Acute Onset Of Chest Pain Research Articles

Serial high-sensitivity troponin T concentrations and long-term outcomes in patients with suspected acute coronary syndrome

Abstract Background High-sensitivity troponin assays allow for accurate and rapid rule-in or rule-out of myocardial infarction (MI) among patients with acute-onset chest pain. However, prognostic implications of serial high-sensitivity troponin concentrations are unknown. Purpose To determine short- and long-term prognostic implications of high-sensitivity troponin T (hsTnT) concentrations and their changes from baseline, in patients with suspected acute coronary syndrome. Methods Retrospective cohort study based on Danish national registries. We identified all patients discharged from the hospital with either MI, unstable angina, suspected MI, or chest pain from January 2012 through December 2019 and merged these individuals with all records of two serial hsTnT measurements obtained ≤7 hours apart during the same hospitalization. The primary outcome was death at days 0–30 and 31–365. Prognostic implications of serial hsTnT were examined in accordance with the 2012 ESC algorithm stratifying patients for normal baseline concentrations and relative changes of 20% and 50% from baseline. In case of a normal baseline concentration, 20% and 50% of the upper reference level (14 ng/l) were used as thresholds instead, i.e., 3 ng/l and 7 ng/l, respectively. Absolute risks were calculated through multivariable logistic regression with average treatment effect modeling (G-formula). Results Complete data were available in 28,902 individuals (median age [25th-75th percentile] 65.2 [53.4–75.4] years, 11,632 [40.2%] women). Of these, 11,116 (38.5%) had a final diagnosis of MI, 1518 (5.3%) of unstable angina, and 16,268 (56.3%) of either suspected MI or chest pain. Median baseline hsTnT was 18 ng/l (25th-75th percentile, 10–69), second hsTnT 21 ng/l (25th-75th percentile, 10–248), relative hsTnT change 3.6% (25th-75th percentile, 0–66.7), and time between samples 4.0 hours (25th-75th percentile, 3.2–5.4). Most patients had either two normal hsTnT concentrations (9483, 32.8%) or two elevated hsTnT concentrations (18,235, 63.1%). At 30 days, 796 (2.8%) individuals had died, while an additional 1287 (4.6% of 30-day survivors) died between days 31–365. Baseline hsTnT and the relative hsTnT change both displayed a significant, non-linear association with death and interacted with each other (P<0.001). Tables 1 and 2 show the standardized, absolute risks of death (with 95% confidence intervals) from days 0–30 and from days 31–365, respectively. Patients with two normal hsTnT concentrations had very low mortality rates, irrespective of the magnitude of relative change. Conversely, patients with two elevated hsTnT concentrations consistently had high mortality rates. Conclusions This is the first study to assess both short- and long-term outcomes as a function of both baseline hsTnT and its change from first to second measurement. In general, patients with two normal hsTnT concentrations have an excellent prognosis while those with two elevated concentrations require scrutiny. Funding Acknowledgement Type of funding sources: None.

Development and validation of a prediction rule for patients suspected of acute coronary syndrome in primary care: a cross-sectional study

ObjectiveTo develop and validate a symptom-based prediction rule for early recognition of acute coronary syndrome (ACS) in patients with acute chest discomfort who call out-of-hours services for primary care (OHS-PC).DesignCross-sectional...

Chest Pain After Cesarean Section

We present a case report of a 35-year-old multiparous female who presented to the emergency department with acute-onset chest pain. She had an uncomplicated cesarean delivery 2 weeks before presentation. Her physical exam, electrocardiogram, laboratory analysis, and bedside echocardiogram findings are presented. Her findings prompted urgent cardiac catheterization to reveal the diagnosis and adjudicate proper therapy. This case highlights a potentially serious etiology of chest pain in an otherwise healthy peripartum female.

Acute Chest Pain due to Single Coronary Artery: Clinical Implications for Diagnostic Work-up and Therapy

Single coronary artery is a rare finding in coronary angiographies. We report a case of a 65-year-old female with first time acute onset of chest pain and discuss the role of multimodality imaging in chest pain as well as diagnostic and therapeutic work-up in coronary anomalies.<

Achy Breaky Heart: A Case of Lymphocytic Myocarditis Mimicking Takotsubo Cardiomyopathy

<h3>Introduction</h3> Myocarditis is an inflammatory disease of the myocardium that may be due to immune system activation, infection or exposure to toxic substances. The clinical presentation and trajectories encompass a wide spectrum. We present a case of cardiogenic shock fulfilling both the Mayo criteria for myocarditis and the WHO criteria for Takotsubo cardiomyopathy, distinguished by endomyocardial biopsy. <h3>Case Report</h3> A 65-year-old female with a history of mitral valve repair, hypertension and diabetes presented with acute onset chest pain and dyspnea. She denied recent viral illness. Upon examination, she was tachycardic with elevated JVP, crackles bilaterally, and bilateral lower extremity edema. EKG showed sinus tachycardia with PVCs and anteroseptal/lateral ischemic changes. Labs revealed troponin peaking in the 90s and leukocytosis. She underwent left and right cardiac catheterization revealing essentially clean coronaries, severely reduced LVEF 10-20%, severe hypokinesis of the inferoapical segments consistent with Takotsubo cardiomyopathy and hemodynamics consistent with cardiogenic shock. Cardiac MRI demonstrated findings consistent with myocarditis. The patient was successfully managed by a multidisciplinary team. Due to differential diagnoses of Takotsubo cardiomyopathy and myocarditis, serologies for cardiotropic viruses, urine toxicology, and autoimmune workup were performed and were negative. Therefore, an endomyocardial biopsy was obtained revealing lymphocytic and histiocytic infiltrates with localized areas of fiber necrosis. The lymphoid infiltrates were predominantly T-cells, highlighted with CD45 and CD3 stains, consistent with findings of lymphocytic myocarditis. <h3>Summary</h3> This case highlights lymphocytic myocarditis presenting similarly to Takotsubo cardiomyopathy in an older female. This is particularly thought-provoking given that myocarditis must be excluded in all cases of Takotsubo cardiomyopathy per the Mayo criteria. It illustrates the importance of recognizing the clinical presentation of myocarditis and distinguishing it from other secondary cardiomyopathies to properly manage these patients.

Lung Ultrasound to Detect Pneumothorax in Children Evaluated for Acute Chest Pain in the Emergency Department: An Observational Pilot Study.

BackgroundSpontaneous pneumothorax is a relatively uncommon and poorly studied condition in children. While several protocols have been developed to evaluate the use of lung ultrasound for dyspneic adult patients in the emergency department, no specific guidelines are present for pediatric emergency physicians.ObjectivesWe prospectively analyzed children with acute chest pain and clinical suspicion of pneumothorax evaluated at the pediatric emergency department.MethodsWe consecutively enrolled children aged 5–17 years presenting to the pediatric emergency department with clinically suspected pneumothorax based on sudden onset of acute chest pain. After clinical examination, all children underwent lung ultrasound followed by chest X-ray (reference standard). We enrolled 77 children, of which 13 (16.9%) received a final diagnosis of pneumothorax.ResultsThe lung point had a sensitivity of 92.3% (95% CI 77.8–100) and a specificity of 100% (95% CI 94.4–100) for the detection of pneumothorax. The “barcode sign” had a sensitivity of 100% (95% CI 75.3–100) and a specificity of 100% (95% CI 94.4–100) for the detection of pneumothorax.ConclusionLung ultrasound is highly accurate in detecting or excluding pneumothorax in children with acute chest pain evaluated in the pediatric emergency department. If pneumothorax is suspected, but the lung point is not visible, the barcode sign should always be sought as it could be a form of massive pneumothorax.

Is It ST-Segment-Elevation Myocardial Infarction?

A 76-year-old man presented with acute-onset chest pain and dyspnea. He had a history of coronary artery disease, ischemic cardiomyopathy (left ventricular ejection fraction, 25%), recent non-ST-segment-elevation myocardial infarction (NSTEMI), and stenting of the left anterior descending coronary artery (LAD) one month before the current presentation. Soon thereafter, he underwent stenting of the left main coronary artery (LMCA), obtuse marginal branch (OMB), and left circumflex coronary artery. His chest pain subsided soon after arrival at the emergency department. His cardiac troponin I level was 22 ng/mL (normal level, &lt;0.03 ng/mL), and his brain natriuretic peptide level was 841 pg/mL (normal level, &lt;100 pg/mL). Figure 1 shows his electrocardiogram (ECG).What is the diagnosis?C) STEMI due to first OMB or ramus intermedius occlusionThe ECG shows sinus rhythm, mild ST-segment elevation (STE) with T-wave inversion in lead aVL, ST-segment depression with positive T waves in leads II, III, aVF, and V3 through V6, and an isoelectric ST segment in leads I and V1 through V2. The Fourth Universal Definition of Myocardial Infarction1 says, “More profound ST-segment shifts or T-wave inversions involving multiple leads/territories are associated with a greater degree of myocardial ischaemia, and a worse prognosis. For example, ST-segment depression ≥1 mm in 6 leads, which may be associated with STE in lead aVR or lead V1 and hemodynamic compromise, is suggestive evidence of multivessel disease or left main disease” (eliminating answer A). This is considered a high-risk ECG pattern for which invasive intervention within 2 hours is recommended, in accordance with the 2020 European Society of Cardiology guidelines for managing acute coronary syndromes without persistent STE.2 Our patient's ECG shows ST-segment depression in 7 leads but no significant STE in lead aVR or V1. In contrast, STE with negative T waves is seen in lead aVL.Patients with a nonischemic early repolarization pattern can have STE in lead aVL. However, the T waves are usually positive, and there is often a J-point notch. The pattern here suggests a reperfused or more advanced stage of STEMI,3 and the patient's clinical presentation (symptom resolution after hospital arrival) supports this diagnosis.New STE in 2 contiguous leads is necessary for the diagnosis of STEMI.1 However, this is an epidemiologic (not pathophysiologic) criterion, to minimize false-positive diagnosis. Acutely occluded arterial branches may cause STE in only one lead with diffuse ST-segment depression.4 The STE in leads aVL and V2 through V5 is caused by LAD occlusion proximal to the first diagonal branch (eliminating answer B),4 and STE in leads aVL and V2 without STE in leads V3 through V5 suggests an occluded first diagonal branch. The ST-segment depression in the anterolateral and inferior leads is incompatible with the typical presentation of takotsubo cardiomyopathy (answer D). The STE in lead aVL, incompatible with ischemic cardiomyopathy (answer E), is accompanied by ST-segment depression in lead V2, suggesting obstruction of the first OMB. Our patient had an isoelectric ST segment in lead V2, so the differential diagnosis is an occluded OMB or ramus intermedius.4 A coronary angiogram on the second day of admission showed subacute thrombotic occlusion of the first OMB (Fig. 2, arrow), and stenting restored patent flow.Disclosures: NoneFunding/support: None

Double Aortic Valve Sign in Aortic Dissection.

A 50-year-old man presented to the emergency department with acute-onset tearing chest pain for 1 h. He was having tachycardia with a heart rate of 100 beats/min and blood pressure was 90/60 mm Hg in both upper limbs. Auscultation revealed a grade 3/6 systolic late peaking murmur and a high pitched early diastolic murmur in the aortic area. Electrocardiogram showed left ventricular hypertrophy with strain pattern. Echocardiogram revealed a dilated ascending aorta along with a thickened calcific aortic valve with moderate aortic stenosis and moderate aortic regurgitation.

698 Acute coronary syndrome in neoatherosclerosis with major stent malapposition and OCT-guided PCI

AimsDue to its bidimensional nature, angiography is not always sufficient to accurately define coronary lesions, in particular when they are ambiguous or indeterminate. Intracoronary imaging, such as intravascular ultrasound or optical coherence tomography (OCT), is often useful in these cases to better characterize the ambiguous angiographic images, to identify the culprit lesion during acute coronary syndrome (ACS) and to guide percutaneous coronary intervention (PCI).Methods and resultsWe report a case of a 61-year-old male with multiple cardiovascular risk factors and a previous ST-segment elevation myocardial infarction treated by PCI of the right coronary artery (RCA) about 7 years before, wo was admitted to our emergency department after acute onset chest pain. At the time of admission, his ECG was normal and cardiac troponin was below the upper reference limit of normality with positive molecular SARS-CoV-2 diagnostic test. Echocardiogram disclosed a mild left ventricular dysfunction with inferior wall hypokinesia. Coronary angiography showed a moderate in-stent restenosis at mid RCA and a hazy, undetermined image at the proximal edge of the previously implanted stent. Left coronary artery angiography showed only diffuse atherosclerotic disease without significant stenoses and a myocardial bridge at the mid tract of left anterior descending artery. OCT pullback of RCA to better characterize the undetermined lesions shown by angiography. OCT revealed significant neointima hyperplasia and a focal area of neoatherosclerosis with unstable features (fissure/microthrombi) at mid RCA. Severe stent strut malapposition embedded neointimal hyperplasia was observed at the proximal stent edge, resulting in ‘dual’ lumen appearance. The two lesions were treated with a single 3.5/48 mm everolimus-eluting stent (stent-in-stent), which was post-dilated with a 3.5/20 mm non-compliant balloon (18 atm) in the mid-to-distal segments, and 4.5/15 mm (16 atm) and 5.0/8 mm (14 atm) semi-compliant balloons in the proximal stent segment. Post-PCI OCT imaging confirmed good stent expansion and apposition. Our case demonstrates the utility of OCT in clarifying the aetiology of ambiguous angiographic lesions and as a guide for PCI. Indeed, the ‘hazy’ appearance on the angiograms corresponded to the major stent malapposition covered by neointima disclosed by OCT as a ‘dual-lumen’. Of note, OCT allowed to confirm the correct guidewire position in the ‘true’ lumen preventing a crush of the previously implanted stent. OCT was also useful as a diagnostic modality for the identification and characterization of the mechanism underlying the ACS (neoatherosclerosis instability).ConclusionsDue to its unprecedented spatial resolution, OCT enables an ‘optical biopsy’ of the coronary artery wall and intrastent tissue. Therefore, OCT imaging should be considered when lesions are ambiguous or indetermined by coronary angiography to guide the diagnosis and treatments of ACS patients. OCT imaging is also useful to guide stenting and to optimize PCI result, and its impact on clinical outcome is under investigation in large randomized clinical trials.

Management of myocarditis in clinical practice.

Myocarditis is an inflammatory heart muscle disease characterized by heterogeneous clinical presentation and outcome. Clinical heterogeneity of myocarditis, ranging from acute onset chest pain with electrocardiographic changes resembling an acute coronary syndrome, to arrhythmic storm and chronic decompensated heart failure, makes diagnosis challenging. However, a correct diagnosis is fundamental to proper patients' management and should always be seeked. Although a definite diagnosis is only provided by endomyocardial biopsy, the European Society of Cardiology task force on myocardial and pericardial diseases provided specific criteria for the diagnosis of clinically suspected myocarditis, which has been facilitated by the advent of noninvasive imaging tests (i.e. cardiovascular magnetic resonance based myocardial tissue characterization). Due to the heterogeneous presentation and disease course of myocarditis, a tailored treatment would be the best strategy, but a standardized management is still not available. However, over the years, new, promising therapies, such as antiviral and immune-suppressive treatment, have come side by side to the standard pharmacological heart treatment, i.e. antiheart failure medications. In this paper we will review the basic principles of myocarditis management in clinical practice, including diagnostic work-up, conventional and disease-specific therapy and patients' follow-up.

PRIMARY INTRATHORACIC SYNOVIAL SARCOMA

TOPIC: Lung Cancer TYPE: Medical Student/Resident Case Reports INTRODUCTION: Synovial sarcomas (SS) are a rare group of malignancies, seen in 0.17 per 100,000 persons, accounting for 7% of all soft tissue sarcomas. These malignant tumors most commonly present as a tumor of the extremities. While they have a high propensity for metastasis to bone and lung, primary intrathoracic malignancy is rare. We present a case of a patient who presented with acute onset shortness of breath, diagnosed with primary synovial sarcoma of the lung. CASE PRESENTATION: A 22-year-old male with no past significant medical history presented with a four-week history of right upper quadrant abdominal pain and acute onset chest pain radiating to his shoulder with associated dyspnea. On arrival to emergency department, patient was tachycardia, otherwise vitally stable. Labs were notable for leukocytosis. Chest x-ray showed a moderate right-sided pleural effusion with associated opacity of the lower hemithorax. A chest tube was placed however no fluid was evacuated. A CT of the chest was obtained which showed a right lower lobe hemithorax, a right lower lobe pleural-based nodule measuring 2x2 x 1.6 cm, and a lesion within the right hemithorax measuring 20x17.9x19.3 cm. The patient was taken for video-assisted thoracoscopic surgery for surgical exploration and chest tube placement. Patient was found to have large tumor invading whole right chest with compression on mediastinal structures including the heart, lung, and IVC. Biopsies were taken. Patient developed acute respiratory distress and obstructive shock and was intubated and placed on vasopressor support. Preliminary pathology was revealing of synovial sarcoma. Operative findings revealed a large right pleural and posterior mediastinal mass invading the right lower lobe through the diaphragm into the peritoneal space and liver capsule. He underwent thoracotomy with excision and resection of the thoracoabdominal and mediastinal tumor, total pulmonary decortication, wedge resection of right lower and middle lobe, and reconstruction of diaphragm. The patient was successfully extubated three days post operatively and soon after discharged home. Post-operative CT showed no definite evidence of gross residual disease. The patient received 3 cycles of doxorubicin/isofosfamide following discharge. DISCUSSION: Reports of primary thoracic SS are rare. Diagnosis is often delayed because of the benign radiographic appearance and indolent nature of these tumors; sequelae of disease often do not manifest until tumor burden is great enough to cause mass effect. Though standard of care is chemotherapy, the patient in this case required emergency palliative resection due to cardiovascular compromise. CONCLUSIONS: Though soft tissue sarcomas account for less than 0.1% of all malignant thoracic neoplasms, it should be considered in the differential for thoracic malignancies as delay in diagnosis could be consequential to patient outcome. REFERENCE #1: Javad Parvizi, Gregory K. Kim, Chapter 218 - Synovial Sarcoma, Editor(s): Javad Parvizi, Gregory K. Kim, High Yield Orthopaedics, W.B. Saunders, 2010, Pages 455-456, ISBN 9781416002369, https://doi.org/10.1016/B978-1-4160-0236-9.00230-3. REFERENCE #2: Nedra Joseph, Samantha St. Laurent, Jeanenne Joy Nelson, Shan Zheng, and Heide Stirnadel-Farrant. Journal of Clinical Oncology 2019 37:15_suppl, e22535-e22535 DISCLOSURES: No relevant relationships by Neiha Kidwai, source=Web Response

"A JAR FULL OF PINK FROTH": AN ATYPICAL CASE OF AMNIOTIC FLUID EMBOLISM AFTER A DILATION AND CURETTAGE AT SEVEN WEEKS GESTATION

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Amniotic fluid embolism (AFE) is one of the leading causes of death during pregnancy in developed countries. It is an uncommon, life-threatening complication often associated with advanced maternal age, multi-parity, and placental rupture. It is extremely rare in the first trimester, as the small amount of amniotic fluid and fetal cells are unlikely to breach the maternal circulation. Here, we present an atypical case of AFE occurring at 7 weeks gestation. CASE PRESENTATION: The patient is a healthy 29-year-old nulliparous woman who developed acute onset chest pain, dyspnea, and productive cough with pink frothy sputum within 30 minutes of dilation and curettage (D&C), which she underwent after spontaneous abortion at 7 weeks gestation. Her symptoms were accompanied by acute hypoxemic respiratory failure, shock, and coagulopathy. She did not have any rash or skin changes. Computed tomography angiography of the chest was negative for pulmonary embolism but showed bilateral patchy opacities in all lobes. Transthoracic echocardiogram showed normal biventricular and valvular function. The patient required supportive care with as many as three vasopressors and Bilevel Positive Airway Pressure at 100% FiO2 and left the intensive care unit after approximately 72 hours. She was discharged home after 7 days, by which time she had fully recovered. DISCUSSION: Amniotic fluid embolism is a diagnosis of exclusion, without rapid and accurate diagnostic options available. For this reason, early and atypical cases of AFE are likely underreported. In AFE, the normal physiology is altered due to increased immunological response upon physical breach of amniotic fluid into maternal circulation, releasing procoagulant and vasoactive mediators to cause anaphylactic reaction to the fetal antigen (1). Hence, the imbalance can cause multi-organ failure, exhibited through a classic triad of hypotension, hypoxia, and coagulopathy that were demonstrated in our case without clear etiology for shock and respiratory decompensation. Management is focused on adequate cardiovascular, pulmonary, and hematologic support. Because no cases of recurrence have been reported, current data suggests successful subsequent pregnancies (2). CONCLUSIONS: Our case highlights a patient at 7 weeks gestation with unexplained shock, respiratory failure, and coagulopathy less than 1-hour status post D&C, and may represent the earliest documented case of AFE. Diagnosis of AFE is based upon clinical findings and symptoms, with treatment focused on providing adequate hemodynamic support. Due to limited understanding of its pathophysiology, an emphasis on early diagnosis and treatment is critical to prevent significant mortality. REFERENCE #1: Society for Maternal-Fetal Medicine (SMFM). Electronic address: pubs@smfm.org, Pacheco LD, Saade G, Hankins GD, Clark SL. Amniotic fluid embolism: diagnosis and management. Am J Obstet Gynecol. 2016 Aug;215(2):B16-24. doi: 10.1016/j.ajog.2016.03.012. Epub 2016 Mar 14. PMID: 26987420. REFERENCE #2: 177: The risk of amniotic fluid embolism reoccurrence in subsequent pregnancy, Irene Stafford, Presley S. Parkes, Amir Moaddab, Miranda Klassen, Steven L. Clark, Michael A. Belfort, Gary A. Dildy, American Journal of Obstetrics and Gynecology, Volume 218, Issue 1, Supplement, https://doi.org/10.1016/j.ajog.2017.10.054. DISCLOSURES: No relevant relationships by Wahaaj Khan, source=Web Response No relevant relationships by Do Yun Kim, source=Web Response No relevant relationships by Andrew Toscano, source=Web Response

Myocarditis Associated with mRNA COVID-19 Vaccination.

Myocarditis Associated with mRNA COVID-19 Vaccination.

Electrocardiographic manifestations in a large right-sided pneumothorax

BackgroundPneumothorax is an extrapulmonary air accumulation within the pleural space between the lung and chest wall. Once pneumothorax acquires tension physiology, it turns into a potentially lethal condition requiring prompt surgical intervention. Common symptoms are chest pain and dyspnea; hence an electrocardiogram (ECG) is often performed in emergent settings. However, early diagnosis of pneumothorax remains challenging since chest pain and dyspnea are common symptomatology in various life-threatening emergencies, often leading to overlooked or delayed diagnosis. While the majority of left-sided pneumothorax-related ECG abnormalities have been reported, right-sided pneumothorax-related ECG abnormalities remain elucidated.Case presentationA 51-year-old man presented to the emergency department with acute-onset chest pain and dyspnea. Upon initial examination, the patient had a blood pressure of 98/68 mmHg, tachycardia of 100 beats/min, tachypnea of 28 breaths/min, and oxygen saturation of 94% on ambient air. Chest auscultation revealed decreased breath sounds on the right side. ECG revealed sinus tachycardia, phasic voltage variation of QRS complexes in V4–6, P-pulmonale, and vertical P-wave axis. Chest radiographs and computed tomography (CT) scans confirmed a large right-sided pneumothorax. The patient’s symptoms, all the ECG abnormalities, and increased heart rate on the initial presentation resolved following an emergent tube thoracostomy. Moreover, we found that these ECG abnormalities consisted of two independent factors: respiratory components and the diaphragm level. Besides, CT scans demonstrated the large bullae with a maximum diameter of 46 × 49 mm in the right lung apex. Finally, the patient showed complete recovery with a thoracoscopic bullectomy.ConclusionsHerein, we describe a case of a large right-sided primary spontaneous pneumothorax with characteristic ECG findings that resolved following re-expansion of the lung. Our case may shed new light on the mechanisms underlying ECG abnormalities associated with a large right-sided pneumothorax. Moreover, ECG manifestations may provide useful information to suspect a large pneumothorax or tension pneumothorax in emergent settings where ECGs are performed on patients with acute chest pain and dyspnea.

Aortic dissection in a young male with isolated interrupted aortic arch: an unusual association

Interruption of the aortic arch (IAA) is a rare congenital anomaly which has been infrequently documented in the adult population. Aortic dissection (AD) is an emergency often presenting as acute chest pain and warranting urgent intervention. A 32-year-old male presented to Emergency Department with acute chest pain. Clinical examination revealed feeble pulses in bilateral lower limbs with a blood pressure difference between upper and lower limbs. Two-dimensional Echocardiography was suggestive of IAA with AD in the descending thoracic aorta. This was confirmed on computed tomography scan of the aorta which revealed complete interruption of the aortic arch distal to left subclavian artery along with the presence of an intimo-medial flap in descending thoracic aorta. A diagnosis of IAA with AD was made. The patient underwent an urgent aortic repair surgery following which he has been largely asymptomatic. A suspicion of AD should always be made in any patient presenting with acute onset chest pain radiating to the back along with accelerated hypertension/feeble pulses in extremity. Occurrence of AD in an adult with IAA is a distinct rarity and has been documented only thrice.

Chest Pain Radiating to the Jaw with Elevated Troponin: Aortic Dissection Masquerading as Myocardial Infarction

Introduction: Chest pain radiating to the jaw, is a classic symptom of acute myocardial infarction (AMI). Electrocardiogram (EKG) changes consistent with ischemia and elevated serum troponin I levels are used to confirm the diagnosis. Prompt management including medical or procedural intervention is required to help reduce mortality in patients with AMI. However, additional conditions may mimic those of classic primary coronary pathology. Case Report: We present the case of a 43-year-old male who came to the emergency department (ED) complaining of acute onset of chest pain radiating to the left jaw. His EKG revealed mild ST changes and T-wave inversion in the antero-lateral leads. Laboratory testing revealed an elevated serum troponin level of 0.18 ng/mL (normal: < 0.04 ng/mL). He was taken for a coronary angiogram and during the procedure, an aortogram was performed revealing a type A aortic dissection. Findings were confirmed by Computed Tomography Angiogram (CTA) showing a dissection extending from the aortic root to the iliac bifurcation. He was promptly taken to the operating room (OR) for surgical repair. Conclusion: Aortic dissection (AD) is included in the differential diagnosis in patients presenting with symptoms and signs consistent with AMI. However, in patients presenting with AD, there are some clues in history and physical exam, such as high blood pressure, history of noncompliance with antihypertensive medications, or location of pain that may provide a clue towards an underlying AD. Our case demonstrates that even if all evidence points towards an AMI, AD should still be on the differential until successfully ruled out by imaging.

ECG of the Month: Wide Complex Tachycardia in an Adult Patient with Surgically Corrected Congenital Heart Disease

A 27-year-old man with history of hypoplastic left-sided heart syndrome, status post-Fontan palliation surgery, and depressed right-sided ventricular function presented to the emergency department with acute-onset chest pain and shortness of breath while walking up steps to his home 90 minutes before presentation. He was ill appearing and diaphoretic on arrival. He was alert but had delayed capillary refill and perioral cyanosis. His initial vital signs were significant for pulse rate of 204 beats/min, respiratory rate of 22 breaths/min, blood pressure 132/75 mm Hg, and oxygen saturation of 88% on 3 L of nasal cannula oxygen.

Utility of HEART Pathway in Identifying Low-Risk Chest Pain in Emergency Department.

Chest pain is a common presenting symptom in the emergency department (ED). The HEART (history, electroencephalogram [ECG], age, risk factors, and troponin I) score, with addition of troponin at 3h, helps to determine appropriate risk stratification of the patients. This study evaluated the utility of the HEART pathway as a decision aid designed for risk stratification of patients with acute-onset chest pain for early and safe disposition. This was a prospective observational study done in a tertiary care center. Focused history, 12-lead ECG, and baseline troponin I level on arrival and at hour 3 were recorded. Subjects were classified as low risk (HEART score 0-3) or high risk (HEART score≥4). Patients with a HEART score of 0-3 with negative troponin I at 3h were discharged and were followed up for major adverse cardiac events (MACEs) within 30days of ED presentation. A total of 250 patients were screened for the study, of which 151 were included for the final analysis. One hundred and two patients (68%) were male and 54% of patients were younger than 45years. HEART scores of 0 (n=16), 1 (n=43), 2 (n=44), and 3 (n=48) were observed. There was only 1 MACE (0.7%) in 30days after ED discharge in the study population. The mean length of ED stay in the low-risk group was 4.5h. Low-risk patients, as per the HEART pathway, can be discharged safely from the ED, which reduces ED stay and health care resource use.

Primary Percutaneous Coronary Intervention in an Anomalous Left Circumflex Artery: Search for the Hidden Culprit

Congenital coronary anomalies are rarely detected in patients undergoing diagnostic coronary angiography. They pose a challenge in delay to identify the anomalous artery as well as difficulty in engaging the anomalous vessel. The present case report was of 56-years-old male patient presented with acute onset of chest pain. On evaluation, his electrocardiogram was suggestive of ST segment elevation in inferior leads. He underwent diagnostic coronary angiogram which revealed totally occluded Left Circumflex Artery (LCx) arising anomalously from right coronary osteum. Primary Percutaneous Coronary Intervention (PCI) of LCx could not be performed with routine guide catheters necessitating the use of special multipurpose guide catheter with balloon support. The case highlights the need for the knowledge of coronary anatomy and anomalous origins of coronary arteries and the selection of appropriate guiding catheters and coronary wires.

Primary meningococcal pericarditis presenting as acute coronary syndrome with angiographically confirmed obstructive lesions

Background: Primary meningococcal pericarditis (PMP) is defined as purulent pericarditis without clinical evidence of meningococcaemia, meningitis, or other foci of meningococcal infection. Meningococcal infections associated with ST segment elevation and raised cardiac enzymes mimicking acute myocardial infarction have been previously reported, but all of these cases had a normal coronary angiogram, which may indeed represent a diagnosis of myocarditis, especially when no endomyocardial biopsies had been conducted. We report a unique case of primary meningococcal pericarditis presenting as acute coronary syndrome with angiographically confirmed obstructive lesions. Case Description: A 68 y old gentleman, an ex-smoker with multiple comorbidities, presented with acute-onset chest pain. There was no fever, skin rashes or meningeal signs. Electrocardiogram revealed hyperacute T at leads V2 to V5 and ST elevation at leads V7 to V9. Bedside echocardiogram disclosed septal wall hypokinesia with a pericardial effusion. Cardiac catheterisation revealed triple-vessel disease with critical stenosing lesion in the mid left anterior descending artery. Plasma troponin I was elevated. 3 d later, patient developed new-onset fever with worsening pericardial effusion and signs of impending cardiac tamponade. Emergent pericardiocentesis yielded pericardial fluid with an exudative picture. Both pericardial fluid and blood culture grew Neisseria meningitidis W-135. Intravenous ceftriaxone 2 g 12 h was initiated. Post-exposure prophylaxis was given to all healthcare workers affected. In spite of appropriate antimicrobial therapy, patient further deteriorated and succumbed due to multiorgan failure. Discussion: Invasive meningococcal infections other than meningitis and meningococcaemia have not been reported in Malaysia before. Neisseria meningitidis W-135 infections in Malaysia are commonly associated with Hajj pilgrimage. PMP usually has a favourable outcome with appropriate and timely antimicrobial administration. However, it was not suspected initially in our case who had no infectious prodrome, history of Hajj pilgrimage or exposure to a known case of meningococcal infection. The infectious process probably acted as an inciting event for acute coronary syndrome secondary to increased coronary vascular resistance induced by inflammatory cytokines. Conclusion: Our case underscores the importance to include infective causes of pericarditis in the differential diagnosis of pericardial effusion in any patient presenting with acute coronary syndrome, especially high-risk groups such as elderly population, diabetics, and those with multiple comorbidities.