Pain may be referred to either arm, the jaw, the neck, the back, or even the abdomen. Troponins (T, I, C) are found in striated and cardiac muscle. Aviles, R.J., et al., Troponin T Levels in Patients with Acute Coronary Syndromes, with or without Renal Dysfunction. 2016 Mar;28:59-64. doi: 10.1016/j.ejim.2015.10.004. and transmitted securely. An exercise treadmill test for patients without abnormal findings on the initial tests, or a nuclear stress test or echocardiographic stress test; 6. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for Abnormal Q waves usually develop within the first day, and T-wave inversion and normalization of ST segments occur within hours to days. 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. A more recent article on acute coronary syndrome is available. Background: Abnormal levels of serum cardiac troponin I (cTnI) are occasionally found in patients presenting with acute coronary syndromes but having insignificant coronary artery disease. Before one concludes that an abnormal cTnI level is a false-positive result, the possibility of coronary vasospasm should be considered. In acute coronary syndrome, common electrocardiographic abnormalities include T-wave tenting or inversion, ST-segment elevation or depression (including J-point elevation in multiple leads), and pathologic Q waves. Is there a clinical way to differentiate between esophageal spasm The presentation is variable and can mimic other conditions such as aortic dissection, pulmonary embolism, and myocardial infarction (MI). During the hospitalization, the patient had another episode of nocturnal dyspnea with chest tightness. Non-ST-elevation myocardial infarction Importantly, an elevated cTn in the absence of ACS is most often associated with a worse prognosis and should not be disregarded as a false positive result. S. Dobrzycki, A. Baniukiewicz, J. Korecki et al., Does gastro-esophageal reflux provoke the myocardial ischemia in patients with CAD? International Journal of Cardiology, vol. Multivariate analysis showed that the variables independently associated with an elevated cTnI level included coronary vasospasm (odds ratio 2.41, 95% CI 1.48-3.18, P <.0001) and hypercholesterolemia (odds ratio 0.64, 95% CI 0.47-0.99, P =.049). Significant Q waves (greater than 0.04 seconds in duration and at least one quarter of the height of the corresponding R wave) suggest myocardial infarction. eCollection 2022. This medicine may help reduce the sensation of pain in the Causes of Non ACS Related Troponin Elevations Liu et al. 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). The term NSTEMI served as a catch-all term to describe both type 1 NSTEMIs and type 2 MIs, but that classification system is no longer valid. The following day, the patient underwent a barium esophagram for evaluation of his symptoms, as an esophagogastroduodenoscopy (EGD) was deferred given recent NSTEMI. A more recent article on acute coronary syndrome is available. He had patent sequential saphenous venous graft to right posterolateral and posterior descending artery and a patent left internal mammary artery to left anterior descending artery (Figures 1(c) and 1(d)). 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. Your email address will not be published. Serum markers such as aspartate transaminase, lactate dehydrogenase, and lactate dehydrogenase subforms no longer are used because they lack cardiac specificity and their delayed elevation precludes early diagnosis.9 Characteristics of the most important serum cardiac markers are summarized in Table 3.1619. Common examples of underlying causes of type 2 MI include acute blood loss anemia (e.g. Heart Vessels. In: Goldman-Cecil Medicine. 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. Vasospastic angina, which was previously referred to as Prinzmetal [ 1] or variant angina, is characterized by episodes of rest angina that promptly respond to short-acting nitrates and are attributable to coronary artery vasospasm. 2022 May 4;4(8):709-720. doi: 10.1016/j.cjco.2022.04.009. (b) Multiple tertiary contractions of the distal esophagus suggestive of dysmotility. cTnI was elevated in 23 patients (25%) and was normal in 70 patients (75%). With older conventional assays, cTnI or T is typically measurable as early as 3-4 hours following myocardial injury. Increased troponin levels may also be due to: Abnormally fast heartbeat; High blood pressure in lung arteries (pulmonary hypertension) Blockage of a lung artery by a blood clot, fat, or tumor cells (pulmonary embolus) Congestive heart failure; Coronary artery spasm When is a troponin elevation an acute myocardial infarction? WebEsophagitis oresophagealspasm Pleurisy Costochondritis Chest wall / musculoskeletal pain Gastritis Hiatal hernia Anxiety Hyperventilation syndrome Biliary colic Peptic Ulcer Other cause(please specify) None of the above/ not applicable 16211628, 1996. 854861, 2009. See permissionsforcopyrightquestions and/or permission requests. Troponin: Elevated troponin levels can indicate heart damage or even a heart attack. Epub 2017 Aug 1. After presenting our case, we review the literature on this atypical presentation of GERD causing acute coronary syndrome and discuss potential mechanisms. K. R. DeVault, Extraesophageal symptoms of GERD, Cleveland Clinic Journal of Medicine, vol. Ohlmann, P., et al., Diagnostic and prognostic value of circulating D-Dimers in patients with acute aortic dissection. WebIn this report we show that coronary arterial and esophageal spasm are sometimes clinically indistinguishable. Assessment of coronary spasms with transluminal attenuation gradient in coronary computed tomography angiography. Admission of patients with an equivocal or positive result. 2020; doi:10.1007/s10388-019-00693-w. Castell DO. Esophageal spasms - Symptoms and causes - Mayo Clinic However, when using hsTn assays, a rising (or falling) pattern may be seen as early as one hour after myocardial injury.4 Importantly, the phenomenon of cTn release is independent of mechanismthus, cardiomyocyte necrosis of any kindischemic, infectious, toxic, or otherwiseis not infrequently detectable. a , nonischemic myocardial injury). In the setting of irreversible myocardial cell injury, the contents of the cTn complex are released into circulation. When is a troponin elevation an acute myocardial infarction? Sepsis without shock: Direct toxicity of circulating cytokines to cardiac myocytes. Chest pain that occurs suddenly at rest or in a young patient may suggest acute coronary vasospasm, which occurs in Prinzmetals angina or with the use of cocaine or methamphetamine. Swinkels, B.M., et al., Prevalence and clinical significance of an elevated cardiac troponin I in patients presenting to the Emergency Department without chest pain. UpToDate (d) Left internal mammary artery graft to distal left anterior descending widely patent. 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. 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. The PubMed wordmark and PubMed logo are registered trademarks of the U.S. Department of Health and Human Services (HHS). Diffuse esophageal spasm (corkscrew esophagus). Kott KA, Bishop M, Yang CHJ, Plasto TM, Cheng DC, Kaplan AI, Cullen L, Celermajer DS, Meikle PJ, Vernon ST, Figtree GA. Pain patterns can be identical, nitroglycerin can bring relief, interval electrocardiograms and exercise electrocardiograms generally disclose no abnormalities, coronary arteriograms may be within normal limits or nearly so, and, WebIn patients with acute coronary syndrome with elevated cTnI and insignificant coronary artery disease, the possibility of coronary vasospasm as a cause of elevated cTnI 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. He was diagnosed with non-ST elevation myocardial infarction based on the electrocardiographic changes and cardiac biomarker elevation. Spasms may cause minor to A normal electrocardiogram does not rule out acute coronary syndrome. 9, pp. 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. 26th ed. Symptoms Association of epicardial adipose tissue with coronary spasm and coronary atherosclerosis in patients with chest pain: analysis of data collated by the KoRean wOmen'S chest pain rEgistry (koROSE). Rings of muscle contract and relax to allow food and liquids to pass through the upper and lower portions. Acute coronary syndrome encompasses a spectrum of coronary artery diseases, including unstable angina, ST-elevation myocardial infarction (STEMI; often referred to as Q-wave myocardial infarction), and non-STEMI (NSTEMI; often referred to as nonQ-wave myocardial infarction). Coronary Vasospastic Angina: A Review of the Pathogenesis, Diagnosis, and Management. The exact mechanism by which cTn release occurs in this setting remains unknown but may be due to right ventricular injury.32. R. Salvador, T. J. Watson, F. Herbella et al., Association of gastroesophageal reflux and O2 desaturation: a novel study of simultaneous 24-h MII-pH and continuous pulse oximetry, Journal of Gastrointestinal Surgery, vol. 167173, 2005. The administration of i/v or per-oral nitroglycerin relieves the symptoms of pain which does not happen if the patient has gastrointestinal diseases.The esophageal 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 troponin level will then begin to fall over the next 4 to 10 days down to a normal level. Before one concludes that an abnormal cTnI level is a false-positive result, the possibility of coronary vasospasm should be considered. Ilva, T.J., et al., The etiology and prognostic significance of cardiac troponin I elevation in unselected emergency department patients. NCI CPTC Antibody Characterization Program. Esophageal Rupture Presenting with ST Based on the coronary anatomy the patient was managed conservatively with optimal medical therapy with no plan for percutaneous intervention or revascularization. 52, no. Troponin elevation in CKD is worth discussion, as the interpretation of elevation of cTn in non-ACS patients may be difficult. Elevated cTn in asymptomatic CKD is common, the frequency which is dependent on the assay (cTnT > cTnI) and cut-off value used. document.getElementById( "ak_js_1" ).setAttribute( "value", ( new Date() ).getTime() ); Dr. Kerley Clinical question: Does initiation of empagliflozin in hospitalized patients with acute decompensated heart failure improve clinical outcomes and symptom burden? The clinician is advised to be familiar with the broad differential diagnosis of an elevated cTn, to avoid false attribution of acute MI to a patient without an ACS. He remained symptom-free until 6-month follow-up visit. History of diabetes mellitus is associated with elevated cardiac troponin I levels in patients with chest pain but no coronary heart disease. 104, no. A. Valiati, Extraesophageal manifestations of gastroesophageal reflux disease, Jornal Brasileiro de Pneumologia, vol. A coronary artery spasm is a temporary tightening (constriction) of the muscles in the wall of an artery that sends blood to the heart. Epub 2015 Oct 27. This widely available marker has low sensitivity and specificity for cardiac damage. Elevated cTn is strongly associated with mortality in acute PE; in a meta-analysis of 20 acute PE studies, patients with an elevated cTn had more than 5-fold increase in mortality (19.7% vs. 3.7%).14, Other relevant cardiac diagnoses that may present with both chest pain and elevated cTn include post-revascularization myocardial injury states, myocarditis (where cTn elevations are common and prognostically meaningful),15-16 acute pericarditis,17 and blunt force trauma to the heart.18, In the context of life-threatening illness, the prevalence of elevated cTn is considerable (table 1). How to Interpret Elevated Cardiac Troponin Levels | Circulation The benefit of its use was a significant reduction in hospital admissions of patients who did not have acute coronary syndrome.26 However, a subsequent study27 suggested that this benefit is not seen unless physicians have been trained in the use of the instrument. 5, pp. The silent myocardial infarction hypothesis is based on the relatively high incidence of ischemic changes noted on screening ECGs in patients with diabetes. This study investigated whether coronary vasospasm could be a reason for elevated cTnI in this patient population. Digestive Diseases Statistics for the United StatesNational Digestive Diseases Information Clearninghouse, March 2012, http://www.niddk.nih.gov/health-information/health-statistics/Pages/digestive-diseases-statistics-for-the-united-states.aspx.