A heart attack happens when blood flow to part of the heart muscle gets blocked long enough for that tissue to start dying. In the vast majority of cases, the blockage comes from a blood clot that forms suddenly inside a coronary artery, the vessels that feed the heart. About 805,000 people in the United States have a heart attack every year, and roughly 1 in 5 of those are “silent,” meaning the damage happens without the person realizing it.
How Plaque Builds Up in Your Arteries
The process behind most heart attacks starts years or even decades before the event itself. It begins when cholesterol particles (LDL, the “bad” cholesterol) seep into the walls of your coronary arteries and get trapped there. Once inside, these particles undergo chemical changes that trigger your immune system to respond. White blood cells rush to the area, swallow the cholesterol, and eventually become bloated “foam cells” that pile up inside the artery wall.
Over time, some of these cells die and aren’t properly cleared away, forming a soft, fatty core inside the artery wall. A thin cap of tissue holds this material in place. As long as the cap stays intact, blood continues flowing. But if the cap becomes too thin or weakened, it can tear open. When it does, the fatty material inside is exposed directly to your bloodstream, and your body reacts the same way it would to an open wound: it forms a clot. That clot can partially or completely block the artery within minutes, cutting off oxygen to the heart muscle downstream. This is a heart attack.
What Makes a Plaque Rupture
Not all plaques are equally dangerous. The ones most likely to rupture tend to have large, soft fatty cores and very thin caps. These “vulnerable” plaques may not even narrow the artery much beforehand, which is why heart attacks sometimes strike people who had no prior warning symptoms.
Several things can push a vulnerable plaque over the edge. A spike in blood pressure or heart rate, driven by your body’s stress response, physically stresses the cap. Increased clotting tendency and more reactive platelets amplify the clot that forms once the cap tears. This is one reason heart attacks cluster around moments of intense physical or emotional stress, and why they happen more often in cold weather or first thing in the morning when stress hormones peak.
Inflammation’s Role
Atherosclerosis is, at its core, an inflammatory disease. Inflammation drives every stage: the initial cholesterol buildup, the growth of the fatty core, and the weakening of the cap that leads to rupture. Scientists now understand that the same type of chronic, low-grade inflammation seen in conditions like arthritis plays a central role in heart disease.
A blood marker called C-reactive protein (CRP) reflects this inflammation. When measured with a high-sensitivity test, CRP levels above 3 mg/L indicate high cardiovascular risk. People with elevated CRP have two to three times the risk of heart attack compared to those with low levels. In one study, high CRP was associated with an eightfold increase in death from cardiovascular disease, with no similar link to other causes of death. CRP doesn’t just predict first events: it also tracks the likelihood of repeat heart attacks in people who already have heart disease.
High Cholesterol and Blood Pressure
High LDL cholesterol is the fuel for plaque formation. Current guidelines from the American Heart Association recommend keeping LDL below 100 mg/dL for people at moderate risk, and below 70 mg/dL for those at high risk of heart disease. The lower LDL goes, the less raw material is available to build new plaques or expand existing ones.
High blood pressure accelerates the damage. Normal blood pressure is below 120/80 mm Hg. Stage 1 hypertension starts at 130/80, and stage 2 begins at 140/90. Elevated pressure puts constant mechanical stress on artery walls, making it easier for cholesterol to penetrate and for existing plaques to destabilize. After age 50, the top number (systolic pressure) becomes an especially important predictor of heart attack risk.
Diabetes and Blood Sugar Damage
Persistently high blood sugar damages the inner lining of your arteries, a layer called the endothelium. Healthy endothelium produces a molecule that keeps arteries relaxed and open. In people with diabetes, high glucose impairs this process and generates harmful molecules called free radicals that accelerate cell death along the artery walls. When patches of the lining die off, the body responds by growing new tissue that can trap even more cholesterol, speeding up plaque formation at those sites. This is a major reason people with diabetes face significantly higher heart attack risk, even when their cholesterol levels aren’t extreme.
Genetics and Lipoprotein(a)
Some people inherit a higher risk of heart attacks regardless of lifestyle. One key genetic factor is lipoprotein(a), often written as Lp(a). This is a cholesterol particle your liver produces in amounts almost entirely determined by your genes. High Lp(a), defined as greater than 50 mg/dL, promotes plaque buildup, increases clotting, and drives inflammation that makes plaques more likely to rupture.
High Lp(a) is common across all racial and ethnic groups but appears more frequently in Black Americans. If heart attacks or strokes run in your family, particularly before age 55 in men or 65 in women, Lp(a) may be a factor worth testing. Unlike regular LDL cholesterol, Lp(a) doesn’t respond much to diet or exercise, which is why people with otherwise “clean” risk profiles can still have early heart attacks.
Coronary Artery Spasm
Not every heart attack involves a ruptured plaque. A coronary artery spasm is a sudden, temporary squeezing of an artery that can slow or completely stop blood flow to part of the heart. If the spasm is severe enough and lasts long enough, it causes the same kind of tissue damage as a clot-based heart attack.
Known triggers for coronary spasm include smoking, cocaine and amphetamine use, extreme emotional stress, and exposure to cold temperatures. This type of heart attack can happen in people with completely clean arteries, making it harder to predict and sometimes harder to diagnose after the fact.
Spontaneous Artery Tears (SCAD)
Spontaneous coronary artery dissection, or SCAD, is a less common but important cause of heart attacks, particularly in women in their 40s and 50s. In SCAD, a tear develops in the inner wall of a coronary artery. Blood seeps between the layers of the artery wall and either forms a clot or creates a flap of tissue that narrows the channel, blocking flow to the heart.
SCAD has no connection to cholesterol or traditional plaque buildup. It’s linked to a condition called fibromuscular dysplasia, which weakens medium-sized arteries and is far more common in women. Hormonal changes and blood vessel stress from pregnancy also play a role, with SCAD sometimes occurring in the weeks after childbirth.
Environmental and Situational Triggers
In someone whose arteries already have vulnerable plaques, certain external conditions can be the final trigger. Cold weather is one of the most well-documented. When you’re exposed to cold, your blood vessels narrow to conserve heat, forcing the heart to pump harder against increased resistance. Blood also becomes slightly thicker and more prone to clotting in cold temperatures. A major international study published in 2023 found that both extreme heat and extreme cold raise the risk of heart disease death, but cold carries the greater danger.
Layering physical exertion on top of cold exposure compounds the risk. Activities like shoveling snow are a classic example: the combination of cold-induced vessel narrowing, increased blood pressure, higher clotting tendency, and sudden physical demand can overwhelm a heart that’s already compromised. Intense emotional stress works through a similar pathway, triggering surges of adrenaline that spike heart rate and blood pressure while making platelets stickier.
These triggers don’t cause heart attacks in healthy arteries. They act as the match that lights a fire in someone who already has the fuel, whether that’s advanced plaque disease, uncontrolled blood pressure, or an undiagnosed coronary artery condition.