Heart Attack (Myocardial Infarction)

A heart attack — what doctors call a myocardial infarction (MI) — happens when blood flow to part of the heart muscle is suddenly cut off, almost always by a blood clot that forms on top of a ruptured cholesterol plaque inside a coronary artery. Starved of oxygen, the affected muscle begins to die within minutes. This is why cardiologists repeat a simple, life-or-death phrase: time is muscle. The faster a blocked artery is reopened, the more heart muscle survives, and the better the odds of a full recovery. In the United States alone, roughly 800,000 people have a heart attack every year. Most survive — and survival, along with long-term quality of life, depends heavily on how quickly the warning signs are recognized and how fast emergency care arrives.

If you think you or someone near you may be having a heart attack, do not wait and do not try to "tough it out." Call 911 (or your local emergency number) right now. The rest of this page explains what a heart attack is, how to recognize it — including the quieter signs that are easy to miss, especially in women — exactly what to do in the first minutes, and how modern treatment and prevention have transformed the outlook for survivors.

What Is a Heart Attack?
Warning Signs & Symptoms
When to Call 911
Types: STEMI, NSTEMI & Unstable Angina
Causes & Risk Factors
Diagnosis
Emergency Treatment
Recovery & Cardiac Rehabilitation
Preventing a First or Second Heart Attack
Complications
Key Research Papers
Connections

What Is a Heart Attack?

The heart is a muscular pump, and like every muscle it needs a constant oxygen supply. That oxygen is delivered by the coronary arteries, a network of vessels that wrap around the outside of the heart. A heart attack occurs when one of those arteries is suddenly and severely blocked, and the region of muscle it feeds is left without oxygen.

The usual sequence unfolds in three steps:

Plaque builds up. Over years or decades, cholesterol-rich deposits called atherosclerotic plaques accumulate in the artery wall. This underlying process is atherosclerosis, the same disease behind coronary artery disease. Many plaques cause no symptoms and never fully block the vessel.
A plaque ruptures. The trigger for most heart attacks is not a slow, gradual narrowing but a sudden event: the thin cap over a vulnerable plaque cracks or erodes, exposing its fatty, inflammatory core to the bloodstream.
A clot forms and blocks the artery. The body treats the ruptured plaque like a wound and forms a blood clot (thrombus) over it. If that clot grows large enough to choke off flow, the heart muscle downstream begins to die — an infarction.

The dying muscle cannot be replaced; heart cells do not regenerate meaningfully. Once an area of muscle is lost, it is replaced by scar tissue, which does not contract. That is why the size and location of a heart attack matter so much, and why reopening the artery quickly — before the muscle is dead — is the single most important thing modern medicine can do. Every minute of blockage destroys more tissue, so the goal of emergency care is measured in minutes, not hours.

Warning Signs & Symptoms

The classic, best-known symptom is chest pain, but heart attacks announce themselves in many ways — and some are surprisingly subtle. The most common signs include:

Chest discomfort — pressure, squeezing, tightness, heaviness, or an ache in the center or left side of the chest. It may last more than a few minutes, or go away and come back. Many survivors describe pressure ("an elephant on my chest") rather than sharp pain.
Pain that spreads to one or both arms, the shoulders, neck, jaw, upper back, or upper stomach.
Shortness of breath, with or without chest discomfort.
Cold sweat, clammy skin.
Nausea, vomiting, or indigestion-like discomfort.
Lightheadedness, dizziness, or fainting.
Unusual or extreme fatigue, sometimes for days beforehand.
A sense of impending doom — an overwhelming feeling that something is seriously wrong.

How symptoms can differ in women

Heart disease is often wrongly thought of as a "man's disease," and this misconception costs lives. Women do experience chest pain during heart attacks — it remains their most common symptom too — but women are more likely than men to also have symptoms other than chest pain, or to describe the discomfort differently. These include shortness of breath, nausea or vomiting, pain in the back or jaw, and unusual, unexplained fatigue. Because these signs are easy to dismiss as the flu, indigestion, anxiety, or simple exhaustion, women (and the people around them, sometimes including clinicians) may delay seeking care. That delay is dangerous. Any woman with new, unexplained chest discomfort, breathlessness, or the symptoms above should be evaluated urgently, not reassured away.

The "silent" heart attack

Not every heart attack hurts. A silent myocardial infarction causes few or no recognizable symptoms and is often discovered later — sometimes months or years afterward — when an electrocardiogram or imaging test reveals old scar tissue. Silent MIs are more common in people with diabetes (whose nerve signaling can be blunted) and in older adults. They are not harmless: they cause real muscle damage and raise the risk of future events, which is one reason routine risk screening matters for higher-risk adults.

When to Call 911

Call 911 — or your local emergency number — immediately if you or someone else has chest discomfort that lasts more than a few minutes or comes and goes, especially when combined with shortness of breath, a cold sweat, nausea, or pain spreading to the arm, jaw, neck, or back. When in doubt, make the call. It is far better to be evaluated and sent home than to wait at home during a heart attack. The average person having a heart attack waits hours before seeking help — a delay that destroys heart muscle and costs lives.

While you wait for the ambulance:

Do not drive yourself to the hospital, and do not let the person drive. If the heart's rhythm collapses on the way, no one can help. Emergency medical services (EMS) can start treatment in your home and in the ambulance, restart a stopped heart, and radio ahead so the hospital's catheterization team is ready and waiting the moment you arrive.
Chew an aspirin — one regular 325 mg tablet, or four 81 mg "baby" aspirins — unless you are allergic to aspirin or have been told by a doctor not to take it. Chewing (rather than swallowing whole) speeds absorption. Aspirin helps thin the clot that is blocking the artery and has been shown to save lives during a heart attack.
Sit or lie down and stay as calm as possible. Loosen tight clothing. If the person takes prescribed nitroglycerin, help them use it as directed.
If the person collapses, is unresponsive, and is not breathing normally, begin hands-only CPR immediately: push hard and fast in the center of the chest, about 100–120 pushes per minute, and don't stop until help arrives. If an automated external defibrillator (AED) is available, use it — turn it on and follow the spoken instructions. Most deaths in the first hour of a heart attack are caused by a chaotic rhythm called ventricular fibrillation, which an AED can reverse. This is also how a heart attack can lead to stroke-level emergencies and cardiac arrest if not treated.

The bottom line: recognizing the signs and calling for help within minutes is the most powerful, life-saving action a bystander or patient can take — more powerful than any single drug or procedure that follows.

Types: STEMI, NSTEMI & Unstable Angina

Heart attacks and their close cousins fall under an umbrella called acute coronary syndrome (ACS). Doctors sort ACS into three categories, mainly using the electrocardiogram (ECG) and a blood test for heart-muscle damage (troponin). The distinctions drive treatment urgency.

STEMI (ST-Elevation Myocardial Infarction). The most dangerous form: a coronary artery is completely blocked, and the ECG shows a characteristic pattern called ST-segment elevation. This usually reflects full-thickness injury to the heart wall and demands emergency reperfusion — reopening the artery as fast as humanly possible.
NSTEMI (Non-ST-Elevation Myocardial Infarction). The artery is severely narrowed or only partially or intermittently blocked. There is real muscle damage — troponin is elevated — but the ECG does not show ST elevation. NSTEMI is treated urgently with medication and, in most cases, coronary angiography within hours to a day or two, timed according to the patient's risk.
Unstable angina. Ischemic chest pain occurring at rest or in a suddenly worsening ("crescendo") pattern, without a rise in troponin — meaning no muscle has died yet. It is a warning that a heart attack may be imminent and is treated as an emergency. With today's highly sensitive troponin tests, many episodes once labeled unstable angina are now reclassified as small NSTEMIs.

The internationally accepted framework, the Fourth Universal Definition of Myocardial Infarction, also separates Type 1 MI — the classic plaque rupture with clot formation described above — from Type 2 MI, in which the heart muscle is starved not by a new clot but by a mismatch between oxygen supply and demand (for example during severe illness, a fast arrhythmia, major bleeding, or very low blood pressure). The two types are managed differently, which is why an accurate diagnosis matters.

Causes & Risk Factors

The root cause of most heart attacks is coronary artery disease — the slow buildup of atherosclerotic plaque — with a plaque rupture and clot providing the final trigger. The factors that drive that buildup are largely the same ones that drive cardiovascular disease as a whole.

Modifiable risk factors

Smoking and tobacco use — one of the strongest and most reversible risks; it damages artery linings and makes blood more likely to clot.
High LDL cholesterol and apolipoprotein B (ApoB) — the cholesterol-carrying particles that build plaque. A lipid panel and, increasingly, an ApoB measurement quantify this risk.
High blood pressure — chronic hypertension stresses and stiffens arteries.
Diabetes and insulin resistance — high blood sugar accelerates arterial damage; see diabetes and metabolic syndrome.
Obesity, physical inactivity, and poor diet — interconnected drivers of nearly all the risks above.
Excess alcohol, chronic psychological stress, poor sleep, and untreated sleep apnea.

Non-modifiable and other factors

Age — risk rises with each decade.
Sex — men develop coronary disease earlier on average, though a woman's risk climbs after menopause until it approaches a man's.
Family history and genetics, including elevated lipoprotein(a), an inherited particle that raises risk independently of standard cholesterol.
A prior heart attack or known coronary disease — the single strongest predictor of a future event, which is why secondary prevention is so aggressive.
Less common triggers — coronary artery spasm, spontaneous coronary artery dissection (SCAD, which disproportionately affects younger women), and stimulant drugs such as cocaine.

Diagnosis

When a possible heart attack reaches the hospital, three tools do most of the diagnostic work, and speed is built into every step.

Electrocardiogram (ECG or EKG). Guidelines call for a 12-lead ECG within 10 minutes of arrival. It is the fastest way to separate a STEMI (which needs immediate artery-opening) from NSTEMI or unstable angina, and it can reveal dangerous rhythm disturbances.
Cardiac troponin. Troponin is a protein released into the blood when heart muscle is injured. Modern high-sensitivity troponin assays can detect tiny amounts within an hour or two of symptom onset. A rising and/or falling pattern, with at least one value above the test's normal upper limit, is the biochemical fingerprint of a heart attack. Repeat ("serial") measurements over 1–3 hours are standard.
Coronary angiography. In this procedure, a thin catheter is threaded to the heart and contrast dye is injected while X-ray images are taken, revealing exactly where and how severely the coronary arteries are blocked. For a STEMI, angiography is done emergently and usually flows directly into treatment (angioplasty and stenting) in the same session.

Supporting tests fill in the picture: an echocardiogram (ultrasound of the heart) shows which walls are not moving well and measures the pumping strength (ejection fraction), a chest X-ray checks for fluid, and blood work assesses kidney function, cholesterol, and blood sugar. In selected lower-risk patients, CT coronary angiography can help rule coronary disease in or out.

Emergency Treatment

The overriding goal in a STEMI is reperfusion — physically reopening the blocked artery before the muscle dies. Two strategies do this, and the choice depends mainly on how fast a skilled team can be reached.

Opening the artery

Primary percutaneous coronary intervention (PCI), also called angioplasty and stenting. A catheter with a tiny balloon is guided to the blockage; inflating the balloon crushes the clot and plaque against the wall, and a metal-mesh stent (usually drug-eluting) is deployed to hold the artery open. Primary PCI is the preferred reperfusion strategy when it can be delivered quickly. A landmark meta-analysis by Keeley and colleagues showed primary PCI reduced death, reinfarction, and stroke compared with clot-dissolving drugs. Guidelines set a target of 90 minutes or less from first medical contact to opening the artery (up to 120 minutes when a patient must be transferred between hospitals) — the famous door-to-balloon time.
Fibrinolytic ("clot-buster") therapy. When timely PCI is not available — for example in a rural hospital far from a cath lab — intravenous clot-dissolving drugs such as tenecteplase or alteplase can restore flow, ideally within 30 minutes of arrival (door-to-needle time). The Fibrinolytic Therapy Trialists' overview and the GUSTO trial established that these drugs save lives when given early. After fibrinolysis, patients are usually transferred for angiography.

Medications given right away

Aspirin, chewed at the first suspicion, remains foundational; the historic ISIS-2 trial showed aspirin alone cut vascular death by about a quarter, with an even larger benefit when combined with a clot-dissolving drug.
A second antiplatelet drug (a P2Y12 inhibitor) — ticagrelor, prasugrel, or clopidogrel — is added to aspirin, a combination called dual antiplatelet therapy (DAPT). Trials such as CURE, COMMIT, and PLATO built the evidence for this approach.
An anticoagulant (such as heparin) to prevent the clot from growing.
A high-intensity statin, started early.
Supportive drugs as needed — oxygen only if blood-oxygen levels are low, nitroglycerin and pain relief for symptoms, and a beta-blocker once the patient is stable.

For an NSTEMI, the immediate priority is not always same-minute artery opening; patients receive antiplatelet drugs, an anticoagulant, and a statin, and are risk-stratified to decide how soon to perform angiography — immediately for the highest-risk patients, and typically within 24 hours for other high-risk cases.

Recovery & Cardiac Rehabilitation

For an uncomplicated heart attack, the hospital stay is often just a few days. But recovery is a months-long process, and how it is handled strongly influences whether a second event occurs.

The cornerstone is cardiac rehabilitation — a medically supervised program combining monitored exercise training, education about heart-healthy living, help quitting smoking, nutrition and weight guidance, and emotional support. Cardiac rehab is one of the most consistently proven interventions in cardiology: it lowers the risk of dying, reduces hospital readmissions, and improves day-to-day quality of life. Despite this, it remains badly underused — many eligible patients are never referred. If you or a loved one survives a heart attack, ask specifically about a cardiac rehab referral.

Emotional recovery matters as much as physical recovery. Depression and anxiety are common after a heart attack and are themselves linked to worse outcomes, so screening and support are part of good care. Most survivors gradually return to work, driving, physical activity, and sexual activity on a timeline their cardiologist sets. Practices such as regular exercise, stress-reduction techniques like meditation, and a Mediterranean-style diet support both physical and mental recovery. Above all, taking prescribed medications faithfully is not optional — stopping them early is one of the most common and preventable causes of a repeat heart attack.

Preventing a First or Second Heart Attack

Most heart attacks are preventable, and the strategies overlap whether you have never had one (primary prevention) or are protecting a heart that has already been injured (secondary prevention).

Preventing a first heart attack

Don't smoke, and avoid secondhand smoke.
Know and manage your numbers — blood pressure, LDL cholesterol or ApoB, and blood sugar. A lipid panel is a simple starting point, and a coronary calcium score can refine risk in selected adults.
Eat a heart-healthy pattern, such as a Mediterranean diet rich in vegetables, fruit, legumes, whole grains, nuts, fish, and olive oil.
Move regularly — aim for at least 150 minutes of moderate exercise per week — maintain a healthy weight, limit alcohol, and manage stress and sleep.

The secondary-prevention drug bundle

After a heart attack, guidelines recommend a combination of proven medications. Each one independently lowers risk; together they are powerful. The typical bundle includes:

A high-intensity statin, often combined with ezetimibe and, when needed, a PCSK9 inhibitor, to drive LDL cholesterol as low as possible. The Cholesterol Treatment Trialists' meta-analysis of more than 170,000 people found that each roughly 39 mg/dL (1 mmol/L) reduction in LDL cut major vascular events by about a fifth per year — and the PROVE IT trial showed that more intensive lowering after an acute coronary syndrome beats moderate lowering. European guidelines target an LDL below 55 mg/dL after an MI.
Dual antiplatelet therapy (aspirin plus a P2Y12 inhibitor), usually for about 12 months, followed by lifelong aspirin (or a single antiplatelet) in most patients.
A beta-blocker, particularly valuable when the heart's pumping strength is reduced.
An ACE inhibitor or ARB, especially for patients with reduced ejection fraction, high blood pressure, diabetes, or kidney disease.
Additional agents when indicated — an aldosterone antagonist for those with a weak heart muscle, and an SGLT2 inhibitor or GLP-1 medication for patients with diabetes, both of which also protect against heart failure.

Layered on top of the medications are the same lifestyle pillars — smoking cessation, cardiac rehab, a Mediterranean-style diet, regular activity, weight and blood-pressure control, and treatment of sleep apnea. The 2023 European Society of Cardiology guidelines pull all of this together into a coherent, evidence-based plan for the year after an acute coronary syndrome.

Complications

Most people who reach the hospital quickly and get their artery reopened do well. But a heart attack can cause serious complications, especially when it is large, treated late, or affects a critical area:

Dangerous arrhythmias. Ventricular fibrillation and ventricular tachycardia — chaotic electrical rhythms — are the leading cause of death in the first hour and the reason AEDs and rapid defibrillation save lives. Damage to the heart's wiring can also cause a dangerously slow rhythm or heart block. See arrhythmia.
Heart failure and cardiogenic shock. When enough muscle is lost, the heart cannot pump effectively, leading to heart failure; a catastrophic version, cardiogenic shock, carries a high mortality.
Mechanical complications. Rare but often deadly, these include rupture of a papillary muscle (causing sudden severe mitral valve leakage), rupture of the wall between the ventricles, and rupture of the heart's outer wall. They typically occur in the first days after an untreated or late-treated MI.
Pericarditis. Inflammation of the sac around the heart, either early after the MI or, weeks later, as an immune-mediated reaction known as Dressler syndrome.
Blood clots in the heart. A clot can form inside a damaged, poorly contracting ventricle and travel to the brain, causing a stroke.
Recurrent heart attack and sudden cardiac death. A previously injured heart is at higher risk of another event, which is exactly why the secondary-prevention program above is so important.

Key Research Papers

Thygesen K, Alpert JS, Jaffe AS, et al. Fourth Universal Definition of Myocardial Infarction (2018). Circulation. 2018;138(20):e618-e651.
Anderson JL, Morrow DA. Acute Myocardial Infarction. New England Journal of Medicine. 2017;376(21):2053-2064.
ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction. The Lancet. 1988;332(8607):349-360.
Fibrinolytic Therapy Trialists' (FTT) Collaborative Group. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results. The Lancet. 1994;343(8893):311-322.
The GUSTO Investigators. An international randomized trial comparing four thrombolytic strategies for acute myocardial infarction. New England Journal of Medicine. 1993;329(10):673-682.
Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. The Lancet. 2003;361(9351):13-20.
The Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) Trial Investigators. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. New England Journal of Medicine. 2001;345(7):494-502.
Wallentin L, Becker RC, Budaj A, et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes (PLATO). New England Journal of Medicine. 2009;361(11):1045-1057.
COMMIT (Clopidogrel and Metoprolol in Myocardial Infarction Trial) Collaborative Group. Addition of clopidogrel to aspirin in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. The Lancet. 2005;366(9497):1607-1621.
Cholesterol Treatment Trialists' (CTT) Collaboration. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. The Lancet. 2010;376(9753):1670-1681.
Cannon CP, Braunwald E, McCabe CH, et al. Intensive versus moderate lipid lowering with statins after acute coronary syndromes (PROVE IT–TIMI 22). New England Journal of Medicine. 2004;350(15):1495-1504.
Byrne RA, Rossello X, Coughlan JJ, et al. 2023 ESC Guidelines for the management of acute coronary syndromes. European Heart Journal. 2023;44(38):3720-3826.

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