What triggers a heart attack in an adult with a potential history of cardiovascular disease or risk factors?

Triggers of Heart Attack

Heart attacks are triggered by acute physical exertion, emotional stress, heavy meals, and respiratory infections, which transiently increase cardiovascular risk through sympathetic activation, endothelial dysfunction, and hypercoagulability—particularly in adults with underlying cardiovascular disease or risk factors. 1, 2

Primary Acute Triggers

Physical Exertion

• Physical activity within 1 hour before symptom onset increases the odds of myocardial infarction 2.3-fold, with a population-attributable risk of 7.7% 2
• Heavy physical exertion triggers acute cardiovascular events across all regions, age groups, and in both men and women, with no significant effect modifiers 2
• The risk is largely limited to individuals with known or occult cardiovascular disease 3

Emotional Stress and Anger

• Anger or emotional upset within 1 hour before symptom onset increases the odds of myocardial infarction 2.4-fold, with a population-attributable risk of 8.5% 2
• Acute mental stress caused by earthquakes, high-drama televised events, job strain, or death of a loved one can trigger cardiovascular events 4
• When physical activity and anger occur together in the same hour, the odds of myocardial infarction increase to 3.05-fold 2

Respiratory Infections

• Respiratory infections transiently increase the risk of myocardial infarction, sudden cardiac death, and stroke 1

Heavy Meals

• Heavy meal consumption is recognized as a trigger that increases acute cardiovascular risk 1

Pathophysiological Mechanisms

Sympathetic Activation

• Triggers increase sympathetic output and catecholamine levels, which elevate myocardial oxygen demand while potentially decreasing oxygen supply 5
• Waking in the morning, physical exertion, and mental stress influence blood pressure, heart rate, plasma epinephrine levels, and coronary blood flow 5

Thrombotic Cascade

• Acute mental stress impairs endothelial function and creates a hypercoagulable state by increasing platelet aggregability 4, 5
• Increases in blood pressure and ventricular contractility elevate intravascular shear stress, causing vulnerable atherosclerotic plaques to rupture and form a nidus for thrombosis 5

Circadian Variation

• Myocardial ischemia, myocardial infarction, sudden cardiac death, and thrombotic stroke each occur with circadian variation and peak after waking in the morning 5

High-Risk Populations

Established Cardiovascular Disease

• Patients with established coronary heart disease should be identified for secondary prevention efforts 6
• Approximately 70% of deaths from coronary heart disease occur in patients with a previous history of cardiovascular disease 6

Cardiovascular Risk Equivalents

• Patients with atherosclerosis in other vascular beds, diabetes mellitus, chronic kidney disease, or 10-year risk greater than 20% should receive equally intensive risk factor intervention as those with clinically apparent coronary heart disease 6

Multiple Risk Factors

• Major risk factors include smoking, family history, adverse lipid profiles, diabetes mellitus, and elevated blood pressure 6
• Patients with 2 or more risk factors who are at increased 10-year and lifetime risk have the greatest benefit from primary prevention 6

Additional Environmental and Behavioral Triggers

Specific Circumstances

• Blizzards, Christmas and New Year's holidays, experiencing an earthquake, threat of violence, job strain, and Mondays for the working population are identified clinical triggers 5
• Sexual activity, overeating, smoking cigarettes, smoking marijuana, using cocaine, and particulate air pollution can precipitate myocardial infarction 5

Reversible Causes

• Alcohol intake ("holiday heart syndrome"), surgery, electrocution, pericarditis, myocarditis, pulmonary embolism, hyperthyroidism, and other metabolic disorders may trigger acute events 6

Clinical Presentation Patterns

Symptom Characteristics

• Patients with non-ST-elevation myocardial infarction usually present with angina at rest 6
• Unstable angina presents as new-onset angina, angina at rest, or increasing angina (increasing in intensity, duration, and/or frequency) 6
• Approximately half of all myocardial infarctions have an identifiable clinical trigger 5

Critical Pitfalls

• Do not assume patients with prior myocardial infarction seek help earlier than those developing symptoms for the first time—there is no evidence supporting this assumption 6
• The delay from symptom onset to initiation of reperfusion therapy is an important determinant of treatment benefit: the longer the delay, the less benefit derived from reperfusion 6
• Patients developing ventricular fibrillation in the presence of emergency medical service personnel have improved chances of successful resuscitation 6