Chest Pain — Symptom Overview

Table of Contents

  1. Overview and Emergency Red Flags
  2. Cardiac Causes
  3. Pulmonary Causes
  4. Gastrointestinal Causes
  5. Musculoskeletal Causes
  6. Neurological and Psychiatric Causes
  7. Diagnostic Approach
  8. Risk Stratification and Treatment
  9. Connections
  10. Key Research Papers
  11. Featured Videos

Overview and Emergency Red Flags

Chest pain is the most common presenting complaint in adult emergency departments in the United States, accounting for 5 to 7 million ED visits each year. It is the second most common reason for ambulance transport. Despite this frequency, fewer than 5% of patients presenting to primary care settings have a cardiac cause; however, in the ED — where patients self-select for severity — the proportion is substantially higher. The full differential spans life-threatening emergencies to benign and self-limited conditions, making a systematic approach essential for every clinician who evaluates it.

The most important early task is to exclude six immediately life-threatening diagnoses. These six "can't-miss" causes share the feature that delay in diagnosis or treatment can cause death within minutes to hours. Every patient with chest pain must be assessed for each of these before a more reassuring diagnosis is accepted.

The Six Immediately Life-Threatening Causes

1. Acute Coronary Syndrome (ACS)

Acute coronary syndrome encompasses STEMI, NSTEMI, and unstable angina. The classic presentation is crushing or pressure-like substernal pain — often described as "an elephant sitting on my chest" — radiating to the left arm, jaw, or back, accompanied by diaphoresis (cold sweating), nausea, and dyspnea. The ECG may show ST-segment elevation (STEMI) or depression, T-wave changes, or new left bundle branch block. However, up to one third of ACS presentations are atypical: burning, indigestion-like, or even entirely painless (particularly in women, diabetics, and the elderly). A normal initial ECG does not exclude ACS.

2. Aortic Dissection

Aortic dissection classically presents with an abrupt, tearing or ripping pain of maximal severity at onset — patients frequently describe it as the worst pain of their life. Pain radiates to the back, between the shoulder blades, or into the abdomen depending on the extent of dissection. A critical bedside finding is a blood pressure difference of more than 20 mmHg between the arms, reflecting obstruction of the subclavian artery by the dissection flap. Aortic regurgitation, pulse deficits, and focal neurological deficits may be present. Risk factors include hypertension (the most important), bicuspid aortic valve, Marfan syndrome, Ehlers-Danlos syndrome, and cocaine use. Misdiagnosis as ACS and subsequent anticoagulation or thrombolysis can be fatal.

3. Pulmonary Embolism (PE)

Pulmonary embolism causes pleuritic chest pain — sharp, worse with inspiration — along with acute-onset dyspnea, tachycardia, and hypoxia. Unilateral leg swelling and pain from deep vein thrombosis is an important associated finding present in roughly 30-50% of cases. Massive PE causes hemodynamic collapse. Risk factors include prolonged immobilization, recent surgery, malignancy, oral contraceptive use, prior PE/DVT, and inherited thrombophilias. The diagnosis is frequently missed because symptoms are nonspecific and the ECG finding of S1Q3T3 is present in only a minority.

4. Tension Pneumothorax

Tension pneumothorax occurs when air enters the pleural space and cannot escape, progressively compressing mediastinal structures. It presents with acute respiratory distress, hypotension, absent breath sounds on the affected side, and tracheal deviation toward the contralateral side (a late sign). Jugular venous distension from impaired venous return to the right heart is typical. This is a clinical diagnosis requiring immediate needle decompression without waiting for imaging confirmation.

5. Cardiac Tamponade

Cardiac tamponade results from fluid accumulation in the pericardial sac compressing the heart and restricting filling. Beck's triad — hypotension, jugular venous distension, and muffled heart sounds — is the classic description, though all three are present simultaneously in fewer than 40% of cases. Pulsus paradoxus (a drop in systolic blood pressure of more than 10 mmHg during inspiration) is a sensitive bedside sign. Causes include malignancy, acute pericarditis, aortic dissection extending into the pericardium, post-cardiac surgery, and trauma.

6. Esophageal Rupture (Boerhaave Syndrome)

Spontaneous esophageal perforation follows a sudden large increase in intraesophageal pressure, most commonly from forceful vomiting. The Mackler triad of vomiting followed by lower chest pain followed by subcutaneous emphysema is pathognomonic but present in fewer than 15% of cases. Severe mediastinitis develops rapidly, with fever, septic shock, and a high mortality rate even with early surgical repair. Chest X-ray may show mediastinal widening, pleural effusion (typically left-sided), or pneumomediastinum. A high index of suspicion after any episode of forceful vomiting with subsequent severe chest pain is essential.

Epidemiology

Across all care settings, the most common causes of chest pain are musculoskeletal (40-50%), gastrointestinal (10-20%), pulmonary (5-10%), and psychiatric or anxiety-related (10-15%). Cardiac causes account for 10-15% across all settings but a much higher proportion in the ED, where high-acuity patients concentrate. Knowing the base rates for a given care setting — primary care versus ED versus chest pain unit — is essential for calibrating pre-test probability.

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Cardiac Causes

Cardiac causes of chest pain range from immediately life-threatening to chronic and manageable. Distinguishing among them requires integrating history, examination, ECG, and biomarkers.

Acute Coronary Syndrome (STEMI, NSTEMI, Unstable Angina)

ST-elevation myocardial infarction (STEMI) involves complete occlusion of a coronary artery, producing ST elevation in a coronary distribution and demanding immediate reperfusion with primary percutaneous coronary intervention (PCI) within 90 minutes of first medical contact. NSTEMI and unstable angina involve partial occlusion; troponin is elevated in NSTEMI but normal in unstable angina. All three present similarly: rest pain, exertional pain that is new, accelerating, or more severe than prior angina, and associated diaphoresis, nausea, or radiation to arm, jaw, or back.

Stable Angina

Stable angina is predictable, exertional chest pressure that resolves within minutes with rest or sublingual nitroglycerin. It results from fixed coronary artery stenoses limiting flow during increased myocardial oxygen demand. The Canadian Cardiovascular Society (CCS) classification grades severity from Class I (angina only with strenuous exertion) through Class IV (angina at minimal activity or rest). New-onset angina that is rapidly worsening or occurring at rest is no longer "stable" and should be evaluated urgently as possible ACS.

Pericarditis

Acute pericarditis causes sharp, pleuritic chest pain that is characteristically worse when lying supine and relieved by leaning forward (the position reduces contact between the inflamed pericardium and the diaphragm). A pericardial friction rub — a scratchy, grating sound — may be heard on auscultation. The ECG shows diffuse ST elevation (in multiple leads, not a single coronary distribution) with PR-segment depression, and the pattern evolves in four stages over days to weeks. This ECG pattern is critical for distinguishing pericarditis from STEMI, in which ST elevation is regional and PR depression is absent. Causes include viral infection (most common), bacterial infection, autoimmune disease, malignancy, and uremia.

Myocarditis

Myocarditis is inflammation of the myocardium itself, most commonly caused by viral infection (coxsackievirus B, adenovirus, SARS-CoV-2). It typically affects younger patients (teens through 40s) who present with chest pain (often pleuritic), dyspnea, and fatigue following a viral prodrome one to two weeks earlier. Troponin is elevated, reflecting myocardial necrosis. Echocardiography may show reduced ejection fraction and regional wall motion abnormalities. Cardiac MRI with gadolinium is the gold standard, showing myocardial edema and late gadolinium enhancement in a non-ischemic pattern. Serious complications include arrhythmias, heart failure, and fulminant myocarditis requiring mechanical circulatory support.

Hypertrophic Cardiomyopathy (HCM)

HCM is a genetic disorder (most commonly due to sarcomere protein mutations) characterized by asymmetric left ventricular hypertrophy without a hemodynamic cause. Chest pain in HCM results from microvascular ischemia and left ventricular outflow tract obstruction (LVOTO). The classic triad in young athletes is exertional chest pain, exertional syncope, and palpitations. HCM is the most common cause of sudden cardiac death in competitive athletes under 35 in the United States. Diagnosis is by echocardiography; genetic testing is available for family screening.

Aortic Stenosis Angina

Severe aortic stenosis causes chest pain (along with syncope and heart failure) from a mismatch between myocardial oxygen demand and supply. The hypertrophied left ventricle faces massive afterload, increasing oxygen demand, while the high filling pressures and compressed subendocardial vessels restrict supply. This angina pattern occurs without obstructive coronary artery disease and is one of the classic indications for aortic valve replacement.

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Pulmonary Causes

Pulmonary causes typically produce pleuritic pain — sharp, localized, and worsened by inspiration, coughing, or movement — in contrast to the pressure or squeezing quality of cardiac ischemia.

Pleuritis and Pleurisy

Pleuritis refers to inflammation of the pleural lining. It produces sharp, well-localized, unilateral chest pain that is strongly worsened by deep breathing, coughing, or sneezing and relieved by splinting the affected side. A pleural friction rub — a leathery creaking sound synchronous with respiration — may be heard on auscultation. Pleuritis occurs in the context of infection (viral, bacterial, or fungal), autoimmune disease (systemic lupus erythematosus is a classic cause), pulmonary embolism, and malignancy.

Pneumonia

Bacterial pneumonia commonly produces pleuritic chest pain when infection involves the pleura or produces a parapneumonic effusion. Associated features include fever, chills, productive cough with purulent or rust-colored sputum, and consolidation on chest X-ray. The chest pain is often overshadowed by the respiratory and constitutional symptoms. Streptococcus pneumoniae is the most common bacterial cause; Legionella, Mycoplasma, and viral pneumonias (including influenza) are important in specific epidemiological contexts.

Pneumothorax

Spontaneous pneumothorax causes sudden-onset unilateral pleuritic chest pain and dyspnea without a precipitating cause. Primary spontaneous pneumothorax affects tall, thin young males without underlying lung disease, typically from rupture of small apical bullae. Secondary spontaneous pneumothorax occurs in patients with underlying lung disease — COPD is the most common substrate, and these are more hemodynamically significant because baseline lung reserve is reduced. Diagnosis is by chest X-ray (absence of lung markings with a visible pleural line) or chest CT for subtle cases.

Pulmonary Hypertension

Pulmonary arterial hypertension causes exertional dyspnea and exertional chest pain from right ventricular ischemia, arising because the markedly elevated pulmonary artery pressures strain the right ventricle beyond its perfusion capacity. The chest pain is often pressure-like and may be mistaken for left-sided ischemia. Other features include fatigue, near-syncope on exertion, and signs of right heart failure (peripheral edema, ascites). Echocardiography is the key screening test; right heart catheterization confirms the diagnosis.

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Gastrointestinal Causes

Gastrointestinal causes account for 10-20% of chest pain presentations across all settings and can mimic cardiac pain with remarkable fidelity — the same vagal nerve supply innervates the heart, esophagus, and upper GI tract.

Gastroesophageal Reflux Disease (GERD)

GERD is the most common GI cause of chest pain. Reflux of gastric acid into the esophagus produces a burning, substernal discomfort that is typically postprandial, worse when lying down, and relieved by antacids or upright posture. However, GERD can also produce pressure-like chest pain indistinguishable from cardiac angina. Acid-sensitive esophageal nociceptors share afferent pathways with cardiac ones. A diagnostic trial of a proton pump inhibitor (PPI) is commonly used; ambulatory pH monitoring and endoscopy are available for refractory or atypical cases. Lifestyle modification includes weight loss, elevation of the head of the bed, avoiding meals within three hours of lying down, and reducing alcohol, caffeine, and fatty foods.

Esophageal Spasm

Diffuse esophageal spasm and jackhammer esophagus (hypercontractile esophagus) cause severe, crushing chest pain that may radiate to the jaw and left arm — mimicking ACS so closely that the two were historically confused. The pain may be provoked by cold liquids, hot beverages, or emotional stress and can last minutes to hours. Crucially, sublingual nitroglycerin may relieve esophageal spasm just as it does angina, compounding diagnostic confusion. High-resolution esophageal manometry is the definitive diagnostic test. Treatment includes calcium channel blockers (diltiazem), tricyclic antidepressants, phosphodiesterase inhibitors, and, for severe refractory cases, peroral endoscopic myotomy (POEM).

Peptic Ulcer Disease

Peptic ulcer pain is typically epigastric rather than substernal, with a meal-related pattern (duodenal ulcer pain worsens a few hours after eating and is relieved by food; gastric ulcer pain is often precipitated by meals). Helicobacter pylori infection and NSAID use are the dominant causes. When an ulcer perforates, pain radiates across the upper abdomen and can involve the chest if diaphragmatic irritation develops from free air. Testing for H. pylori (urea breath test, stool antigen, or biopsy at endoscopy) guides eradication therapy.

Pancreatitis

Acute pancreatitis causes severe epigastric pain radiating to the back — a pattern sometimes described as "boring through to the back." Chest pain may occur from diaphragmatic irritation or, in severe cases, from associated pleural effusions (usually left-sided) or acute respiratory distress syndrome (ARDS). Elevated serum lipase (three times the upper limit of normal) is diagnostic. Gallstones and alcohol are the two most common causes.

Cholecystitis and Biliary Colic

Right upper quadrant pain from acute cholecystitis radiates to the right shoulder and right infrascapular region via phrenic nerve irritation. This pattern is sometimes perceived as right-sided chest pain. Murphy's sign (sudden arrest of inspiration during deep palpation of the right upper quadrant) is a useful bedside finding. Biliary colic from gallstone passage follows a distinct pattern: intense, cramping right upper quadrant pain lasting 15 minutes to several hours, often triggered by fatty meals.

Mallory-Weiss Tear

A Mallory-Weiss tear is a mucosal laceration at the gastroesophageal junction caused by forceful or prolonged vomiting, most often in the context of alcohol use. It presents with hematemesis following retching. Chest pain may accompany the tear, raising concern for Boerhaave syndrome; the distinction is that Mallory-Weiss tears are mucosal (not full-thickness), so mediastinitis does not develop. Upper endoscopy is both diagnostic and therapeutic.

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Musculoskeletal Causes

Musculoskeletal etiologies are collectively the most common cause of chest pain in ambulatory settings, accounting for 40-50% of presentations. The key diagnostic feature is reproducibility of the pain by direct palpation of the chest wall or specific movements — a finding that strongly suggests a musculoskeletal rather than cardiac or visceral origin.

Costochondritis

Costochondritis is inflammation of the costochondral junctions — where the ribs meet the costal cartilage. It is the most common musculoskeletal cause of chest pain. Pain is typically sharp or aching, worse with deep breathing, coughing, or movement, and reproducible by palpating the affected junction. It most commonly involves ribs 2 through 5 on the left side. Tietze syndrome is a related condition distinguished by visible and palpable swelling of the costochondral junction. Treatment is conservative: NSAIDs, heat, rest, and reassurance. Most cases resolve within weeks to months.

Rib Fractures

Rib fractures cause well-localized pleuritic chest pain at the fracture site, worsened by breathing, coughing, and direct palpation. They may follow trauma, vigorous coughing (particularly in patients with chronic cough or osteoporosis), or be pathological (from malignancy or metabolic bone disease). Complications include pneumothorax, hemothorax, and, with multiple rib fractures causing a flail segment, respiratory failure.

Chest Wall Muscle Strain

Intercostal and pectoralis muscle strains from exercise, heavy lifting, or repetitive motion produce localized chest pain that worsens with specific movements or positions that stretch the affected muscle. The pain is reproduced by resisted movement of the relevant muscle group. Treatment includes rest, ice, NSAIDs, and gradual return to activity.

Precordial Catch Syndrome (Texidor's Twinge)

Precordial catch syndrome is a benign, self-limited condition most common in children, adolescents, and young adults. It produces sudden, sharp, well-localized stabbing pain at the left lower parasternal or apical region that is dramatically worsened by attempting a deep breath and lasts only seconds to a few minutes. Paradoxically, a forced deep breath through the pain often terminates the episode. The cause is unknown but may involve localized intercostal muscle spasm or pleural irritation. No treatment or investigation is required beyond reassurance.

Fibromyalgia

Fibromyalgia is a central sensitization syndrome characterized by widespread musculoskeletal pain, fatigue, sleep disturbance, and cognitive symptoms. Chest wall tenderness is present in many patients and can be mistaken for cardiac pain or costochondritis. The diagnosis requires widespread pain for at least three months meeting the 2010 or 2016 ACR diagnostic criteria. Management includes aerobic exercise, cognitive behavioral therapy, sleep hygiene, and medications such as duloxetine, milnacipran, or pregabalin.

Thoracic Outlet Syndrome

Compression of the brachial plexus, subclavian artery, or subclavian vein between the clavicle and first rib (or by a cervical rib) causes neurogenic, arterial, or venous thoracic outlet syndrome. Neurogenic type — the most common — produces shoulder and chest pain with radiation into the arm, often with paresthesias in the ulnar distribution. Symptoms are worse with overhead arm positions. Diagnosis is clinical with provocative maneuvers (Adson, Wright, Roos); imaging with CT or MRI angiography defines the anatomy.

Herpes Zoster (Shingles) — Pre-eruption Phase

Reactivation of varicella-zoster virus in a dorsal root ganglion causes prodromal burning, aching, or stabbing pain in the affected dermatome — often days before the characteristic vesicular rash appears. When the affected dermatome involves thoracic nerves (T1-T12), the prodromal chest pain can be intense and unexplained, mimicking pleurisy, cardiac disease, or musculoskeletal injury. The unilateral, dermatomal distribution is the key clue; the subsequent appearance of grouped vesicles on an erythematous base confirms the diagnosis. Early antiviral therapy (acyclovir, valacyclovir, famciclovir) within 72 hours of rash onset reduces duration and severity, and may reduce post-herpetic neuralgia risk.

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Neurological and Psychiatric Causes

Psychiatric and functional causes of chest pain are more common than cardiac causes in most outpatient settings. They are real — not imagined — and cause genuine suffering. They are diagnoses supported by positive clinical evidence, not merely exclusion of other causes.

Panic Disorder and Panic Attacks

Panic attacks produce a constellation of physical and psychological symptoms that occur abruptly and peak within minutes: chest tightness or chest pain, palpitations, shortness of breath, trembling, dizziness, paresthesias, and an overwhelming sense of impending doom or fear of dying. The autonomic surge of a panic attack — driven by catecholamine release — produces genuine tachycardia, diaphoresis, and hyperventilation, all of which can be misinterpreted as cardiac symptoms. Panic disorder is common, affecting 2-3% of the US population, and is particularly prevalent in patients presenting to the ED with chest pain; several studies have found rates of 15-25% in this population. Treatment is highly effective: selective serotonin reuptake inhibitors (SSRIs) and cognitive behavioral therapy (CBT) are first-line. Benzodiazepines may be used for acute attacks but should be used cautiously and short-term given dependence risk.

Generalized Anxiety Disorder

Chronic, pervasive anxiety produces persistent low-level sympathetic activation with physical manifestations including chest tightness, palpitations, muscle tension (including chest wall tension), fatigue, and sleep disturbance. Unlike panic attacks, the physical symptoms are less paroxysmal and more continuous. Differentiating anxiety-related chest pain from cardiac disease requires excluding organic causes while also positively identifying the anxiety features. SSRIs, SNRIs, buspirone, and CBT are effective treatments.

Somatic Symptom Disorder

In somatic symptom disorder (formerly somatization disorder), patients experience one or more somatic symptoms — including chest pain — that are distressing and disproportionately disruptive to daily functioning. The distress is not about the symptom itself but about its perceived meaning (fear of serious illness) and associated behaviors (repeated health-care seeking, avoiding activity). Acknowledging the reality and impact of the symptom while building a therapeutic alliance is essential; reassurance alone is rarely sufficient and may paradoxically worsen health anxiety. Treatment includes CBT, antidepressants (for comorbid depression or anxiety), and regular scheduled follow-up.

Functional Chest Pain

Functional chest pain of presumed esophageal origin (now classified under disorders of gut-brain interaction) refers to recurrent, unexplained chest pain after negative cardiac and GI workup. Central sensitization — in which visceral afferent pathways become amplified — is the leading mechanistic hypothesis. Low-dose tricyclic antidepressants (amitriptyline 10-25 mg at bedtime) are the most evidence-supported pharmacological treatment. SSRIs, venlafaxine, and psychological therapies including CBT and hypnotherapy also show benefit.

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Diagnostic Approach

A systematic diagnostic approach to chest pain integrates history, physical examination, and targeted testing. The history alone correctly identifies the diagnosis in a substantial proportion of cases.

History

The OPQRST mnemonic structures the chest pain history effectively:

Physical Examination

Key Diagnostic Tests

ECG

The ECG should be obtained within 10 minutes of presentation in any patient with possible cardiac chest pain and is the single most important first test. ST elevation in a regional coronary distribution with reciprocal depression identifies STEMI and mandates immediate PCI activation. Diffuse ST elevation with PR depression in multiple leads (particularly with PR elevation in aVR) indicates pericarditis. ST depression or T-wave inversion suggests NSTEMI or ischemia. Right heart strain pattern (S1Q3T3, right bundle branch block, sinus tachycardia) raises concern for PE. Wellen's warning — deep symmetrical T-wave inversions or biphasic T waves in V1-V4 — indicates critical proximal LAD stenosis, even in a patient who is currently pain-free.

High-Sensitivity Cardiac Troponin

High-sensitivity troponin assays have largely replaced conventional troponin in major centers. Their key advantage is detecting very low-level myocardial injury and enabling rapid rule-out protocols. The European Society of Cardiology 0h/1h (RAPID) protocol and the 0h/2h protocol, using validated absolute delta change thresholds, can rule out NSTEMI in approximately 60-75% of patients at 1-2 hours of presentation. A negative troponin at 0 hours and 2 hours in a patient with a low HEART score (0-3) has a negative predictive value exceeding 99.5% for 30-day major adverse cardiac events (MACE), enabling safe discharge.

Chest X-Ray

Chest radiography identifies pneumothorax (absent lung markings, visible pleural line), pneumonia (consolidation, infiltrate), widened mediastinum (dissection, lymphoma), cardiomegaly (heart failure, pericardial effusion), and pleural effusion. It is not sufficient to exclude PE, dissection, or early pneumonia.

D-Dimer

D-dimer is used to exclude PE in patients with low or intermediate pre-test probability. In high-risk patients, imaging is mandatory regardless of D-dimer level. The PERC rule (Pulmonary Embolism Rule-out Criteria) can identify low-risk patients in whom D-dimer testing is unnecessary: if all 8 PERC criteria are met (age under 50, heart rate under 100, SpO2 ≥ 95%, no unilateral leg swelling, no hemoptysis, no recent surgery or trauma, no prior PE/DVT, no exogenous estrogen), PE prevalence is below 2% and testing can be safely omitted.

Echocardiography

Point-of-care ultrasound and formal echocardiography identify pericardial effusion/tamponade, regional wall motion abnormalities (ACS), right ventricular strain (PE), reduced EF (myocarditis or ischemic cardiomyopathy), and valvular disease. In hemodynamically unstable patients with undifferentiated shock, emergency bedside echo distinguishes tamponade, massive PE (dilated right ventricle), and severe LV dysfunction.

CT Angiography

CT pulmonary angiography (CTPA) is the standard test for PE in patients with elevated pre-test probability or elevated D-dimer. CT aortography with contrast detects aortic dissection with sensitivity and specificity approaching 100%. CT coronary angiography (CCTA) is increasingly used in low-to-intermediate risk chest pain in the ED for rapid anatomical exclusion of significant coronary disease.

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Risk Stratification and Treatment

Risk stratification tools guide the intensity and urgency of further workup and the safety of discharge versus hospital admission.

HEART Score (ACS)

The HEART score (History, ECG, Age, Risk factors, Troponin) is the most validated chest pain risk stratification tool for use in the ED, outperforming TIMI and GRACE in this setting. Each of the five domains is scored 0-2, for a maximum of 10 points. Interpretation: 0-3 (low risk) — 1.7% 30-day MACE rate, safe for early discharge; 4-6 (moderate risk) — 12-16.6% MACE, serial troponins and observation required; 7-10 (high risk) — 65% MACE, early invasive strategy (coronary angiography within 24-72 hours) is indicated.

TIMI Score (ACS)

The TIMI risk score for unstable angina/NSTEMI assigns one point each for age ≥65, ≥3 CAD risk factors, known CAD (stenosis ≥50%), ST deviation on ECG, ≥2 anginal events in prior 24 hours, aspirin use in prior 7 days (suggesting aspirin inadequacy), and elevated cardiac markers. Scores of 0-2, 3-4, and 5-7 correspond to 4.7%, 13.2%, and 26.2% rates of all-cause mortality, MI, or severe recurrent ischemia at 14 days, respectively.

PERC Rule (PE)

If all 8 PERC criteria are satisfied in a patient the clinician pre-test estimates as low risk for PE (less than 15%), D-dimer testing is unnecessary. The rule was validated to reduce unnecessary D-dimer testing and downstream CT exposure without increasing missed PE rates. In intermediate pre-test probability, the Wells PE score (or revised Geneva score) guides D-dimer versus CTPA.

ADD-RS (Aortic Dissection)

The Aortic Dissection Detection Risk Score (ADD-RS) assigns scores based on high-risk conditions (Marfan syndrome, aortic disease history, aortic valve disease, prior aortic surgery), high-risk pain features (abrupt onset, tearing/ripping quality), and high-risk exam features (BP differential, pulse deficit, focal neurological deficit, aortic regurgitation murmur). A score of 0 with D-dimer below 500 ng/mL has been proposed (validated in ADVISED trial) as a rule-out strategy, though it requires validation in broader populations before replacing CT aortography in clinically suspicious cases.

Treatment Summary by Cause

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Connections

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Key Research Papers

  1. Six AJ, Backus BE, Kelder JC. Chest pain in the emergency room: value of the HEART score. Neth Heart J. 2008;16(6):191-196. PMID: 18665203.
  2. Backus BE, Six AJ, Kelder JC, et al. Chest pain in the emergency room: a multicenter validation of the HEART score. Crit Pathw Cardiol. 2010;9(3):164-169. PMID: 20806056.
  3. Mahler SA, Riley RF, Hiestand BC, et al. The HEART Pathway randomized trial: identifying emergency department patients with acute chest pain for early discharge. Circulation. 2015;132(12):1186-1195. PMID: 25776647.
  4. Imazio M, Bobbio M, Cecchi E, et al. Colchicine in addition to conventional therapy for acute pericarditis: results of the COlchicine for acute PEricarditis (COPE) trial. Circulation. 2005;112(13):2012-2016. PMID: 16186437.
  5. Imazio M, Brucato A, Cemin R, et al. A randomized trial of colchicine for acute pericarditis. N Engl J Med. 2013;369(16):1522-1528. PMID: 23992557.
  6. Swap CJ, Nagurney JT. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA. 2005;294(20):2623-2629. PMID: 16304077.
  7. Body R, Carley S, McDowell G, et al. Rapid exclusion of acute myocardial infarction in patients with undetectable troponin using a high-sensitivity assay. J Am Coll Cardiol. 2011;58(13):1332-1339. PMID: 21920260.
  8. Pauker SG, Kassirer JP. The threshold approach to clinical decision making. N Engl J Med. 1980;302(20):1109-1117. PMID: 7366635.
  9. Fruergaard P, Launbjerg J, Hesse B, et al. The diagnoses of patients admitted with acute chest pain but without myocardial infarction. Eur Heart J. 1996;17(7):1028-1034. PMID: 8809520.
  10. Kline JA, Mitchell AM, Kabrhel C, Richman PB, Courtney DM. Clinical criteria to prevent unnecessary diagnostic testing in emergency department patients with suspected pulmonary embolism. J Thromb Haemost. 2004;2(8):1247-1255. PMID: 15304025.
  11. Wells PS, Anderson DR, Rodger M, et al. Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and D-dimer. Ann Intern Med. 2001;135(2):98-107. PMID: 11453709.
  12. de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982;103(4 Pt 2):730-736. PMID: 7063014.

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