A 60-year-old male patient with a history of dyslipidemia presented to the emergency department with worsening chest pain. He first developed chest pain 1 week prior while riding his bicycle. He described left-sided dull chest pain with a pressure quality that radiated down his left arm. The pain lasted 10 minutes and resolved with rest. Over the subsequent week, he developed chest pain with less exertion, including walking up a flight of stairs and, more recently, preparing for bed. He now presented with chest pain that started 6 hours ago and occurred while lying in bed, again lasting approximately 10 minutes. His medications include aspirin 81 mg and fish oil daily. He is a nonsmoker and works as an electrician. He has a family history of early coronary artery disease; his father died from a myocardial infarction (MI) at the age of 55.
On arrival, his blood pressure was 145/80 mmHg, and his heart rate was 67 bpm. Physical exam demonstrated a man in no acute distress lying comfortably in bed. Cardiac exam demonstrated regular rate and rhythm with normal heart sounds and without murmurs or rubs. He had no jugular venous distention. His lungs were clear to auscultation, and he had no peripheral edema.
A 12-lead electrocardiogram (ECG) demonstrated normal sinus rhythm and was otherwise unremarkable with no ischemic changes. Chest x-ray was normal. Laboratory work-up obtained included a hemoglobin of 14.5g/dL, creatinine of 1.1mg/dL (estimated glomerular filtration rate >60 mL/min/BSA), and an initial fourth generation cardiac troponin T (cTnT) of <0.01 ng/mL (99th percentile upper reference limit <0.01 ng/mL) at presentation. He was admitted for concerns of suspected acute coronary syndrome (ACS) and underwent serial cTnT measurements at 3 and 6 hours, which were both <99th percentile (<0.01 ng/ml).
Based on the above information, what is the most appropriate next step?
Show Answer
The correct answer is: B. Invasive coronary angiography
The patient was ruled out for acute MI with serial cTnT measurement below the 99th percentile. However, given his clinical presentation and symptoms, there was concern for unstable angina. He was risk-stratified during the index admission with exercise ECG testing in which he was able to exercise for 6.4 minutes on the Bruce protocol (9.5 metabolic equivalents of task, 67% predicted). He developed chest pain during the exercise stress test, and ECG demonstrated 2.5 mm downsloping ST depressions in leads V4-V6. He underwent subsequent invasive coronary angiography that demonstrated a 99% occlusion of his first obtuse marginal artery and 90% stenosis of the second obtuse marginal artery for which he underwent percutaneous coronary intervention (PCI) with successful stenting to each vessel. He also had a 70% mid-left anterior descending artery lesion with an instantaneous wave-free ratio of 0.88 that underwent staged PCI.
The patient's symptoms are consistent with non-ST elevation ACS given the progressively worsening chest pain with less exertion and chest pain at rest. Therefore, discharge is inappropriate.1 It is a Class IIa recommendation that patients with possible ACS who have normal ECGs and troponins undergo stress testing for risk stratification.1 For a lower-risk patient outpatient, stress testing can be considered. However, this patient's history puts him at an elevated risk; therefore, inpatient stress testing would be preferred. One can also consider computed tomographic angiography because there is also no history of coronary artery disease.1
For investigational purposes, his initial blood sample at presentation was measured with the fifth generation high-sensitivity cTnT assay. His fifth generation cTnT result was increased above the corresponding sex-specific 99th percentile, 28.7 ng/L (sex-specific 99th percentile <15 ng/L), indicating myocardial injury. In this setting, given the strong history and presentation, coronary angiography would have been the best next step in management rather than risk stratification with stress testing because his presentation would be consistent with non-ST-segment elevation MI.
Our case illustrates how high-sensitivity cTn assays may improve the detection of myocardial injury and lead to the reclassification of unstable angina to non-ST-segment elevation MI. The use of these high-sensitivity assays will allow for more rapid risk stratification of patients with suspected ACS and expedite the identification of patients at low risk for whom early discharge is possible and also facilitate the earlier detection of patients at high risk for whom appropriate therapies and/or further diagnostic studies can be considered if indicated.2-4 The use of these high-sensitivity assays may increase the detection of myocardial injury in circumstances other than acute MI. Therefore, it is important to keep other etiologies of cTn release in the differential diagnosis, such as myocarditis, cardiomyopathies, heart failure, renal failure, and skeletal muscle diseases.2,5
References
Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;64:e139-e228.
Sandoval Y, Jaffe AS. Using High-Sensitivity Cardiac Troponin T for Acute Cardiac Care. Am J Med 2017;130:1358-65.
Kozinski M, Krintus M, Kubica J, Sypniewska G. High-sensitivity cardiac troponin assays: From improved analytical performance to enhanced risk stratification. Crit Rev Clin Lab Sci 2017;54:143-72.
Sandoval Y, Apple FS, Smith SW. High-sensitivity cardiac troponin assays and unstable angina. Eur Heart J Acute Cardiovasc Care 2018;7:120-8.
Melki D, LugnegÄrd J, Alfredsson J, et al. Implications of Introducing High-Sensitivity Cardiac Troponin T Into Clinical Practice: Data From the SWEDEHEART Registry. J Am Coll Cardiol 2015;65:1655-64.