A heart attack happens when blood flow to part of the heart muscle gets blocked, starving that tissue of oxygen. In about 75% of cases, the blockage comes from a ruptured plaque inside a coronary artery. Every year, roughly 805,000 people in the United States have a heart attack, and someone in the U.S. has one every 40 seconds.
How a Blocked Artery Causes a Heart Attack
The process starts years or even decades before the actual event. Cholesterol particles in your blood slip through damaged spots in the lining of your coronary arteries and settle inside the artery wall. Your immune system treats this buildup as a threat, sending inflammatory cells to the area. Those cells absorb the cholesterol and form a fatty deposit called plaque.
Over time, a fibrous cap forms over the plaque, keeping it contained. But inflammation weakens that cap. Immune cells release enzymes that eat away at the cap’s structure until it cracks open. The moment it ruptures, the material inside is exposed to your bloodstream, and your body responds the same way it would to a wound: it forms a blood clot. That clot can partially or completely block the artery, cutting off blood flow to the heart muscle downstream. Within minutes, heart cells begin to die.
Not every plaque that ruptures causes a heart attack. Your body has its own clot-dissolving system, and sometimes it breaks the clot down before serious damage occurs. The balance between clot formation and clot dissolution in that moment determines whether you walk away unaware or end up in an emergency room.
The Major Risk Factors
High Blood Pressure
Sustained high blood pressure damages the inner lining of your arteries, making it easier for cholesterol to penetrate the artery wall and start the plaque-building process. It also forces the heart to work harder with every beat, thickening the heart muscle over time and increasing its oxygen demand. When combined with diabetes, the danger compounds: people with high blood pressure are about 2.5 times more likely to develop type 2 diabetes, and the two conditions together accelerate artery damage significantly.
Diabetes
Diabetes is one of the strongest independent risk factors for a heart attack. The age-adjusted risk of dying from a cardiovascular event is roughly three times higher in people with type 2 diabetes than in the general population. That elevated risk persists even after accounting for blood pressure, cholesterol levels, smoking, and age. High blood sugar damages blood vessels from the inside and promotes inflammation, both of which speed up plaque formation.
The risk is not equal between sexes. After adjusting for other factors, the increased mortality risk from heart disease is about 2.4 times greater for men with diabetes and 3.5 times greater for women with diabetes compared to their non-diabetic counterparts.
High Cholesterol
Elevated LDL cholesterol (the “bad” kind) is the raw material for plaque. The more LDL circulating in your blood, the more that infiltrates your artery walls. Reducing LDL levels slows plaque growth and can even stabilize existing plaques, making them less likely to rupture.
Smoking
Smoking damages the artery lining, raises blood pressure, reduces the oxygen-carrying capacity of your blood, and makes blood more likely to clot. It accelerates every step of the process that leads to a heart attack. Quitting reverses much of this damage over time, with cardiovascular risk dropping substantially within the first few years.
Genetic Causes
Some people are genetically wired for higher heart attack risk regardless of lifestyle. Familial hypercholesterolemia is a hereditary condition affecting about 1 in 311 people that causes abnormally high LDL cholesterol from birth. If left untreated, 50% of men with this condition will have a heart attack by age 50, and 30% of women will have one by age 60.
About 60% to 80% of people with familial hypercholesterolemia carry a specific identifiable gene mutation. Genetic testing can confirm the diagnosis and help guide treatment decisions. Because the condition runs in families, discovering it in one person often leads to testing relatives, some of whom may not know they’re at risk.
Beyond this specific condition, a family history of early heart disease (a father or brother before age 55, or a mother or sister before age 65) raises your risk even when no single gene is responsible. Multiple common genetic variants can each nudge cholesterol, blood pressure, or inflammation slightly higher, and their effects add up.
Acute Triggers That Set Off an Attack
Most heart attacks happen in people who already have plaque buildup, but something in the hours before the event tips the balance. The INTERHEART study, a large international study of heart attack patients, identified two triggers that stand out.
Physical exertion in the hour before a heart attack was associated with 2.3 times the odds of having the event. Anger or intense emotional upset carried similar odds, at 2.4 times. When both occurred together, the odds jumped to about 3 times higher. Both triggers work through the same mechanism: they activate your body’s stress response, releasing adrenaline, constricting blood vessels, raising heart rate and blood pressure, and increasing the heart’s oxygen demand. In someone with a vulnerable plaque, that surge of pressure and turbulence can be enough to crack it open.
This doesn’t mean exercise is dangerous. Regular physical activity actually protects the heart. The risk comes from sudden, intense exertion in someone who isn’t conditioned for it or who already has significant artery disease.
Heart Attacks Without Major Blockages
Between 5% and 15% of heart attacks occur in people whose coronary arteries show no significant blockage on imaging. This category, sometimes called MINOCA, has several possible explanations.
Coronary artery spasm is one cause. The muscular wall of a coronary artery clamps down temporarily, choking off blood flow even though no permanent blockage exists. Stimulant drugs, particularly cocaine, are a well-known trigger. Cocaine causes the smooth muscle cells in artery walls to constrict by overstimulating certain receptors while simultaneously reducing the natural compounds that keep arteries relaxed. It also increases heart rate and blood pressure, drives up the heart’s oxygen demand, and makes the blood more prone to clotting. All of these effects can converge to cause a heart attack, even in someone with otherwise healthy arteries.
Another less common cause is spontaneous coronary artery dissection, where the inner lining of a coronary artery tears without warning, and blood collects within the artery wall. This narrows or blocks the channel through which blood flows. About 90% of cases occur in women, and while it was once thought to mainly affect younger women, it can happen at any age, including after menopause. The triggers are not fully understood but may include hormonal changes, extreme physical stress, and connective tissue disorders.
Tiny clots that form elsewhere and travel to the heart’s smaller blood vessels, or dysfunction in the heart’s microcirculation (the smallest blood vessels that feed the heart muscle directly), can also cause a heart attack without visible blockages in the larger arteries.
Silent Heart Attacks
About 1 in 5 heart attacks are silent, meaning the person experiences no obvious chest pain and may not realize anything happened. The damage still occurs. Heart muscle cells still die and form scar tissue, which can weaken the heart over time. Silent heart attacks are often discovered later during a routine electrocardiogram or imaging test. They’re more common in people with diabetes, partly because nerve damage from the disease can blunt the pain signals that would normally alert someone to the problem.
The cumulative toll of heart attacks in the U.S. is substantial. Coronary heart disease killed 371,506 people in 2022, making it the most common type of heart disease. Of the 805,000 annual heart attacks, about 605,000 are a first event, and 200,000 occur in people who have already survived one.