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Journal articles on the topic 'Acute Chest Syndrome'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 June 2025

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1

Yusuf, BelloJamoh, AbdullahA Abba, and Mohammed Tasiu. "Acute Chest Syndrome." Sub-Saharan African Journal of Medicine 1, no. 3 (2014): 111. http://dx.doi.org/10.4103/2384-5147.138930.

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2

Johnson, Cage S. "The Acute Chest Syndrome." Hematology/Oncology Clinics of North America 19, no. 5 (2005): 857–79. http://dx.doi.org/10.1016/j.hoc.2005.08.001.

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3

Panteghini, Mauro. "Acute Coronary Syndrome." Chest 122, no. 4 (2002): 1428–35. http://dx.doi.org/10.1378/chest.122.4.1428.

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4

Aslam Lashari, Naveed, Nadia Irum Lakho, Sarfaraz Ahmed Memon, Ayaz Ahmed, and Muhammad Fahad Waseem. "ACUTE CORONARY SYNDROME;." Professional Medical Journal 24, no. 03 (2017): 409–13. http://dx.doi.org/10.29309/tpmj/2017.24.03.1544.

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Introduction: ACS is defined as the cluster of symptoms arising due to the rapiddrop of blood flow to the heart because of coronary artery obstruction. It is stated that worldwidearound 17 million people die due to cardiovascular diseases of which half of the deaths arereported due to ACS. Chest pain is known to be the most leading factor associated with ACS.Objectives: To determine the frequency of acute coronary syndrome, its types and commoncontributing factors in patients presenting with typical chest pain in a secondary care hospital.Study Design: Cross sectional study. Setting: Medical Unit, PAF Hospital Mushaf Sargodha.Period: October 2013 to March 2014. Methodology: A total of 280 patients of either gender,aged 20 to 80 years presented with typical chest pain with or without conventional risk factorswere included in the study. Results: Majority (68.9%) was males and 31.1% were female. Acutecoronary syndrome was observed in 131(46.8%) patients. Out of these 131 patients, 55% hadNSTEMI, 28.2% had unstable angina and 16.8% had STEMI. A higher proportion of femaleswere found to have ACS as compared to males (75.9% vs 33.7%, P-value<0.0001). Out of131 patients, 40.5% were diabetic, 29.8% were hypertensive 16% were hyperlipidemic, while13.7% were smokers. Conventional risk factors except smoking were observed more in femalesas compared to males. Conclusion: Majority of patients with acute coronary syndrome werefemales and diabetic. NSTEMI was the most common type of ACS. Prevalence of conventionalrisk factors was found more in females with ACS.
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5

Ibrahim, Aliyu. "Empyema thoracis complicating acute chest syndrome." Journal of Mahatma Gandhi Institute of Medical Sciences 20, no. 1 (2015): 74. http://dx.doi.org/10.4103/0971-9903.151748.

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6

Chambers, Charles E., and David M. Leaman. "Management of Acute Chest Pain Syndrome." Critical Care Clinics 5, no. 3 (1989): 415–34. http://dx.doi.org/10.1016/s0749-0704(18)30416-0.

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7

Mekontso Dessap, Armand. "Radiographic patterns of acute chest syndrome." Thorax 70, no. 8 (2015): 792.2–792. http://dx.doi.org/10.1136/thoraxjnl-2015-207088.

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8

VOULALAS, DEBRA. "Albuterol Inhalations in Acute Chest Syndrome." Archives of Pediatrics & Adolescent Medicine 145, no. 6 (1991): 603. http://dx.doi.org/10.1001/archpedi.1991.02160060019011.

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9

Paul, Rabindra N., Oswaldo L. Castro, Anita Aggarwal, and Patricia A. Oneal. "Acute chest syndrome: sickle cell disease." European Journal of Haematology 87, no. 3 (2011): 191–207. http://dx.doi.org/10.1111/j.1600-0609.2011.01647.x.

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10

Lee, J. G., E. Nap-Hill, and B. Bressler. "A128 ACUTE GASTRIC VOLVULUS DISGUISED AS ACUTE CORONARY SYNDROME." Journal of the Canadian Association of Gastroenterology 4, Supplement_1 (2021): 111–12. http://dx.doi.org/10.1093/jcag/gwab002.126.

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Abstract Background Acute gastric volvulus is a rare but potentially life-threatening condition that warrants emergent assessment. Its clinical presentation may encompass the Borchardt’s triad of vomiting, epigastric pain, and inability to insert a nasogastric tube. However, it can also present as chest pain and is often not cited within the typical differential diagnosis of non-cardiac causes of chest pain. We report the first known case of mesenterico-axial gastric volvulus presenting as acute coronary syndrome with a normal electrocardiogram, complete with radiographic and endoscopic images. Aims To present a case of acute gastric volvulus disguised as an acute coronary syndrome and describe its management. Methods Case report and review of literature. Results A 68 year-old female with history of recent coronary artery bypass graft surgery presented to hospital with sudden onset chest pain radiating to her left shoulder and jaw while having dinner. Initial high sensitivity troponin (normal &lt;9ng/L) was 15ng/L, which increased to a modest peak at 115ng/L. ECG at presentation and through admission consistently showed normal sinus rhythm x 5. She was assessed by Cardiology and given her rising troponin and chest pain, she was treated as a non-ST elevation myocardial infarction with dual antiplatelet therapy. She underwent cardiac catheterization showing distal graft anastomotic site stenosis and was stented x2. Post procedure, her severe retrosternal chest pain recurred. GI was consulted for dysphagia and odynophagia, which was then noted to be present concurrent with her initial chest pain presentation. An urgent CT scan of the abdomen and pelvis revealed acute mesenterico-axial gastric volvulus (Figure 1A), a rarer form of gastric volvulus in the adult population compared to its organo-axial counterpart. After a failed nasogastric decompression, an emergent upper endoscopy was attempted and demonstrated mucosal necrosis (Figure 1B) but was unsuccessful in relieving the volvulus. The patient then underwent overnight surgery, which showed gastric volvulus with contained perforation and 50% necrosis of the stomach with sparing of the cardia and antrum. This resulted in a subtotal gastrectomy, hiatus hernia repair, pyloromyotomy, jejunostomy, and bilateral chest tube insertion. She then recovered in ICU before being successfully discharged home from hospital. Conclusions Acute gastric volvulus can present while disguised as more common causes of chest pain, such as acute coronary syndrome. Those who present with chest pain who also have a history of a large hiatal hernia, or an intrathoracic stomach should be evaluated with gastric volvulus in the differential diagnosis as its prompt management is critical to reduce morbidity and mortality. Funding Agencies None
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11

Hui, David S. C., and Joseph J. Y. Sung. "Severe Acute Respiratory Syndrome." Chest 124, no. 1 (2003): 12–15. http://dx.doi.org/10.1378/chest.124.1.12.

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12

Chaturvedi, Shruti, Djamila L. Ghafuri, Jeffrey Glassberg, Adetola A. Kassim, Mark Rodeghier, and Michael R. DeBaun. "Rapidly progressive acute chest syndrome in individuals with sickle cell anemia: a distinct acute chest syndrome phenotype." American Journal of Hematology 91, no. 12 (2016): 1185–90. http://dx.doi.org/10.1002/ajh.24539.

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13

Saussine, Max, Pascal Colson, Michel Mauzen, and Henri Mary. "Postoperative Acute Respiratory Distress Syndrome." Chest 102, no. 3 (1992): 980–81. http://dx.doi.org/10.1378/chest.102.3.980.

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14

Yale, Steven H., Nahed Nagib, and Troy Guthrie. "Acute chest syndrome in sickle cell disease." Postgraduate Medicine 107, no. 1 (2000): 215–22. http://dx.doi.org/10.3810/pgm.2000.01.835.

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15

Laurie, G. A. "Acute chest syndrome in sickle cell disease." Internal Medicine Journal 40, no. 5 (2010): 372–76. http://dx.doi.org/10.1111/j.1445-5994.2010.02129.x.

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16

Warrier, R. P., Rafael Ducos, and Lolie C. Yu. "Acute chest syndrome in sickle cell disease." Journal of Pediatrics 109, no. 4 (1986): 731. http://dx.doi.org/10.1016/s0022-3476(86)80260-8.

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17

Corradi, Francesco, Claudia Brusasco, and Paolo Pelosi. "Chest ultrasound in acute respiratory distress syndrome." Current Opinion in Critical Care 20, no. 1 (2014): 98–103. http://dx.doi.org/10.1097/mcc.0000000000000042.

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18

Freixa, Marta, Glória Nunes da Silva, Fernanda Paula Santos, and Filipe Froes. "Acute Chest Syndrome: An Unrecognized Progressive Condition." Open Respiratory Archives 2, no. 4 (2020): 300–301. http://dx.doi.org/10.1016/j.opresp.2020.08.004.

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19

Mehta, Nilesh, Iain MacIntosh, Rodney Rivers, and Simon Nadel. "Acute chest syndrome of sickle cell disease." Journal of Pediatrics 137, no. 4 (2000): 589. http://dx.doi.org/10.1067/mpd.2000.107634.

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20

Farooq, Sajid, Mohannad Abu Omar, and Gary A. Salzman. "Acute chest syndrome in sickle cell disease." Hospital Practice 46, no. 3 (2018): 144–51. http://dx.doi.org/10.1080/21548331.2018.1464363.

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21

Golden, Carla, Lori Styles, and Elliott Vichinsky. "Acute chest syndrome and sickle cell disease." Current Opinion in Hematology 5, no. 2 (1998): 89–92. http://dx.doi.org/10.1097/00062752-199803000-00002.

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22

White, Dorothy A., Lee S. Schwartzberg, Mark G. Kris, and George J. Bosl. "Acute chest pain syndrome during bleomycin infusions." Cancer 59, no. 9 (1987): 1582–85. http://dx.doi.org/10.1002/1097-0142(19870501)59:9<1582::aid-cncr2820590909>3.0.co;2-#.

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23

Dourakis, Spyros P., Alexandra Alexopoulou, Constantin Papageorgiou, Andreas Kaloterakis, and Stephanos J. Hadziyannis. "Acute chest syndrome in sickle-cell trait." European Journal of Internal Medicine 15, no. 4 (2004): 248–50. http://dx.doi.org/10.1016/j.ejim.2004.03.010.

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24

Livesay, Sarah, and Susan D. Ruppert. "Acute Chest Syndrome of Sickle Cell Disease." Critical Care Nursing Quarterly 35, no. 2 (2012): 183–95. http://dx.doi.org/10.1097/cnq.0b013e3182456630.

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25

Ballas, Samir K. "Acute Chest Syndrome in Sickle Cell Anemia." Journal of Intensive Care Medicine 15, no. 3 (2000): 123–25. http://dx.doi.org/10.1177/088506660001500301.

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26

Honoré, P., A. Williams, C. Ozanne, and K. Clark. "Acute Chest Syndrome in Sickle Cell Anaemia." Acta Clinica Belgica 48, no. 5 (1993): 344–47. http://dx.doi.org/10.1080/17843286.1993.11718328.

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27

Ballas, Samir K. "Acute Chest Syndrome in Sickle Cell Anemia." Journal of Intensive Care Medicine 15, no. 3 (2000): 123–25. http://dx.doi.org/10.1046/j.1525-1489.2000.00123.x.

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28

Stone, Michael B. "Acute chest syndrome diagnosed by lung sonography." American Journal of Emergency Medicine 27, no. 4 (2009): 516.e5–516.e6. http://dx.doi.org/10.1016/j.ajem.2008.08.002.

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29

Werberich, Gabriel Madeira, Miriam Menna Barreto, and Edson Marchiori. "Acute Chest Syndrome in Sickle Cell Disease." Archivos de Bronconeumología (English Edition) 56, no. 3 (2020): 188–89. http://dx.doi.org/10.1016/j.arbr.2019.08.010.

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30

Werberich, Gabriel Madeira, Miriam Menna Barreto, and Edson Marchiori. "Acute Chest Syndrome in Sickle Cell Disease." Archivos de Bronconeumología 56, no. 3 (2020): 188–89. http://dx.doi.org/10.1016/j.arbres.2019.08.016.

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31

Hering, Justin, Stefano Schena, Barney Dillard, James Doherty, Don Fishman, and Steven Salzman. "Acute chest syndrome following blunt liver laceration." Injury Extra 39, no. 6 (2008): 216–18. http://dx.doi.org/10.1016/j.injury.2007.10.026.

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32

Pangestika, Destiya Dwi, Yanny Trisyani, and Aan Nuraeni. "The Effect of Dhikr Therapy on the Cardiac Chest Pain of Acute Coronary Syndrome (ACS) Patients." Nurse Media Journal of Nursing 10, no. 2 (2020): 200–210. http://dx.doi.org/10.14710/nmjn.v10i2.25638.

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Background: Cardiac chest pain is a typical complaint experienced by patients with Acute Coronary Syndrome (ACS) in Emergency Departments (EDs). Pharmacological therapy is one major intervention used to reduce cardiac chest pain due to ACS. However, this therapy does not optimally and completely reduce cardiac chest pain; therefore, additional therapy is greatly required.Purpose: This study aimed to examine the effect of Dhikr therapy as one of the additional therapies for the cardiac chest pain experienced by patients with ACS in EDs.Methods: This quasi-experimental research was conducted using a pretest-posttest control group design. As many as 52 patients with ACS were recruited using a consecutive sampling technique and then equally divided to the intervention and control group. The intervention group received both pharmacological and Dhikr therapy approximately for 17 minutes, while the control group only received the pharmacological therapy based on the hospital’s protocol. The Numeric Pain Rating Scale (NPRS) was used to measure the intensity of cardiac chest pain, and both paired and independent t-tests were utilized to analyze the data.Results: The results showed that there was a significant difference in pain reduction in both groups (p=0.000), although the decrease in the intervention group was higher than that in the control group. Furthermore, the pain reduction was significantly different between groups (p=0.021)Conclusion: Dhikr combined with the pharmacological therapy reduced the intensity of cardiac chest pain in ACS patients better than the use of pharmacological therapy alone. Therefore, this study recommends the combination of pharmacological and Dhikr therapy for patients with ACS.
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33

Dina, Ayodeji, Peter Barlis, and William van Gaal. "Clozapine-Induced Myocarditis or Acute Coronary Syndrome? Optical Coherence Tomography to the Rescue." Case Reports in Cardiology 2018 (July 19, 2018): 1–3. http://dx.doi.org/10.1155/2018/5026107.

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Chest pain and troponin elevation may be due to an acute coronary syndrome, myocarditis, acute cardiomyopathy, or other less common conditions. Management differs depending on the aetiology, and the pathophysiologic diagnosis has direct implications on treatment and patient outcomes. History and clinical examination is supplemented by selected investigations including the electrocardiogram, chest X-ray, echocardiography, coronary angiography, and even myocardial perfusion scintigraphy or cardiac magnetic resonance imaging. Intravascular imaging can provide important insights into the underlying mechanism of acute coronary syndromes, especially when angiography is ambiguous.
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34

Aspromonte, Nadia, Stefania A. Di Fusco, Roberto Latini, et al. "Natriuretic peptides in acute chest pain and acute coronary syndrome." Coronary Artery Disease 24, no. 1 (2013): 33–39. http://dx.doi.org/10.1097/mca.0b013e32835b6741.

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35

Maldonado, Lorena, Emiliano Descotte, Martin Chertcoff, Alejandro Salvado, and Miguel Angel Blasco. "Everolimus Related Acute Respiratory Distress Syndrome." Chest 144, no. 4 (2013): 301A. http://dx.doi.org/10.1378/chest.1703449.

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36

Hui, David S. C., and Joseph J. Y. Sung. "Treatment of Severe Acute Respiratory Syndrome." Chest 126, no. 3 (2004): 670–74. http://dx.doi.org/10.1378/chest.126.3.670.

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37

Eichhöfer, Jonas, Cara Hendry, and Douglas Fraser. "Management of Non-STEMI and suspected Acute Coronary Syndrome." Acute Medicine Journal 8, no. 1 (2009): 3–9. http://dx.doi.org/10.52964/amja.0223.

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Chest pain is a common complaint of patients presenting to the Emergency Department, but there is a wide variety of underlying causes. These include ischaemic chest pain (acute coronary syndromes (ACS) and stable angina), non-ischaemic cardiovascular chest pain (aortic dissection, pulmonary embolism, pericarditis) and a wide variety of non cardiovascular causes (musculoskeletal, psychiatric and gastrointestinal causes).
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38

&NA;. "Morphine: acute chest syndrome in sickle cell anaemia." Reactions Weekly &NA;, no. 1002 (2004): 4. http://dx.doi.org/10.2165/00128415-200410020-00011.

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39

Quinn, Charles T., and George R. Buchanan. "The acute chest syndrome of sickle cell disease." Journal of Pediatrics 135, no. 4 (1999): 416–22. http://dx.doi.org/10.1016/s0022-3476(99)70162-9.

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40

Autore, Camillo, Luciano Agati, Marco Piccininno, Stefano Lino, and Salvatore Musarò. "Role of echocardiography in acute chest pain syndrome." American Journal of Cardiology 86, no. 4 (2000): 41–42. http://dx.doi.org/10.1016/s0002-9149(00)00991-7.

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41

Wieler, Jane, and Ahmed Mamdouh Taha Mostafa. "Cocaine induced chest pain and acute coronary syndrome." Visual Journal of Emergency Medicine 16 (July 2019): 100589. http://dx.doi.org/10.1016/j.visj.2019.100589.

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42

Platt, Orah S. "The Acute Chest Syndrome of Sickle Cell Disease." New England Journal of Medicine 342, no. 25 (2000): 1904–7. http://dx.doi.org/10.1056/nejm200006223422510.

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43

Haynes, Johnson, and Michael B. Kirkpatrick. "The Acute Chest Syndrome of Sickle Cell Disease." American Journal of the Medical Sciences 305, no. 5 (1993): 326–30. http://dx.doi.org/10.1097/00000441-199305000-00013.

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44

GLADWIN, MARK T, ALAN N SCHECHTER, JAMES H SHELHAMER, and FREDERICK P OGNIBENE. "The Acute Chest Syndrome in Sickle Cell Disease." American Journal of Respiratory and Critical Care Medicine 159, no. 5 (1999): 1368–76. http://dx.doi.org/10.1164/ajrccm.159.5.9810094.

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45

Desai, Payal C., and Kenneth I. Ataga. "The acute chest syndrome of sickle cell disease." Expert Opinion on Pharmacotherapy 14, no. 8 (2013): 991–99. http://dx.doi.org/10.1517/14656566.2013.783570.

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46

Saint-Jacques, Henock, Valentine J. Burroughs, Justyna Watkowska, Michelle Valcarcel, Pedro Moreno, and Myo Maw. "Acute Coronary Syndrome Critical Pathway: Chest PAIN Caremap." Critical Pathways in Cardiology: A Journal of Evidence-Based Medicine 4, no. 3 (2005): 145–60. http://dx.doi.org/10.1097/01.hpc.0000175896.05417.5e.

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47

Farsi, Khalil Al, Vinodh K. Panjwani, and Salam Alkindi. "Acute Chest Syndrome During Pregnancy: Presentation and Outcome." Blood 116, no. 21 (2010): 4812. http://dx.doi.org/10.1182/blood.v116.21.4812.4812.

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Abstract Abstract 4812 Background: There is very little data on acute chest syndrome (ACS) during pregnancy in patients with sickle cell disease (SCD). Having been following a treatment protocol that necessitates exchange transfusions during pregnancy in patients who have a severe course of sickle cell disease and history of previous maternal and/or fetal complications as well as prophylactic chest physiotherapy in patients who are at risk of ACS, we planned to study the rate and course of ACS during pregnancy at our institution. Methods: As chest X-rays (CXR) are not commonly done during pregnancy, we defined ACS as an acute respiratory illness with lower respiratory tract symptoms and signs that are likely reflecting or are equivalent to a finding of a new pulmonary infiltrate. We reviewed the electronic records of women with SCD over the age of 18 years who were admitted to our hospital between the period of June 2006 and June 2010. Results: We identified a total of 60 patients who had one or more pregnancies during this period, 5 of whom met our definition of ACS. Median age was 26 years (range: 25–34). Two, 2 and 1 were in their first, second and fourth pregnancies, respectively. ACS occurred during different trimesters of pregnancy (first: 1, second: 2 and third: 2). ACS was the reason for admission in 2, while acute painful episodes and decreased fetal movement were the reason in 2 and 1, respectively (with ACS developing within a median of 1 day post-admission; range: 1–6, in the latter two groups). All patients presented with fever and shortness of breath, 4 had cough and 4 had decreased oxygen saturation < 95%. All had decreased breath sounds and dullness to percussion, 4 had coarse crackles and 3 also had wheezes. There was a tendency to involve the lower lobes (Right in 1 and bilateral in 4). Two patients had pleural effusions (one seen on ultrasound and one on CXR done immediately after delivery in a patient who had ACS late in the third trimester). Only one had a positive culture (E. coli on blood culture). All patients had an increase in lactate dehydrogenase, LDH, compared to their baseline (median increase from baseline: 173, range: 101–530) and C-reactive protein, CRP (median increase from baseline: 90; range: 23 – 170). All episodes of ACS resolved completely with a median duration of hospitalization of 13 days (range: 4 – 23) with a treatment protocol consisting of intravenous hydration, morphine for pain control, chest physiotherapy, broad-spectrum antibiotics, bronchodilators and red cell transfusions (simple in one and simple + exchange in 4). Only one patient required admission to the intensive care unit where she received non-invasive positive pressure ventilation. All pregnancies ended up in live births. However, 2 of these were preterm. Conclusions: Our analysis indicates that the rate of ACS during pregnancy is low and its course is uncomplicated at our institution, which might reflect the pre-emptive strategy that we have been following. A prospective study with a control group to examine the exact incidence, risk factors, course and outcome of ACS during pregnancy is warranted. Disclosures: Alkindi: Sultan Qaboos University: Employment, Research Funding.
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48

Gentile, Michael, Jose Pineda, Ira Cheifetz, and Jon Meliones. "HIGH FREQUENCY OSCILLATORY VENTILATION IN ACUTE CHEST SYNDROME." Critical Care Medicine 27, Supplement (1999): 135A. http://dx.doi.org/10.1097/00003246-199901001-00380.

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49

Desideri, Giovambattista, Giuseppe Limongelli, and Ezio De Pratti. "Oesophagus perforation mimicking an acute chest pain syndrome." Internal and Emergency Medicine 10, no. 6 (2015): 749–51. http://dx.doi.org/10.1007/s11739-015-1216-6.

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50

Chaumont, Martin, Marc Blaimont, Rachid Briki, Philippe Unger, and Nadia Debbas. "Acute Coronary Syndrome Mimicking Takotsubo Cardiomyopathy or Takotsubo Cardiomyopathy Mimicking Acute Coronary Syndrome?" Case Reports in Cardiology 2020 (February 24, 2020): 1–3. http://dx.doi.org/10.1155/2020/6562316.

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A healthy 66-year-old female presented to the emergency department with acute chest pain, T-wave inversion in the anterior leads, and elevated troponin-I. Coronary angiography showed a stenosis in the midportion of the left anterior descending coronary artery (LAD), which did not wrap the left ventricle (LV) apex. LV angiography demonstrated a large LV apical akinetic systolic ballooning with a 45% ejection fraction. Fractional flow reserve (FFR) of LAD lesion was 0.71. Percutaneous intervention was performed. At six months, transthoracic echocardiography was normal. Fifteen months later, the patient presented with chest pain and a small rise in troponin-I. Coronary angiogram was unchanged. Repeat FFR in distal LAD was 0.86 and left ventriculography was normal. Diagnostic criteria for Takotsubo cardiomyopathy (TTC) require the absence of obstructive coronary artery disease. In the present case, TTC was highly suspected on the basis of typical LV apex ballooning. However, significant ischemia in the same territory was demonstrated by positive FFR, which could not be falsely positive in this context. Current TTC diagnostic criteria increase specificity for diagnosing TTC. This case reminds us that it is at the price of reduced sensitivity, since there is no reason to believe that coronary lesions may protect from TTC.
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