Heart attacks happen when blood flow to part of the heart muscle gets blocked, starving that tissue of oxygen. The most common cause is a buildup of fatty deposits inside the coronary arteries that eventually ruptures and triggers a blood clot. But several other conditions, substances, and even sudden events can also cause one, sometimes in people who seem perfectly healthy.
How Most Heart Attacks Start
The vast majority of heart attacks trace back to a slow process called atherosclerosis. It begins when cholesterol particles in the blood get trapped in the walls of the coronary arteries. Over years, those deposits attract immune cells and trigger inflammation, gradually forming a plaque made of fat, dead cells, fibrous tissue, and calcium.
A heart attack typically occurs when one of these plaques ruptures. Not all plaques are equally dangerous. The ones most likely to rupture have a large, soft core of dead cells and fat covered by an extremely thin fibrous cap. When that cap tears open, it exposes the interior of the plaque to the bloodstream. The body treats this like a wound and rapidly forms a blood clot at the site. If the clot is large enough to block the artery, the heart muscle downstream loses its blood supply within minutes. The longer that blockage lasts, the more permanent the damage.
The Major Risk Factors
Some risk factors you can change, others you can’t. But even the ones you can’t change are worth knowing, because they tell you how aggressively to manage the ones you can.
Risks You Can Control
- High blood pressure damages artery walls over time, making it easier for cholesterol to penetrate and form plaques.
- High cholesterol directly fuels plaque growth. LDL cholesterol is the primary driver, but a genetic blood fat called lipoprotein(a), or Lp(a), independently raises risk. Levels above 50 mg/dL are considered high, and roughly one in five people have them. Unlike regular cholesterol, Lp(a) is mostly determined by genetics and doesn’t respond much to diet.
- Smoking accelerates plaque formation, promotes blood clotting, and can trigger coronary artery spasms on its own.
- Diabetes and high blood sugar damage blood vessels from the inside, increasing both the speed of plaque development and the likelihood of clotting.
- Obesity and physical inactivity worsen nearly every other risk factor on this list while also contributing to chronic inflammation.
- Poor sleep is increasingly recognized as a cardiovascular risk factor. The American Heart Association now includes sleep alongside diet, exercise, and smoking in its core measures of heart health.
Risks You Can’t Control
Age is the strongest non-modifiable risk factor. Risk climbs sharply after 45 in men and after 55 in women. A family history of early heart disease (a parent or sibling who had a heart attack before age 55 for men or 65 for women) signals a genetic predisposition that goes beyond shared lifestyle habits. Elevated Lp(a) is one measurable piece of that genetic puzzle, though it’s far from the only one.
Risks Unique to Women
Heart attacks are often framed as a men’s health problem, but cardiovascular disease kills more women than any other condition. Women share the same core risk factors as men, yet face several additional ones tied to hormones, pregnancy, and autoimmune conditions.
Preeclampsia, a dangerous rise in blood pressure during pregnancy, makes a person 75% more likely to die of cardiovascular disease later in life. Gestational diabetes raises the lifetime risk of developing full diabetes, which in turn raises heart attack risk. Even having four or more pregnancies has been linked to higher cardiovascular risk.
Menopause is a turning point. Estrogen helps protect blood vessels, and when levels drop after menopause, that protection fades. The body also becomes more sensitive to sodium after menopause, making blood pressure harder to control. Women account for about 80% of autoimmune disease diagnoses in the U.S., and conditions like lupus and rheumatoid arthritis significantly increase the risk of heart attack and heart failure through chronic inflammation that damages arteries from the inside.
Coronary Artery Spasm
Not every heart attack involves a ruptured plaque. Sometimes a coronary artery suddenly squeezes shut on its own, temporarily cutting off blood flow. This is called a coronary artery spasm, and it can happen even in arteries with little or no plaque buildup. Common triggers include tobacco use, cocaine or amphetamine use, exposure to extreme cold, and severe emotional stress. Spasms tend to strike at rest, often in the early morning hours, and the chest pain they cause can be intense but typically passes within minutes. In rare cases, a prolonged spasm causes enough oxygen deprivation to produce a full heart attack.
Spontaneous Coronary Artery Dissection
Spontaneous coronary artery dissection, or SCAD, is a tear in the wall of a coronary artery that allows blood to collect between the layers, creating a bulge that blocks flow. It overwhelmingly affects women and may account for up to 35% of heart attacks in women under 50. Most people who experience SCAD have few or no traditional risk factors like high cholesterol or high blood pressure.
The strongest associated condition is fibromuscular dysplasia, a disorder of blood vessel walls found in 25% to 86% of SCAD patients depending on how thoroughly doctors screen for it. Connective tissue disorders like Ehlers-Danlos syndrome and Marfan syndrome also increase risk, though they account for a small fraction of cases. Pregnancy-related SCAD is well documented but relatively uncommon, occurring in 2% to 8% of cases in large studies. Hormonal therapies, including oral contraceptives and fertility treatments, have been linked to SCAD as well.
Acute Triggers That Push a Vulnerable Heart Over the Edge
In someone with existing plaque buildup, certain acute events can be the final trigger that causes a rupture. The plaque was already unstable; the trigger is what breaks it open.
Sudden, intense physical exertion is one of the best-documented triggers, particularly in people who are not regularly active. Shoveling heavy snow is a classic example, and case reports have linked it to plaque rupture, heart attacks, and dangerous heart rhythm disturbances. The combination of straining, cold air, and a spike in blood pressure is especially risky.
Severe emotional distress can do something similar. Intense anger, grief, or fear triggers a surge of stress hormones that raise heart rate, spike blood pressure, and make blood more prone to clotting. This is the mechanism behind “broken heart syndrome” and the well-documented rise in heart attacks after earthquakes, major sporting events, and personal loss. The stress itself doesn’t create the disease, but it can set off a crisis in someone whose arteries are already compromised.
Substances and Medications
Cocaine is one of the most potent heart attack triggers at any age. It causes coronary artery spasm, raises heart rate and blood pressure dramatically, and promotes blood clotting, all at the same time. Amphetamines and other stimulants carry similar risks.
Some prescription and over-the-counter medications can also raise heart attack risk over time. Common anti-inflammatory painkillers (the class that includes ibuprofen and naproxen) can increase the risk of clotting events, especially with long-term use or high doses. Certain hormonal therapies and some antipsychotic medications have also been associated with elevated risk through mechanisms that include blood vessel dysfunction, increased clotting tendency, and metabolic changes like weight gain and higher blood sugar.
How a Heart Attack Gets Confirmed
When you arrive at a hospital with chest pain, doctors look for a specific pattern: a rise or fall in a protein called troponin in your blood, combined with at least one other sign that your heart muscle is being damaged. Troponin is released when heart cells die, so a spike above normal confirms injury is happening. The other evidence can come from your symptoms, changes on an electrocardiogram (ECG), or imaging that shows part of the heart isn’t contracting normally. Both pieces are required. Elevated troponin alone could come from other causes of heart stress, and symptoms alone aren’t specific enough. Together, they confirm the diagnosis and guide how urgently treatment needs to begin.