esophageal spasm and elevated troponin

Patients at intermediate risk may be monitored in a telemetry bed in an inpatient setting or a chest pain unit. doi: 10.1371/journal.pone.0271189. 2018 Jan;33(1):17-24. doi: 10.1007/s00380-017-1029-9. 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. GERD is caused by an impaired antireflux barrier and defective lower esophageal sphincter, leading to reflux of gastric acid into the esophagus. Misdiagnosis can have downstream repercussions. The symptoms lasted for an hour and he was taken to the hospital due to persistent discomfort. spontaneous), and bradyarrhythmias. Rapezzi, C., et al., Risk factors for diagnostic delay in acute aortic dissection. An elevated troponin T or I level is helpful in identifying patients at increased risk for death or the development of acute myocardial infarction.16 Increased risk is related quantitatively to the serum troponin level. However, many patients with GERD may present with extraesophageal symptoms such as chest pain or discomfort mimicking angina, chronic cough, wheezing, dyspnea, globus sensation, hoarseness, or recurrent pneumonia as their primary presentation [57]. Of these, 2,344 patients (3.3% overall, or 7.0% of those that had a cTn measured) had an elevated cTn concentration. 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. 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. Park JY, Kang EJ, Kim MH, Yong HS, Rha SW. PLoS One. Current Surgical Therapy. Sometimes an antidepressant, such as imipramine (Tofranil), may be prescribed. The cardiac troponins may remain elevated up to two weeks after symptom onset, which makes them useful as late markers of recent acute myocardial infarction.9. 2016;23(2):149-54. doi: 10.5603/CJ.a2015.0072. WebGastrointestinal causes (eg, gastroesophageal reflux, esophageal spasm, peptic ulcer, pancreatitis, biliary disease) Musculoskeletal causes (eg, costochondritis, cervical radiculopathy) Psychiatric disorders. J. P. Liuzzo and J. While cTn elevation in CKD necessarily leads to a higher risk for false positive ACS diagnosis, cTn values in this setting are to be taken seriously; a true positive cTn related to ACS in patients with CKD is associated with a heightened risk for mortality29 compared to non CKD patients, while an asymptomatic elevation in cTn in severe CKD is associated with an increased incidence of ACS30 and a 2- to 5-fold increase in mortality.31 Serial measurement, observing for a rise and/or fall of an elevated cTn value in a patient with CKD is recommended to differentiate ACS from non-ACS causes of cTn elevations. doi: 10.7759/cureus.26193. Task Force 5: coronary artery disease. Mayo Clinic does not endorse companies or products. 4, pp. A. Ambrose, Chest pain from gastroesophageal reflux disease in patients with coronary artery disease, Cardiology in Review, vol. The esophagus is a muscular tube that connects your mouth and your stomach. We report a case of an 83-year-old man with history of coronary artery disease and gastroesophageal reflux disease (GERD) who presented with sudden onset nocturnal dyspnea. Elevated cardiac troponin concentration in the absence of an acute coronary syndrome. Occasionally, reciprocal ST-segment depression occurs in leads that are electrically opposite to the area of injury. Gastroesophageal reflux disease , also known as GERD, is a digestive disorder that affects the ring of muscle between your esophagus and stomachthe lower esophageal sphincter, or LES. Conclusions: 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. Abnormal levels of serum cardiac troponin I (cTnI) are occasionally found in patients presenting with acute coronary syndromes but having insignificant coronary artery disease. These include: food and drink, such as red wine or spicy food. In general, renal failure in the absence of symptoms/signs of ischemia is best classified as a non-MI troponin elevation. Two mechanisms have been proposed to be responsible for respiratory symptoms induced by gastric reflux: (1) vagal reflex response from stimulation of the vagus nerve by gastric acidic content, resulting in bronchoconstriction and (2) microaspiration of gastric contents causing direct irritation or trauma to the upper airway [57]. Unauthorized use of these marks is strictly prohibited. https://www.uptodate.com/contents/search. Pruszczyk, P., et al., Cardiac troponin T monitoring identifies high-risk group of normotensive patients with acute pulmonary embolism. However, elevated troponin doesnt always mean cardiac damage. Acute pulmonary embolism: Result of acute right ventricular wall stretch/strain, not from myocardial ischemia. Vedovati, and G. Agnelli, Prognostic value of troponins in acute pulmonary embolism: a meta-analysis. A Case of Elevated Troponin I Level After Packed Red Blood Cell Transfusion With Normal Coronary Angiography. Stroke/intracranial hemorrhage: Mechanisms of myocardial injury and troponin elevation are incompletely understood, but may include catecholamine surges that injure the heart. Myoglobin has low cardiac specificity but high sensitivity, which makes it most useful for ruling out myocardial infarction if the level is normal in the first four to eight hours after the onset of symptoms.9, Time changes in the myoglobin value also can be extremely helpful. Waxman, D.A., et al., A model for troponin I as a quantitative predictor of in-hospital mortality. Furthermore, Swiatowski et al. Coronary Vasospastic Angina: A Review of the Pathogenesis, Diagnosis, and Management. Coronary vasospasm, documented by an ergonovine provocation test, was found in 38 patients (41%). CK-MB2 is found in myocardial tissue, and CK-MB1 is found in plasma. 3, pp. 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. Relationship between dobutamine echocardiography and the elevation of cardiac troponin I in patients with acute coronary syndromes. You may also feel pain in the right side of the chest alone. Isolated small Q waves in leads II, III, and aVF (in the electrically vertical heart) and leads I and aVL (in the electrically horizontal heart) frequently are normal. 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. Wallace, T.W., et al., Prevalence and determinants of troponin T elevation in the general population. However, patient declined the elective EGD on his follow-up visit as he had no further episodes of nocturnal dyspnea on higher doses of antireflux medication. 2022 Jun 22;14(6):e26193. Atypical symptoms do not necessarily rule out acute coronary syndrome. Apple, F.S., et al., Predictive value of cardiac troponin I and T for subsequent death in end-stage renal disease. Merck Manual Professional Version. Esophageal neuromuscular function and motility disorders. Although GERD classically presents with symptoms of heartburn and regurgitation of food contents, some patients may present with less typical extraesophageal cardiac or respiratory symptoms. 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)). Accessed Oct. 6, 2020. A comprehensive literature search was conducted from November 11, 2017, to May 1, 2020, encompassing randomized and nonrandomized trials, observational studies, registries, reviews, and other evidence conducted on human subjects that were published in English from PubMed, EMBASE, the Cochrane Collaboration, Agency for Healthcare This is an open access article distributed under the, http://www.worldgastroenterology.org/assets/downloads/pdf/wdhd/2008/events/map_of_digestive_disorders_2008.pdf, http://www.niddk.nih.gov/health-information/health-statistics/Pages/digestive-diseases-statistics-for-the-united-states.aspx. 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). 14446, Lippincott-Raven, Philadelphia, Pa, USA, 4th edition, 2009. 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. Epub 2015 Oct 27. Cardiac catheterization revealed chronic three-vessel coronary artery disease, with 2 patent grafts and 2 chronically occluded grafts. Barium esophagram demonstrated a smooth short narrowing in the distal esophagus proximal to the gastroesophageal junction, suggesting a stricture or spasm from yet controlled reflux disease (Figures 2(a) and 2(b)). 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 In general, the prevalence of cTn elevation in the general population is low when currently available assays are used. The term acute coronary syndrome encompasses a range of thrombotic coronary artery diseases, including unstable angina and both ST-segment elevation and nonST-segment elevation myocardial infarction. Medication adjustment resulted in resolution of nocturnal symptoms, which were likely a manifestation of GERD and angina. 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). 6772, 2005. Cells. Indeed, independent of mechanism, non-ACS cTn elevations are most often prognostically meaningful (Figure 1). Liu et al. Chui Man Carmen Hui and Santosh K. Padala contributed equally to the paper and share first authorship. Given this fact, and the emerging use of hsTn assays, clinicians should understand that cTn is not solely a biomarker of ischemic myocardial infarction (MI), and such clinicians must be well-versed in the differential diagnosis of an elevated cTn value outside of ACS, in order to avoid unnecessary and potentially harmful misdiagnosis and treatment for presumed ACS, while also avoiding delay in the correct treatment for the underlying cause of the elevated value. Although protocols for chest pain units may vary somewhat, one protocol28 that has been shown to be safe and cost-effective in an intermediate-risk population consists of the following: 1. NCI CPTC Antibody Characterization Program. Four patients staffed by one full-time nurse; 4. Scholl, F.G., et al., Interval or permanent nonoperative management of acute type A aortic dissection. Reproduction of previous documented angina, Known history of coronary artery disease, including myocardial infarction, New transient mitral regurgitation, hypotension, diaphoresis, pulmonary edema or rales, New or presumably new transient ST-segment deviation (> 0.05 mV) or T-wave inversion (> 0.2 mV) with symptoms, Elevated cardiac troponin T or I, or elevated CK-MB, ST-segment elevation greater in lead III than in lead II, ST-segment elevation of > 2.5 mm in lead V, ST-segment depression of > 1 mm in leads II, III, and aVF, ST-segment depression of 1 mm or ST-segment elevation in leads II, III, and aVF, Measured 4 hours after onset of chest pain, Measured 10 hours after onset of chest pain. 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. 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. 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). Peroral endoscopic myotomy for esophageal motility disorders. A violet-colored or dusky red rash develops, most commonly on your face and eyelids and on your knuckles, elbows, knees, chest and back. When there is only elevated troponin levels (or even a rise and fall in troponin) without new symptoms or ECG/imaging evidence of myocardial ischemia, it is most appropriate to document a non-MI troponin elevation due to a nonischemic mechanism of myocardial injury. Assays for cTn, namely cTnI and cardiac troponin T (cTnT), are the preferred diagnostic tests for ACS, in particular nonST-segmentelevation myocardial infarction, because of the tissue-specific expression of cTnI and cTnT in the myocardium. 2020; doi:10.1007/s10388-019-00693-w. Castell DO. 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). Chauhan et al. Major disorders of esophageal hyperperistalsis: Clinical features, diagnosis and management. 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. 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. Esophageal spasms are sometimes associated with conditions such as heartburn or gastroesophageal reflux disease (GERD). Cardiac troponin (cTn) is the standard blood-based test to confirm the diagnosis of acute myocardial infarction. Troponin levels typically start to elevate in the circulation within 2 to 3 hours of the onset of chest pain. Jensen, J.K., et al., Frequency and significance of troponin T elevation in acute ischemic stroke. cTnI was elevated in 23 patients (25%) and was normal in 70 patients (75%). The silent myocardial infarction hypothesis is based on the relatively high incidence of ischemic changes noted on screening ECGs in patients with diabetes. A 12-lead ECG should be obtained within 10 minutes of presentation in patients with ongoing chest pain. High-sensitivity troponin tests can detect elevated troponin levels in people without symptoms of cardiovascular disease, according to a 2019 study. Despite the value of cTn for ACS diagnosis, risk stratification and management, it has become quite evident that non-ACS elevation of the marker is not uncommon. MeSH It is also possible that myocardial ischemia in our patient was due to esophagocardiac reflex, which describes myocardial ischemia associated with chemical esophageal stimulation. Esophageal spasms typically occur only occasionally and might not need treatment. J Am Coll Cardiol. Furthermore, the prevalence of GERD in patients with CAD is higher, with some studies reporting prevalence ranging from 40% to 78% [4]. K. R. DeVault, Extraesophageal symptoms of GERD, Cleveland Clinic Journal of Medicine, vol. One study5 found the syndrome in 22 percent of 596 patients who presented to emergency departments with sharp or stabbing pain. Troponins (T, I, C) are found in striated and cardiac muscle. 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. If you experience squeezing chest pain, seek immediate medical care. However, in a prospective observational study6 of 528 patients with symptoms suggestive of coronary artery disease on presentation to the emergency department of a cardiac referral center, symptoms did not differ significantly in patients with and without diabetes. 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. 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. 2022 May 4;4(8):709-720. doi: 10.1016/j.cjco.2022.04.009. Based on Marriotts criteria,15 epicardial injury is diagnosed when the J point (origin of the ST segment at its junction with the QRS complex) is (1) elevated by 1 mm or more in two or more limb leads or precordial leads V4 to V6 or by 2 mm or more in two or more precordial leads V1 to V3; or is (2) depressed by 1 mm or more in two or more precordial leads V1 to V3. 10, no. This lack of blood supply can be due to an acute absolute or relative deficiency in coronary artery blood flow. Many people find that there are specific triggers that prompt esophageal spasms. Thus, it is critically important to recognize this association and initiate treatment with PPIs in appropriate patients with CAD and concomitant GERD as it might improve GERD and prevent future adverse cardiac events. Feng J, et al. In a single-center study by Salvador et al., 30 patients with GERD underwent simultaneous 24-hour multichannel intraluminal impedance pH monitoring and continuous O2 saturation monitoring via pulse oximetry [8]. CJC Open. However, a combination of atypical symptoms improves identification of low-risk patients. Troponin elevation in CKD is worth discussion, as the interpretation of elevation of cTn in non-ACS patients may be difficult. Thygesen, K., et al., Universal definition of myocardial infarction. Very high levels of troponin typically indicate that a person has had a heart attack, which can occur if the blood supply to some of the heart muscle suddenly Troponin is a protein found in all muscles. This tube is called the esophagus. A chest pain unit is a specialized unit within an emergency department or a medical center; the unit is dedicated to careful monitoring and aggressive implementation of diagnostic protocols (clinical guidelines) for the evaluation of acute coronary syndrome. The squeezing chest pain associated with esophageal spasms also can be caused by a heart attack. Esophagus. Spasms may cause minor to It can be detected in the serum as early as two hours after myocardial necrosis begins. Bethesda, MD 20894, Web Policies Distinguishing a type 1 NSTEMI from a type 2 MI depends mainly on the clinical context and clinical judgment. Kim MN, Kim HL, Park SM, Shin MS, Yu CW, Kim MA, Hong KS, Shim WJ. A. Valiati, Extraesophageal manifestations of gastroesophageal reflux disease, Jornal Brasileiro de Pneumologia, vol. S20S32, 2003. Please enable it to take advantage of the complete set of features! The site is secure. Abnormal Q waves usually develop within the first day, and T-wave inversion and normalization of ST segments occur within hours to days. Esophageal spasms are sometimes associated with conditions such as heartburn or gastroesophageal reflux disease (GERD). Given extensive prior cardiac history, anginal equivalent symptoms, ischemic ECG changes, and elevated troponin I levels, non-ST elevation myocardial infarction (NSTEMI) was diagnosed and patient was started on appropriate optimal medical therapy for acute coronary syndrome. (b) Left anterior descending with 99% ostial and 100% mid occlusion and circumflex 99% distal occlusion. The test results should be available within 30 to 60 minutes, because elevated troponins are helpful in identifying the patients who benefit most from early Daniels, L.B., et al., Minimally elevated cardiac troponin T and elevated N-terminal pro-B-type natriuretic peptide predict mortality in older adults: results from the Rancho Bernardo Study. Hospitalists encounter troponin elevations daily, but we have to use clinical judgment to determine if the troponin elevation represents either a myocardial infarction (MI), or a non-MI troponin elevation (i.e. Pain radiating to the shoulder, left arm, or both arms somewhat increases the likelihood of acute coronary syndrome (likelihood ratio [LR]: 1.6).3, Typical angina is described as pain that is substernal, occurs on exertion, and is relieved with rest. Although the ECG may be completely normal in a patient with myocardial ischemia and evolving infarction, classic ECG changes occur in STEMI.14 Within minutes, there is J-point elevation, and tall, peaked, hyperacute T waves develop; ST-segment elevation and reciprocal-lead ST-segment depression also occur. The physical examination in patients with acute coronary syndrome frequently is normal. A community-based sample of 3557 participants showed that the frequency of elevated cTnT using was 0.7%,5 and typically associated with risk factors for heart disease or heart failure (HF). From 1 to 4 percent of patients ultimately proven to have acute coronary syndrome are sent home from the emergency department.24 Patients with acute coronary syndrome who are sent home without further evaluation are more likely to be women, to be nonwhite, to present without chest pain, or to have ECGs that are normal or show nonspecific changes.18, A suggested approach to the evaluation of patients with chest pain or symptoms consistent with acute coronary syndrome is provided in Figure 1. Subsequently, patient underwent an early invasive strategy of cardiac catheterization and angiography that revealed chronic, severe, native 3-vessel CAD (Figures 1(a) and 1(b)).

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