It is important to identify risk factors for atherosclerotic disease when assessing the likelihood of unstable angina. Key among these is assessing patient history of coronary artery disease (CAD), peripheral vascular disease, and cerebrovascular disease, with positive responses to any of these questions leading to increased likelihood that current ischemic symptoms are due to ACS. Additionally, if the patient has a history of CAD, then determining how the current symptoms compare to usual symptoms of CAD is vital to assessing whether current symptoms are associated with previously known disease or changes to existing disease. Any patient who presents must be asked about classic risk factors including age ≥ 55 in men, age ≥ 65 in women, diabetes, smoking, hypertension, and family history of early CAD. These questions help to risk stratify patients and determine next steps in management.
ACS, including unstable angina, is most commonly caused by a cascade of chronic inflammatory processes in coronary vessels that leads to the development of stable and/or unstable plaques with or without embolisms, leading to a mismatch between cardiac myocyte demand and oxygenated blood delivery. Beginning with endothelial damage thought to be precipitated by elevated levels of circulating low-density lipoproteins and/or increases in free radicals, the endothelium creates an environment conducive to platelet aggregation and the formation of pro-coagulant signals, pro-inflammatory signals, and increasing endothelial permeability. In this environment, smooth muscle cells proliferate and can lead to fibrosis or focal necrosis of the arterial wall. Cholesterol and inflammatory cells (foam cells) can accumulate within the lesion as well and lead to calcification and hardening. The vessel dilates to maintain blood flow distal to the lesion, but it will eventually be unable to compensate adequately, altering the blood flow in the region. The fibrous cap is unstable and can rupture, leading to embolism of the plaque contents with distal obstruction or exposure of the pro-thrombotic core, leading to localized thrombosis. Either outcome can lead to complete obstruction of the vessel with cardiac myocyte damage and changes to the ECG (consistent with STEMI) or transient or incomplete obstruction of the vessel with or without myocyte damage or ECG changes, which would be consistent with NSTEMI or unstable angina.
Unstable angina can present in a variety of ways. Classically, acute ischemic disease presents with substernal heaviness or pressure that lasts for ≥ 10 minutes. If radiation exists, classic regions include the neck, jaw, shoulder, and left arm. The pain / pressure is classically worse with exertion and improves with rest and nitrates and can be associated with shortness of breath, nausea and vomiting, diaphoresis, syncope, lightheadedness, palpitations, or abdominal pain. Less commonly, patients can present without chest pain and with any of the associated features alone. Isolated nausea and vomiting is more common in women, and the absence of chest pain is more common in people with diabetes. Other atypical symptoms include epigastric pain, indigestion, fatigue, stabbing pain, pleuritic pain, and increasing dyspnea above baseline.
Each presentation of unstable angina has its own risk for progression of underlying cardiac disease. Any change from usual angina symptoms must be evaluated for presence of unstable angina or more severe ACS.
- New-onset angina: New-onset angina that occurs only with heavy exertion poses a risk similar to that of chronic stable angina, while angina that is provoked with minimal activity and prolonged in duration carries increased risk.
- Angina with rest: Poses increased risk if prolonged or associated with ST changes.
- Early post-myocardial infarction (MI) angina: Poses high risk in the absence of intervention.
- Late post-MI angina: More than 30 days after stent or coronary artery bypass grafting (CABG); can represent progression of disease or stent / graft re-stenosis.
- Angina without evidence of cardiovascular disease: Typically present in women and younger individuals, who usually have a better prognosis. This may indicate vasospasm, which would suggest different treatment modalities.
I20.0 – Unstable angina
4557003 – Preinfarction syndrome
- NSTEMI – no ST elevation on ECG but with acute elevations of cardiac markers
- STEMI – ST or T wave changes across a vascular region with acute elevations of cardiac markers
- Acute pericarditis – sharp pain, positional (improved with leaning forward), recent illness or MI (or other risk factors), pericardial friction rub, diffuse ST elevations on ECG
- Musculoskeletal chest pain (costochondritis) – sharp, localized, reproducible history of traumatic injury
- Stress-induced cardiomyopathy
- Microvascular angina
- Pulmonary embolism – pleuritic chest pain, tachycardia, shortness of breath, syncope, evidence of R heart strain on ECG, CT angiograph
- Aortic dissection – tearing chest pain, hypotension, tachycardia, CT
- Gastroesophageal reflux disease – burning pain, pain on abdominal examination
- Pneumonia – pleuritic chest pain, cough, fever
- Panic attack – history of psychiatric disease with admissions
- Expanding aortic aneurysm – positive risk factors (many are the same), ultrasound, or CT
- Esophageal spasm
- Peptic ulcer disease – positive risk factors
- Pancreatitis – positive risk factors, pancreatic enzyme levels
- Biliary disease (ie, acute cholecystitis) – positive risk factors, liver function tests
- Sickle cell crisis – positive history, CBC
- Herpes zoster – look for rash
Last Updated: 10/01/2019