A heart attack happens when blood flow to part of the heart muscle gets blocked, usually by a blood clot that forms inside a coronary artery. Without blood flow, heart cells begin dying within minutes. The most common underlying cause is a slow buildup of fatty deposits in artery walls that eventually becomes unstable and ruptures, but heart attacks can also strike people with clean arteries under the right circumstances.
How Plaque Builds Up in Your Arteries
The process that leads to most heart attacks starts years or even decades before any symptoms appear. It begins with damage to the inner lining of a coronary artery. High blood pressure, smoking, high blood sugar, and chronic inflammation all wear down this lining over time, making it sticky and permeable.
Once the lining is damaged, cholesterol particles (specifically LDL, the “bad” cholesterol) slip through and get trapped inside the artery wall. The immune system treats this like an infection. White blood cells rush in, swallow the cholesterol, and become bloated “foam cells” that pile up beneath the surface. These foam cells release chemical signals that recruit even more immune cells, creating a self-reinforcing cycle of inflammation. Over years, this mass of fat, dead cells, and immune debris grows into what’s called plaque.
The plaque develops a fibrous cap that separates it from the bloodstream. As long as that cap holds, blood continues flowing. The real danger comes when the cap weakens.
The Moment a Heart Attack Begins
Inflammatory cells inside the plaque release enzymes that eat away at the fibrous cap from the inside. The thinnest, most vulnerable spot is typically at the edges of the plaque. When the cap tears open, the fatty core is suddenly exposed to flowing blood. The body reacts the same way it would to a cut on your skin: platelets swarm to the site and a blood clot rapidly forms.
In a coronary artery, which may already be narrowed by plaque, that clot can completely seal off blood flow in seconds. About 54% of heart attacks are triggered by this kind of plaque rupture. The remaining cases, roughly 46%, involve a different process called plaque erosion, where the surface of the plaque wears away without a dramatic rupture, but still triggers clot formation.
Once the artery is blocked, the clock starts immediately. Heart muscle begins dying from the inside out, starting with the innermost layers closest to the blockage. Research using cardiac MRI shows that if blood flow isn’t restored within about two hours, the damage typically extends through the full thickness of the heart wall. This is why emergency treatment focuses on reopening the artery as fast as possible.
Chronic Inflammation as a Driver
Inflammation isn’t just part of the plaque-building process. It’s an independent force that raises heart attack risk even when cholesterol levels look normal. One way to measure this is through a blood marker called high-sensitivity CRP. Levels below 1 mg/L indicate low cardiovascular risk. Levels between 1 and 3 mg/L signal moderate risk. Levels above 3 mg/L reflect significantly elevated risk of heart attack and stroke. In head-to-head comparisons, CRP has outperformed several other newer risk markers at predicting future cardiac events.
Chronic inflammation can come from many sources: excess body fat (especially around the abdomen), poor sleep, gum disease, autoimmune conditions, or a diet high in processed foods. It accelerates every stage of artery disease, from the initial damage to the artery lining all the way to the final weakening of the plaque cap.
High Blood Pressure and Blood Sugar
Persistently high blood pressure acts like sandpaper on artery walls. The 2025 guidelines from the American Heart Association define normal blood pressure as below 120/80 mm Hg. Stage 1 hypertension starts at 130/80, and stage 2 at 140/90. People with readings at or above 130/80 who also have diabetes, kidney disease, or an estimated 10-year cardiovascular risk of 7.5% or higher are considered candidates for blood pressure medication on top of lifestyle changes.
Insulin resistance, the metabolic state where your cells stop responding properly to insulin, compounds the problem. When insulin can’t do its job efficiently, the body produces more of it, and that excess insulin directly damages the artery lining. It promotes oxidative stress, stiffens blood vessels, and fuels the same inflammatory pathways that destabilize plaque. This is one reason why people with type 2 diabetes have such a sharply elevated risk of heart attack, even when their cholesterol numbers are under control.
Genetic Factors You Can’t Control
Some people inherit a high level of a cholesterol particle called lipoprotein(a), often written as Lp(a). Unlike regular LDL cholesterol, Lp(a) levels are almost entirely determined by your genes and don’t change much with diet or exercise. About one in five people has elevated levels.
Lp(a) is a triple threat. It sticks to artery walls more aggressively than regular LDL, promoting plaque buildup. It triggers inflammation by increasing the signals that pull immune cells into the artery lining. And it interferes with the body’s natural clot-dissolving system, making dangerous clots more likely to persist. Optimal Lp(a) is below 14 mg/dL. Levels between 31 and 50 mg/dL are considered high risk, and anything above 50 mg/dL puts you in the highest risk category. If you have a strong family history of early heart attacks, Lp(a) testing is worth asking about, since standard cholesterol panels don’t include it.
Heart Attacks Without Clogged Arteries
Not every heart attack follows the plaque-rupture script. In spontaneous coronary artery dissection (SCAD), the wall of a coronary artery tears on its own, and blood collects between the layers of the vessel wall. This pinches the artery shut from the outside. SCAD accounts for a small but significant percentage of heart attacks, and it looks nothing like typical heart disease.
About 93% of SCAD patients are women, with an average age around 48. Many have no traditional risk factors like high blood pressure or diabetes. Instead, the strongest associations are with pregnancy (which raises SCAD risk roughly sevenfold), extreme emotional or physical stress, hormonal factors like menopause or fertility treatments, and a blood vessel condition called fibromuscular dysplasia, found in about 22% of SCAD cases. This is one reason heart attacks in younger women are sometimes missed or dismissed.
Stimulant Use and Coronary Spasm
Cocaine and other stimulants can trigger a heart attack through a different mechanism entirely. These drugs cause coronary arteries to clamp down in intense spasm, cutting off blood flow even in arteries with little or no plaque. At the same time, stimulants spike heart rate and blood pressure, dramatically increasing the heart’s demand for oxygen at the exact moment its supply is being choked off. They also make platelets stickier, promoting clot formation.
If there is any existing plaque, the effect is amplified. Diseased segments of artery are especially prone to spasm because their damaged lining can’t produce the chemical signals that normally keep vessels relaxed. This combination of spasm, increased oxygen demand, and clot formation is why cocaine-related heart attacks can happen in otherwise young, healthy-looking people.
Environmental and Acute Triggers
Air pollution is a less obvious but well-documented trigger. Fine particulate matter (tiny particles from vehicle exhaust, industrial emissions, and wildfire smoke) can enter the bloodstream through the lungs and provoke inflammation in artery walls. For every 10 micrograms per cubic meter increase in fine particulate pollution, the risk of acute heart attack rises by roughly 8%. Brief spikes in pollution, not just years of exposure, can set off events in people with vulnerable plaque.
Other acute triggers that can push an already-vulnerable heart over the edge include sudden intense physical exertion in someone who is normally sedentary, extreme emotional stress (sometimes called “broken heart syndrome,” though the mechanism differs), cold weather exposure, and heavy meals. These don’t cause heart disease on their own, but they can be the final stressor that ruptures a weakened plaque or triggers a dangerous spasm.