.
- High LDL cholesterol provides more raw material for plaque formation. The higher your LDL, the faster plaques can grow.
- Smoking damages blood vessel linings and promotes clotting. Even regular exposure to secondhand smoke raises the risk of coronary heart disease by 25 to 30 percent.
- Diabetes accelerates atherosclerosis through multiple pathways, including chronic inflammation and damage to blood vessel walls from elevated blood sugar.
- Obesity and physical inactivity contribute to all of the above conditions and add independent risk.
These risk factors don’t just add up. They multiply each other. Someone with high blood pressure, high cholesterol, and diabetes faces a far greater risk than the sum of each factor alone.
Genetics and Early Heart Attacks
Some people have heart attacks despite doing everything “right,” and genetics is often the reason. One inherited risk factor that many people have never heard of is lipoprotein(a), or Lp(a). Unlike regular cholesterol, Lp(a) levels are almost entirely determined by your genes and don’t respond much to diet or exercise.
High Lp(a) significantly increases the likelihood of heart attack, stroke, and aortic valve disease. Your doctor may suspect elevated Lp(a) if you or a close family member had a heart attack or stroke before age 55 (for men) or 65 (for women), especially without obvious risk factors like high cholesterol, smoking, diabetes, or obesity. If one family member has high Lp(a), first-degree relatives (parents, siblings, children) should be tested as well.
Heart Attacks Without Typical Plaque Buildup
Not every heart attack is caused by cholesterol plaques. Spontaneous coronary artery dissection, or SCAD, occurs when the wall of a coronary artery tears on its own, allowing blood to collect between the layers and block flow. It accounts for 1 to 4 percent of all heart attacks overall, but plays a much larger role in younger people.
SCAD is overwhelmingly more common in women. It may cause up to 35 percent of heart attacks in women under 50 and is the most common cause of heart attacks related to pregnancy, accounting for 43 percent of those cases. The average age at pregnancy-related SCAD ranges from 33 to 36. Because these patients are young and often have no traditional risk factors, SCAD is frequently misdiagnosed or missed entirely. Some patients are even sent home from the emergency department because they don’t fit the expected profile of someone having a heart attack.
Why Symptoms Differ Between Women and Men
The classic heart attack image of crushing chest pain applies more reliably to men. Women more often experience subtler symptoms: unusual fatigue, sweating, nausea, dizziness, shortness of breath, and pain in the back, jaw, lower chest, or upper abdomen. These symptoms can appear during rest or even during sleep, making them easier to dismiss as something else.
This difference has real consequences. Many women downplay their symptoms or delay seeking care, sometimes until significant heart damage has already occurred. The vagueness of the symptoms also leads to misinterpretation by both patients and healthcare providers. Coronary heart disease killed over 371,000 people in the United States in 2022 alone, and delayed recognition of symptoms contributes to that toll, particularly among women.
What You Can Actually Control
The majority of heart attacks are driven by atherosclerosis, and atherosclerosis is heavily influenced by modifiable risk factors. Keeping blood pressure below 120/80, maintaining healthy cholesterol levels, not smoking, staying physically active, and managing blood sugar if you have diabetes all directly slow plaque formation and reduce inflammation in artery walls.
Of the 805,000 heart attacks that occur each year in the U.S., about 605,000 are first-time events and 200,000 happen in people who have already had one. That second number is a reminder that even after a heart attack, the same risk factors continue to matter. The arterial damage that caused the first event doesn’t stop progressing on its own. Whether you’re trying to prevent a first heart attack or a second one, the biology works the same way: less inflammation, less plaque growth, more stable arteries.