Acute Coronary Syndromes without Persistent ST-Segment Elevation Initial Assessment

Last updated: 22 May 2026

Clinical Presentation

Ischemic-type Chest Discomfort or Anginal Equivalent  

Retrosternal chest pain presents as angina or ischemic-type chest discomfort and is usually described as heaviness, pressure, tightness, squeezing or burning in nature. Pain that is usually central or in the left chest may radiate to the jaw, left or both arms, back or shoulder. It may occur at rest or during activity that may be associated with physical exertion or emotional stress. The pain is prolonged and usually not fully relieved by rest or Glyceryl trinitrate (GTN). Chest pain-equivalent symptoms (also referred to as atypical or possible cardiac symptoms): Pain develops in the epigastrium, arm, shoulder, wrist, jaw or back without occurrence in the chest. Discomfort that presents solely as jaw, neck, ear, arm, or epigastric pain and is associated with exertion or stress or is relieved promptly with GTN should be considered an anginal equivalent. Older persons, females, and diabetics often present with anginal equivalents. Accompanying symptoms of ischemic-type chest discomfort may include nausea and vomiting, dyspnea, diaphoresis, lightheadedness, abdominal (epigastric) pain, dizziness, fatigue, weakness and loss of consciousness.


Acute Coronary Syndromes w.out Persistent ST-Segment Elevation_Intial AssesmentAcute Coronary Syndromes w.out Persistent ST-Segment Elevation_Intial Assesment





Patients with ACS may present with a broad range of signs and symptoms, from asymptomatic at presentation to patients with ongoing chest discomfort (eg pain, pressure, tightness, heaviness, burning). Patients may also present with cardiac arrest, electrical or hemodynamic instability or cardiogenic shock. Older patients frequently have an atypical presentation with symptoms of weakness, confusion, delirium or syncope. Patients typically present with ischemic-type chest pain as described above, except episodes may be more severe and prolonged, and may occur at rest or may be caused by less exertion than previous episodes. Chest-pain equivalent symptoms are often observed in younger (25 to 40 years old), and older (>75 years old) patients, in women, and in patients with diabetes mellitus (DM), chronic renal failure or dementia. Chest pain-equivalent symptoms include pain that occurs predominantly at rest, epigastric pain, recent onset of unexplainable indigestion, belching, stabbing chest pain, chest pain with some pleuritic features or increasing dyspnea. 

Common features of UA include:

  • Rest angina: Angina occurring at rest and prolonged, usually >20 minutes
    • Classified as acute if it occurred within the past 48 hours and subacute if it occurred within the past month but not within the preceding 48 hours
  • No angina at rest
    • New-onset severe angina: Patient usually has marked limitation on ordinary physical activity (angina occurs on walking one to two blocks on level or climbing one flight of stairs under normal conditions and at a normal pace)
    • Increasing or crescendo angina: Previously diagnosed effort-related angina that has become distinctly more frequent, longer in duration or more easily provoked (by less effort than before)
  • Post-MI angina: Occurs within 2 weeks of an acute MI

Physical Examination

The major objectives of doing a physical examination in patients suspected with ACS are to identify precipitating causes (eg uncontrolled hypertension, thyrotoxicosis, infection, anemia or gastrointestinal [GI] bleeding) and comorbid conditions (eg lung disease, diabetes and complications, obesity, peripheral vascular disease, chronic kidney disease [CKD], heart failure or cancer), to identify very high-risk and high-risk ACS features, to assess the hemodynamic impact of the ischemic event, to exclude non-cardiac causes of chest pain (eg pneumothorax, pulmonary embolism, pneumonia, pleural effusion, esophageal discomfort, gallstones, pancreatitis, or musculoskeletal origin), and to assess for non-ischemic cardiac disorders (eg pericarditis, valvular disease, aortic stenosis, aortic dissection, acute pericarditis, hypertrophic cardiomyopathy, cardiac tamponade).

Vital signs are also measured (eg blood pressure [BP] in both arms, heart rate [HR], respiratory rate [RR], and temperature). A thorough cardiovascular and chest exam are also performed which includes auscultation of the heart, neck veins, liver, and peripheral pulses to check for murmurs, bruits or pulse deficits which signify severe underlying CAD. It must be noted that new-onset murmurs may be due to ventricular sepal rupture and mitral regurgitation. Left ventricle (LV) dysfunction and shock should be suspected if the patient has cold extremities, hypotension, pulmonary rales, S3 gallop, displaced apex beat or S1<S2 at the apex. Aortic dissection may be present if there is pain in the back, unequal pulses, or a murmur of aortic regurgitation. While acute pericarditis is suspected by a presence of pericardial friction rub. Cardiac tamponade may be present as pulsus paradoxus.  

Patients with pneumothorax may have acute dyspnea, pleuritic chest pain, and differential breath sounds. Lastly, chest pain caused by musculoskeletal chest wall syndromes may be found by performing palpation of the chest wall. 

Diagnosis or Diagnostic Criteria

It is important that patients with suspected ACS must be evaluated quickly to identify acute coronary occlusion early and avoid delays in reperfusion therapy. Diagnosis and initial short-term risk stratification of ACS should be based on a thorough, targeted clinical history, symptoms, vital signs, and other physical findings, electrocardiogram (ECG) results, and concentration of high-sensitivity cardiac troponin (hs-cTn).  

MI is diagnosed by a rise and/or fall in cTns, with at least one value >99th percentile of the upper reference limit (URL), together with at least one of the following:

  • Clinical history consistent with chest pain of ischemic origin lasting >30 minutes
  • ECG changes of ischemia/infarction and/or development of pathologic Q waves
  • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
  • Identification of an intracoronary thrombus by angiography or autopsy