Patients with all three of these features have a greater likelihood of having acute coronary syndrome than patients with none, one, or even two of these features. 13th ed. The PubMed wordmark and PubMed logo are registered trademarks of the U.S. Department of Health and Human Services (HHS). Esophageal spasms can feel like sudden, severe chest pain that lasts from a few minutes to hours. As of Oct. 1, 2017, ICD-10 and the Centers for Medicare & Medicaid Services have a new ICD-10 diagnosis code for type 2 MI (I21.A1), distinct from NSTEMI (I21.4) based on updated definitions from the American College of Cardiology, American Heart Association, European Society of Cardiology, and World Heart Federation. For example, hypertensive emergency, severe aortic valve stenosis, hypertrophic cardiomyopathy, and tachyarrhythmias (including atrial fibrillation with rapid ventricular response) may cause increased myocardial oxygen demand, and in patients with underlying CAD, could precipitate a type 2 MI. 32, no. Risk stratification then should be performed using the criteria in Table 1.1 Alternatively, the Acute Cardiac Ischemia Time-Insensitive Predictive Instrument can be used.26 This is a computerized decision-making program that is built into the ECG machine. This study investigated whether coronary vasospasm could be a reason for elevated cTnI in this patient population. A person viewing it online may make one printout of the material and may use that printout only for his or her personal, non-commercial reference. This site needs JavaScript to work properly. Admission of patients with an equivocal or positive result. He also denied any nausea, vomiting, or epigastric discomfort. This medicine may help reduce the sensation of pain in the Ominous physical findings include a new mitral regurgitation murmur, hypotension, pulmonary rales, a new third heart sound (S3 gallop), and new jugular venous distention. Troponin is a protein found in all muscles. 26th Bethesda conference: recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities. Esophageal spasms are sometimes associated with conditions such as heartburn or gastroesophageal reflux disease (GERD). Copyright 2015 Chui Man Carmen Hui et al. Combining a doubling of the baseline myoglobin level at two hours after symptom onset with an abnormal myoglobin test at six hours after symptom onset increases the sensitivity to 95 percent at six hours.25. GI bleed), acute hypoxia (e.g. The prevalence of GERD ranged from 11% to 38.8% worldwide per Map of Digestive Disorders & Disease (MDD) with Mexico, Spain, Malaysia, and Yemen at the top quartile of prevalence, and Asian countries in the lowest quartile [1]. Subendocardial ischemia classically results in ST-segment depression and T-wave inversion.14 Approximately 25 percent of patients with ST-segment depression and elevated creatine kinaseMB isoenzyme (CK-MB) levels eventually develop STEMI, and 75 percent have NSTEMI. In patients with acute coronary syndrome with elevated cTnI and insignificant coronary artery disease, the possibility of coronary vasospasm as a cause of elevated cTnI should be considered. 2023 American College of Cardiology Foundation. Esophageal spasms typically occur only occasionally and might not need treatment. Troponin T or I generally is the most sensitive determinant of acute coronary syndrome, although the MB isoenzyme of creatine kinase also is used. Troponin: Elevated troponin levels can indicate heart damage or even a heart attack. NSTEMI (acute coronary artery plaque rupture/erosion), Supply/demand mismatch (heterogeneous underlying causes), Sudden cardiac death with ECG evidence of acute myocardial ischemia before cardiac troponins could be drawn, MI due to percutaneous coronary intervention (PCI), MI due to coronary artery bypass grafting (CABG). Unauthorized use of these marks is strictly prohibited. Bookshelf Distinguishing the diagnose of type 2 MI vs. non-MI troponin elevation depends on documenting whether there are ancillary ischemic symptoms, ECG findings, imaging, and/or cath findings of acute myocardial ischemia. This tube is called the esophagus. doi: 10.7759/cureus.26193. There are two types of esophageal spasms distal esophageal spasm and hypercontractile esophagus, also referred to as jackhammer esophagus. Coronary vasospasm (positive ergonovine provocation test) could explain 74% of elevated cTnI levels in patients with insignificant coronary stenosis. Most high-risk patients should be hospitalized. Serum cardiac marker determinations play a vital role in the diagnosis of acute myocardial infarction. Furthermore, the high prevalence of O2 desaturation was found mostly in GERD patients with primary respiratory complaints [8]. Accessed Oct. 6, 2020. However, they appear to be related to atypical functioning of nerves that control the muscles you use when you swallow. Pain from esophageal spasm is one distinct possibility for precipitating ischemia in this patient. Acute (on chronic) systolic or diastolic heart failure: Usually due to acute ventricular wall stretch/strain. University of Florida, Gastroesophageal Reflux Disease, Office of Medical Informatics. The levels will continue to rise at that time until a peak is reached, generally between 12 and 48 hours. 10, no. Diseases of the esophagus. The CK-MB subform assay takes about 25 minutes to perform.21 A CK-MB2 level greater than 1 U per L in combination with a subform ratio greater than 1.5 suggests myocardial injury.9,22 One large study23 involving 1,110 patients with chest pain found that CK-MB subform analysis is 96 percent sensitive and 94 percent specific when the marker is measured six hours after symptom onset. For our patient, high dose of PPI was initiated to control his reflux symptoms along with further optimization of medical therapy for his CAD in order to augment efforts at secondary prevention of future ischemic events. spontaneous), and bradyarrhythmias. A normal electrocardiogram does not rule out acute coronary syndrome. According to National Digestive Disease Information Clearinghouse (NDDIC), 20% of the population had reflux symptoms at least once a week in 2004; 8.9 million ambulatory visits in 2009 and 4.7 million hospitalizations in 2010 were attributed to GERD [3]. Elsevier; 2021. https://www.clinicalkey.com. M. J. Cousins, P. O. Bridenbaugh, D. B. Carr, and T. T. Horlocker, Neural blockade: impact on outcome, in Cousins and Bridenbaughs Neural Blockade in Clinical Anesthesia and Pain Medicine, C. L. Wu and S. S. Liu, Eds., pp. The symptoms lasted for an hour and he was taken to the hospital due to persistent discomfort. Various mechanisms for HF-related cTn elevation have been proposed, including subendocardial ischemia from wall tension, apoptosis, spontaneous necrosis, as well as inflammation. Your provider might recommend a proton pump inhibitor to treat GERD. However, there are also many mechanisms of myocardial injury unrelated to reduced coronary artery blood flow, and these should be more appropriately termed non-MI troponin elevations. The cardiac troponins typically are measured at emergency department admission and repeated in six to 12 hours.20 Patients with a normal CK-MB level but elevated troponin levels are considered to have sustained minor myocardial damage or microinfarction, whereas patients with elevations of both CK-MB and troponins are considered to have had acute myocardial infarction. In type 2 MI, myocardial injury occurs secondary to an underlying process, and therefore requires correct documentation of the underlying cause as well. We present a case of an atypical presentation of GERD leading to NSTEMI, likely from demand ischemia in the setting of known severe 3-vessel native CAD as well as chronic total occlusions of venous grafts. The serum CK level rises within three to eight hours after myocardial injury, peaks by 12 to 24 hours, and returns to baseline within three to four days.16 A serum CK level may be used as a screening test to determine the need for more specific testing. 8600 Rockville Pike A. Ambrose, Chest pain from gastroesophageal reflux disease in patients with coronary artery disease, Cardiology in Review, vol. S20S32, 2003. 6772, 2005. After presenting our case, we review the literature on this atypical presentation of GERD causing acute coronary syndrome and discuss potential mechanisms. The silent myocardial infarction hypothesis is based on the relatively high incidence of ischemic changes noted on screening ECGs in patients with diabetes. When used by trained physicians, the Acute Cardiac Ischemia Time-Insensitive Predictive Instrument (a computerized, decision-making program built into the electrocardiogram machine) results in a significant reduction in hospital admissions of patients who do not have acute coronary syndrome. and transmitted securely. R. S. Irwin and J. M. Madison, Diagnosis and treatment of chronic cough due to gastro-esophageal reflux disease and postnasal drip syndrome, Pulmonary Pharmacology & Therapeutics, vol. An official website of the United States government. Accessed Oct. 6, 2020. You may also feel pain in the right side of the chest alone. Over the previous five to six years, the patient experienced recurring episodes of nocturnal coughing and difficulty breathing during his sleep which was typically precipitated after intake of a heavy meal. Iser, D.M., et al., Prospective study of cardiac troponin I release in patients with upper gastrointestinal bleeding. https://www.uptodate.com/contents/search. reported similar findings of longer duration and higher incidence of ischemic events in patients with CAD and gastric reflux [12]. Despite multiple mechanisms suggested to explain its pathophysiology, there is increasing evidence that supports direct neuroadrenergic myocardial stimulation with concomitant transient, reversible, coronary vasospasm as the inciting event, either at the epicardial or arteriolar level. Esophageal rupture is a rare but potentially fatal cause of chest pain. NCI CPTC Antibody Characterization Program. This investigation enrolled 93 patients who presented to the emergency department with suspected coronary ischemia and had insignificant coronary artery disease. Furthermore, the prevalence of GERD in patients with CAD is higher, with some studies reporting prevalence ranging from 40% to 78% [4]. Cureus. However, these same conditions could cause a non-MI troponin elevation in patients without CAD and could also cause myocardial injury and troponin release by causing acute left ventricular stretch/strain. The diagnosis of a type 1 MIs (STEMI and NSTEMI) is supported by the presence of an acute coronary thrombus or plaque rupture/erosion on coronary angiography or a strong suspicion for these when angiography is unavailable or contraindicated. eCollection 2022. (a) Smooth short stricture in the distal esophagus slightly proximal to the gastroesophageal junction. National Library of Medicine Feldman, A.M. and D. McNamara, Myocarditis. Some patients may present without chest pain; in one review,2 sudden dyspnea was the sole presenting feature in 4 to 14 percent of patients with acute myocardial infarction. ESRD patients who present with volume overload due to missed dialysis also typically have a non-MI troponin elevation. WebThe diagnosis of esophageal spasm is used quite freely among physicians, including gastroenterologists. The cTn complex is found both in the sarcomere (accounting for ~95% of cTn in the heart) as well as to a lesser extent in the cytosol of cardiomyocytes. If the test result is elevated (in a range that indicates damage to heart tissue), this can mean that the patient had a heart attack very recently. However, in a patient presenting with other or vague complaints where an elevated troponin was found amongst a battery of tests, a type 2 MI may be favored, particularly if there is evidence of an underlying trigger for a supply-demand mismatch. Diagnosing a type 2 MI requires evidence of acute myocardial ischemia (Figure 2) with an elevated troponin but must also have at least one of the following:2. Cells. In: Goldman-Cecil Medicine. J. P. Liuzzo and J. 261266, 2002. Before https://www.merckmanuals.com/professional/gastrointestinal-disorders/esophageal-and-swallowing-disorders/diffuse-esophageal-spasm#. J Am Coll Cardiol. Accessed Oct. 8, 2020. Januzzi, and R.H. Christenson, Increases of cardiac troponin in conditions other than acute coronary syndrome and heart failure. demonstrated that esophageal acid stimulation in patients with documented CAD on angiogram resulted in typical chest discomfort and a significant reduction in coronary blood flow as measured by intracoronary Doppler in 9 of 14 (64%) patients [10]. Cardiac Tn is elevated in up to 18% of patients with AAD,8 indicative of the high acuity of illness than specific to aortic dissection itself, although coronary artery occlusion in this setting is well-described.9 Misdiagnosis of AAD may potentially result in incorrect administration of anticoagulation therapy, or lead to a risky delay in the correct diagnosis.10, Another common non-ACS cause of chest pain and cTn elevation is pulmonary embolism (PE).11 The frequency of elevated cTn is 10-50% in such patients,12-13 and may be related to a combination of acute right ventricular strain and injury, hypoxia and tachycardia.
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