A myocardial infarction, commonly called a heart attack, happens when blood flow to part of the heart muscle is blocked long enough to cause tissue death. The most common cause is a buildup of fatty deposits in a coronary artery that ruptures and triggers a blood clot, choking off the oxygen supply. In the United States, roughly 605,000 people experience a first heart attack each year, with another 200,000 having a recurrent one.
How a Blocked Artery Causes a Heart Attack
The process starts years or even decades before the heart attack itself. Cholesterol and other fatty substances gradually collect inside the walls of the coronary arteries, forming deposits called plaques. Over time, these plaques develop a soft, fatty core surrounded by a fibrous cap that keeps the contents sealed off from the bloodstream. In stable plaques, this cap is thick enough to hold. In vulnerable plaques, it thins to less than 65 micrometers (roughly the width of a human hair) as inflammatory cells eat away at it.
When that thin cap tears open, the fatty core is suddenly exposed to flowing blood. The body treats this like an open wound. Platelets rush to the site and begin sticking to the exposed tissue, changing shape and releasing chemical signals that recruit even more platelets. At the same time, a protein called tissue factor, which is found in high concentrations inside diseased artery walls, kicks off the clotting cascade. Within minutes, a blood clot can form large enough to partially or completely block the artery.
Even a clot that doesn’t fully seal the artery can still cause a heart attack. The clot releases chemicals that make the artery walls constrict, and in a vessel already narrowed by plaque, that added tightening can be enough to cut off blood flow entirely. Without oxygen, heart muscle cells begin dying within 20 to 40 minutes.
Major Risk Factors
Several conditions accelerate plaque buildup and make rupture more likely. Smoking is one of the strongest: current smokers have roughly three times the risk of a heart attack compared to nonsmokers, based on large population studies. High blood pressure damages artery walls and promotes plaque formation, with each standard increase in systolic blood pressure raising heart attack risk by about 23%. Elevated cholesterol, particularly non-HDL cholesterol (the types that deposit in artery walls), independently increases risk as well.
Diabetes accelerates artery disease through multiple pathways, including chronic inflammation and damage to the blood vessel lining. Obesity, physical inactivity, and a diet high in processed foods all compound these effects. Family history matters too. A genetic marker called lipoprotein(a), which is largely determined by your DNA and not significantly changed by diet or exercise, is linked to heart attacks at younger ages when levels reach 50 mg/dL or higher. People with elevated lipoprotein(a) tend to have more extensive coronary artery disease at the time of their first event.
Heart Attacks Without a Ruptured Plaque
Not every heart attack follows the classic pattern of plaque rupture and clot formation. In what’s classified as a Type 2 myocardial infarction, the heart muscle is starved of oxygen because of a mismatch between supply and demand, without a new clot forming. Common triggers include severe infection (sepsis), significant anemia with hemoglobin below 10 g/dL, dangerously fast or slow heart rhythms, respiratory failure, and sudden drops in blood pressure. In one study, more than half of Type 2 heart attack patients had sepsis, and roughly half had anemia, with most patients having two or more of these conditions simultaneously.
These heart attacks typically happen in people who are already critically ill or recovering from surgery. The underlying coronary arteries may have some degree of narrowing, but it’s the added stress of another illness that tips the balance.
Coronary Spasm and MINOCA
Some people have heart attacks despite having coronary arteries that look normal or near-normal on imaging. This condition, known as MINOCA (myocardial infarction with non-obstructive coronary arteries), has several possible explanations, but coronary artery spasm appears to be the most common one. Studies estimate that spasm accounts for anywhere from 16% to 71% of MINOCA cases, with most research placing it at the higher end when both large-vessel and small-vessel spasm are tested for.
Coronary spasm is an intense, temporary constriction of an artery that can reduce blood flow enough to damage heart tissue. It can affect the larger coronary arteries or the tiny microvessels deeper in the heart wall. In some patients, spasm occurs in segments where the artery dips into the heart muscle itself, a normal anatomical variant called a myocardial bridge. About 60% of patients with a significant myocardial bridge show severe spasm in the bridged segment during provocative testing. Other causes of MINOCA include spontaneous tearing of a coronary artery wall (coronary dissection) and small blood clots that travel to the heart from elsewhere in the body.
External Triggers
Heart attacks don’t happen randomly. They cluster around certain environmental and behavioral triggers that can push a vulnerable plaque past its breaking point. Cold temperatures increase blood pressure and make blood more prone to clotting, and heart attack rates consistently rise during winter months. Air pollution, particularly fine particulate matter from traffic and industrial sources, triggers inflammation in the blood vessels and is now considered a modifiable risk factor for heart attacks. Intense physical exertion in someone who is otherwise sedentary, severe emotional stress, and heavy meals can all acutely raise heart rate and blood pressure enough to trigger plaque rupture.
Two Types Based on ECG Patterns
When a heart attack is diagnosed, it’s classified into two main categories based on what the electrocardiogram (ECG) shows. A STEMI involves a complete blockage of a coronary artery and shows a characteristic elevation pattern on the ECG tracing. This type causes damage through the full thickness of the heart wall and requires emergency treatment to reopen the artery as quickly as possible.
An NSTEMI traditionally indicates a partial blockage with damage limited to the inner layer of the heart muscle, without the same ECG elevation pattern. However, this distinction isn’t as clean as it sounds. Roughly 25% to 30% of patients initially classified as NSTEMI actually have a completely blocked artery when imaging is performed. Some ECG patterns that don’t meet the technical STEMI criteria, such as unusually tall, peaked T-waves or certain conduction abnormalities, can still indicate a total blockage requiring urgent intervention.
How a Heart Attack Is Confirmed
The key blood test for diagnosing a heart attack measures a protein called troponin, which leaks out of damaged heart muscle cells into the bloodstream. Modern high-sensitivity troponin tests can detect extremely small amounts of this protein, picking up heart damage earlier than older tests could. A heart attack is confirmed when troponin levels rise and then fall in a characteristic pattern, with at least one measurement above a threshold called the 99th percentile upper reference limit. This threshold varies depending on which specific test a hospital uses, and it differs between men and women. A rising troponin level, combined with symptoms like chest pain, ECG changes, or imaging showing a new area of damaged heart muscle, confirms the diagnosis.