Introduction Acute coronary syndrome (ACS) can be divided into subgroups of ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), and unstable angina. ACS carries significant morbidity and mortality and the prompt diagnosis, and appropriate treatment is essential. STEMI diagnosis and management are discussed elsewhere. NSTEMI and Unstable angina are very similar, with NSTEMI having positive cardiac biomarkers. The presentation, diagnosis, and management of NSTEMI are discussed below.[1][2][3]
Go to: Etiology The etiology of NSTEMI varies as there are several potential causes.
Go to: Epidemiology The median age at the time of presentation for ACS in the United States is 68 years. Males outnumber females by a 3:2 ratio. The incidence of ACS in the United States is over 780,000, and of those, approximately 70% will have NSTEMI.
Go to: Pathophysiology ACSs are simply a mismatch in the myocardial oxygen demand and myocardial oxygen consumption. While the cause of this mismatch in STEMI is nearly always coronary plaque rupture resulting thrombosis formation occluding a coronary artery, there are several potential causes of this mismatch in NSTEMI. There may be a flow-limiting condition such as a stable plaque, vasospasm as in Prinzmetal angina, coronary embolism, or coronary arteritis. Non-coronary injury to the heart such as cardiac contusion, myocarditis, or presence of cardiotoxic substances can also produce NSTEMI. Finally, conditions relatively unrelated to the coronary arteries or myocardium itself such as hypotension, hypertension, tachycardia, aortic stenosis, and pulmonary embolism lead to NSTEMI because the increased oxygen demand cannot be met.[4][5]
Go to: History and Physical The “typical” presentation of NSTEMI is a pressure-like substernal pain, occurring at rest or with minimal exertion. The pain generally lasts more than 10 minutes and may radiate to either arm, the neck, or the jaw. The pain may be associated with dyspnea, nausea or vomiting, syncope, fatigue, or diaphoresis. Sudden onset of unexplained dyspnea with or without associated symptoms is also a common presentation. Risk factors for ACS include male sex, older age, family history of coronary artery disease, diabetes, personal history of coronary artery disease, and renal insufficiency. Atypical symptoms may include a stabbing or pleuritic pain, epigastric or abdominal pain, indigestion, and isolated dyspnea. While all patients presenting with ACS are more likely to present with typical symptoms than atypical symptoms, the likelihood of atypical presentations increases with age over 75, women and those with diabetes, renal insufficiency, and dementia.
Physical Exam for ACS and NSTEMI is often nonspecific. Clues such as back pain with aortic dissection or pericardial friction rub with pericarditis may point to an alternative diagnosis for a patient’s chest pain, but no such exam finding exists that indicates ACS as the most likely diagnosis. Signs of heart failure should increase concern for ACS but are, again, nonspecific findings.[6][7][8]
Go to: Evaluation History, ECG, and cardiac biomarkers are the mainstays in the evaluation. An ECG should be performed as soon as possible in patients presenting with chest pain or those with a concern for ACS. A normal ECG does not exclude ACS and NSTEMI. ST elevation or anterior ST depression should be considered a STEMI until proven otherwise and treated as such. Findings suggestive of NSTEMI include transient ST elevation, ST depression, or new T wave inversions. ECG should be repeated at predetermined intervals or if symptoms return.
Cardiac troponin is the cardiac biomarker of choice. Troponin is more specific and more sensitive than other biomarkers and becomes elevated relatively early in the disease process. While contemporary cardiac troponin may not be elevated within the first 2 to 4 hours after symptom onset, newer high sensitivity troponin assays have detectable elevations much earlier. It is also true that the amount of troponin released, and therefore the time to elevation, is proportional with infarct size, so it is unlikely to have a negative initial troponin with larger infarcts. Regardless of infarct size, most patients with true ischemia will have elevations in troponin within 6 hours, and negative troponins at this point effectively rule out infarct in most patients. Most assays use a cutoff value of greater than a 99th percentile as a positive test. In older, contemporary troponin assays, no detectable troponin is reported in most healthy individuals without the disease. Newer high sensitivity troponin assays often will report a normal detectable range in healthy individuals without the disease.
Several tools and scores have been developed to assist in the workup of ACS. These tools must be used with caution and in the appropriate context as none have been definitively