Developed Chest Pain Research Articles

Refractory Coronary Vasospasm After Spine Surgery; A Rare Case Report

Refractory vasospastic angina (RVSA) is a rare condition leading to several episodes of constriction of coronary arteries which eventually leads to myocardial ischemia. Calcium-channel blockers (CCBs) and nitrates are usually used, however, sometimes the vasospasm is refractory and recurrent leading to high morbidity and mortality. A 35-year-old man known case of hypertension underwent two times operation due to T9-T10 discopathy and decompressive laminectomy of three segments T8/T9/ T10 following a previous car accident 4 months before this admission. Three days postoperatively he developed chest pain, dyspnea and diaphoresis. Electrocardiography showed inverted T wave in leads I, II and ST elevation in pericardial leads of V1-V4. Left anterior descending (LAD) artery stenosis was present (99%) at mid part that resolved after Trinitroglycerin (TNG) injection during angiography. Totally, he underwent 3 times coronary angiography due to recurrent chest pain refractory to conventional management of Prinzmetal’s angina. Coronary stent could not be placed due to severe spasm. Finally, he developed refractory chest pain and dyspnea and cardiac arrest in the CCU despite receiving intravenous high dose TNG, Diltiazem, Nicorandil and Hydrocortisone. He expired after several times of cardiopulmonary resuscitation. Refractory VSA after spine surgery has not been reported in the literature yet. This patient was resistant to available medications. There is no consensus regarding the treatment unfortunately. Randomized clinical trials have to be done to find ways regarding unconventional treatment options such as alpha-2-agonists, Corticosteroids, rho-kinase-inhibitors, statins and magnesium. Despite the fact, some surgical interventions with sympathetic denervation like left-stellate-ganglion denervation must be assessed.

EBUS-TBNA-INDUCED PURULENT PERICARDITIS: A RARE COMPLICATION OF A COMMON PROCEDURE.

Endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) has a good safety profile and is used to investigate peritracheal and peribronchial lesions, but severe complications have occurred so prophylactic measures should be implemented.Risk factors for infections due to EBUS-TBNA have not been properly established, but the presence of necrotic or cystic lesions and an elevated number of punctures during TBNA seem to be relevant.Although severe complications are rare, awareness of their existence may allow faster diagnosis and, consequently, a better prognosis.

Takotsubo Syndrome Occurring after mRNA COVID-19 Vaccination in a Patient with Graves’ Disease

Cardiovascular events such as myocarditis following mRNA COVID-19 vaccination are increasing. We present a 67-year-old postmenopausal woman with Takotsubo Syndrome and Graves' disease after mRNA COVID-19 vaccination. She developed chest pain and shortness of breath one week after vaccination. An electrocardiogram revealed ST elevation in the precordial leads. Coronary angiography revealed the absence of obstructive coronary artery disease, and the left ventriculography showed a typical feature with apical ballooning. Laboratory workup showed the elevation of free T4 and thyrotropin receptor antibodies. It was presumed that Takotsubo Syndrome and Graves' disease were probably related to the COVID-19 mRNA vaccination. The patient was treated with low-dose bisoprolol, diuretics, carbimazole, and steroid and discharged uneventfully. The mRNA COVID-19 vaccination is still safe and effective to defend against COVID-19 pandemic. However, clinicians should be aware of the possible cardiovascular adverse events other than myocarditis following vaccination.

Феназепам® и Дексмедетомидин при плановых чрескожных коронарных вмешательствах. Сравнительный анализ

INTRODUCTION: Intraprocedural analgosedation in planned percutaneous coronary interventions is a priority method of anesthesia, since it provides comfort for patient in comparison with when it is absent; it leads to a fast recovery of patients and reduction of the incidence of complications in comparison with the general anesthesia. The question of the optimal sedation method is still open. AIM: To carry out a comparative analysis of sedation with Phenazepam® and Dexmedetomidine in planned percutaneous coronary interventions in patients with stable coronary heart disease. MATERIALS AND METHODS: A prospective randomized study was conducted from September 2021 to January 2022. The study included patients with stable ischemic heart disease (serum troponin T level less than 0.32 ng/ml; absence of anginous pain at the beginning of X-ray endovascular intervention), who had planned percutaneous coronary intervention. The Phenazepam® sedation group included 40 patients, including 30.0% (n = 12) women and 70.0% (n = 28) men. 40 patients were included in the Dexmedetomidine sedation group: 30.0% (n = 12) women, 70.0% (n = 28) men. RESULTS: There was a statistically significant (p < 0.001) reduction of blood pressure and heart rate in patients in the group of sedation with Dexmedetomidine at the stage of stenting of the coronary artery, compared with analogous parameters in the group of sedation with Phenazepam®. Patients in the group of sedation with Dexmedetomidine developed chest pain at the stage of coronary artery stenting reliably 3.13 times less often (p = 0.024) than patients of the group of sedation with Phenazepam® (OR: 0.32; 95% CI: 0.13–0.80). With use of Dexmedetomidine, relief of anginal pain with narcotic analgesics was required 20 times less often (p < 0.001) than with Phenazepam® (OR: 0.05; 95% CI: 0.01–0.38). One can confidently speak about the superiority and safety of analgosedation with Dexmedetomidine in planned percutaneous coronary interventions over sedation with Phenazepam®. CONCLUSIONS: Dexmedetomidine provides deeper sedation and sufficient pain relief in patients in planned percutaneous coronary interventions than Phenazepam®. At the same time, Dexmedetomidine has a more pronounced hypotensive and a negative chronotropic effect.

Congenital Absence of Left Coronary Artery Ostium in a Patient Presenting With Anterior ST-Elevation Myocardial Infarction

A 73-year-old man developed chest pain 12 hours before arriving at our hospital. An electrocardiogram revealed ST-segment elevation in leads V2–V6 (Figure 1A); therefore, an emergent coronary angiography was performed. Several attempts were made to engage the left coronary artery (LCA), but they were unsuccessful. Left coronary cusp angiography and subsequent right coronary angiography demonstrated a single right coronary artery (RCA) with blood flow to the left circumflex coronary artery (LCX) and the congenital absence of the LCA ostium at the left, right, and posterior Valsalva sinuses (Figure 1B, Video 1).

1935. Cardiac Tamponade Following COVID-19 Vaccination

Abstract Background While numerous, most described cases of myocarditis and pericarditis following COVID-19 vaccination are mild and self-limited. We present two cases of life-threatening cardiac tamponade following COVID-19 vaccination. Methods Two cases of cardiac tamponade in temporal association with COVID-19 vaccination were reviewed Results Case 1 : 75-year-old male with rheumatoid arthritis admitted with chest pressure and hypotension 2 days after his 1st dose of Pfizer-BioNTech COVID-19 vaccine. Pericardiocentesis removed 275 ml of exudative effusion with 14,140 nucleated cells/ml. Fluid bacterial and fungal cultures were negative; cytology was inconsistent with malignancy. He had no Epstein-Barr virus (EBV) or cytomegalovirus (CMV) viremia. Symptoms resolved on prednisone and colchicine. A week later, he had an uneventful second COVID-19 vaccine. He went on to have 3 recurrences of pericarditis starting two months after his first. One was within 48 hours of his COVID-19 booster. He is on long term prednisone. Case 2: 66-year-old male with non-Hodgkin’s lymphoma in remission. He developed chest pain a day after his 2nd dose of Pfizer-BioNTech COVID-19 vaccine. Admitted 4 days later with pericardial effusion and managed medically. Readmitted a week later with fever and chest pain. Echocardiogram now showed cardiac tamponade. Pericardiocentesis removed 400 ml of exudative fluid with 1,191 nucleated cells/mL. Cultures for bacteria, fungi, and mycobacteria were negative. Cytology didn't show malignancy. Serologies for CMV, EBV and parvovirus represented past infection. He was discharged with a pericardial drain, colchicine, and NSAIDs. He was later readmitted with fevers. Echocardiogram only showed small pericardial effusion, which did not require drainage. Figure 1Circumferential pericardial effusion seen on trans-thoracic echocardiography from patient in case 1. Conclusion Given the proximity to COVID-19 vaccination and lack of alternative explanations, we believe that tamponade was a direct result of post-vaccine inflammatory pericarditis. Neither patient had a prior history of pericardial effusion. Both tested negative for SARS-CoV-2 by nasopharyngeal swab excluding active infection. Healthcare providers should consider the possibility of pericardial effusion and tamponade in patients with chest pain, shortness of breath, or hypotension following COVID-19 vaccination. Disclosures All Authors: No reported disclosures.

Abstract 11380: Exercise Induced ST Segment Elevation Caused by Coronary Vasospasm

Case Presentation: A 52-year-old male with no known medical history was seen in the cardiology clinic for occasional pressure-like chest pain on exertion. Due to an intermediate pretest probability of CAD, ischemic workup with a nuclear perfusion exercise stress test was planned. Patient achieved maximum predicted heart rate after 12 minutes of exercising, with no anginal symptoms, ST segment changes or arrhythmias during the entire period. However, 3 minutes into the recovery phase, he developed chest pain and diaphoresis, with EKG now showing 7mm ST elevations in the inferior leads and BP falling to 77/56 mmHg. STEMI code was called, and patient was emergently taken to the cardiac cath lab for coronary angiogram and possible PCI. Angiogram found the coronary arteries to be non-obstructive but revealed vessels possibly having vasospasm. Intra coronary nitroglycerin was given with no further PCI. The patient’s symptoms subsided after the angiogram, and he remained asymptomatic thereupon and was eventually discharged on Verapamil and nitrate therapy. Discussion: Typically, vasospastic angina occurs at rest. Exercise induced and post-exercise recovery phase ST segment elevation on EKG is associated with severe atherosclerotic disease with significant coronary obstruction. However, exercise induced ST elevations in the post exercise recovery phase caused by non-obstructive, vasospastic coronary arteries, as seen in this patient, is a rare occurrence. The vasospasm is hypothesized to be due to coronary vascular smooth muscle hyperactivity and endothelial cell dysfunction. Treatment is usually with calcium channel blockers, nitrates and lifestyle modification such as smoking cessation and alcohol restriction. This case illustrates the importance of identifying the etiology of the angina, noting that post exercise ST segment elevations are not always associated with coronary vessel obstruction and vasospasm should be considered as a possible etiology.

Abstract 14188: An Unexpected Cause of Anterior ST Segment Elevation After Coronary Intervention

Background: ST elevation (STE) in V1 to V3 is traditionally labeled as anteroseptal infarction due to occlusion of the LAD proximal to the septal branches. An important and uncommon cause for similar ECG findings is an isolated RV myocardial infarction due to occlusion of the proximal RCA and/or its branches. We present a case of anteroseptal ST elevation after jailing of a conus branch during percutaneous coronary intervention (PCI) to the RCA. CASE: 89-year-old female with history of moderate aortic stenosis (AS), hypertension, hypercholesterolemia, and prior stroke presented with progressive dyspnea on exertion and 3 days of chest tightness. Initial echocardiogram showed an EF of 64% and severe AS with peak velocity of 4.27 m/s, mean gradient of 45 mmHg and aortic valve area of 0.43 cm 2 . Coronary angiography showed severe stenosis of the proximal RCA successfully treated with intravascular lithotripsy and drug-eluting stent deployment with jailing of the conus branch. The LAD and LCX had mild nonobstructive disease. Patient developed chest pain after the procedure with new STE in V1 to V3. She was taken for emergent cardiac angiogram due to suspected occlusion of the LAD however this showed unchanged anatomy with patent stent in the RCA and no new severe stenosis or occlusion of the left coronary arteries. There was no flow in the jailed conus branch that was not intervened on due to small vessel size. A repeat echocardiogram showed new mild RV dilatation with unchanged EF and normal LV wall motion. Patient had resolution of the chest pain and STE within 2 hours and was discharged home in stable condition. Conclusion: Occlusion of a conus branch artery with associated isolated RV myocardial infarction is an uncommon cause of STE in anteroseptal leads. High index of suspicion is important to anticipate and manage potential complications like ventricular arrhythmias and RV failure.

TYPE II AND III KOUNIS SYNDROME AFTER PEANUT ANAPHYLAXIS

<h3>Introduction</h3> Acute coronary syndrome (ACS) associated with allergic or anaphylactic reactions, described in 1991 as "allergic angina", is known as Kounis syndrome (KS). Triggers include food, drugs, and coronary stents. This case highlights ACS following peanut anaphylaxis. <h3>Case Description</h3> A 61 year-old smoker with peanut allergy and diabetes presented with pruritus and urticaria following accidental peanut ingestion. He was treated with diphenhydramine, famotidine, methylprednisolone, and epinephrine with symptomatic improvement. He experienced sudden hypotension and pruritus and received additional epinephrine. EKG revealed inferolateral ST elevations with reciprocal depressions. He underwent catheterization with stents to LAD and RCA and received clopidogrel. After intervention, he developed chest pain with recurrent inferolateral ST elevations; progressed to pulseless ventricular tachycardia requiring CPR, revascularization, balloon pump placement, and CVICU transfer. Ultimately, he discharged on prasugrel. <h3>Discussion</h3> KS has three variants: type I and II are defined by absence or presence of coronary artery disease, respectively. Type III describes DES thrombosis. Our patient had evidence of underlying CAD. Anaphylaxis-induced coronary vasospasm was further exacerbated by epinephrine administration, likely resulting in plaque rupture, consistent with Type II KS. Ruptured plaques increase mast cells, histamine, and other cytokines. Histamine is well-described in coronary vasoconstriction. Non-allergic ischemia patients are shown to have increased histamine. Stent thrombosis is a multifactorial process; with common causes ruled out, Type III KS became more plausible. Treatment includes offending-agent removal, corticosteroids, antihistamines, and revascularization. KS management requires detailed history, cardiovascular and anaphylactic pathophysiology focus, mast cell degranulation inhibiting agents, and allergy desensitization.

PSAT018 Management of Pheochromocytoma in the Setting of a Patient with Multiple Vasculopathies

Abstract A 66-year-old male with history of Type 2 diabetes and adrenal incidentaloma presented to the hospital with significant left lower limb edema and was found to have severe peripheral vascular disease. CT surgery was consulted and performed an angiogram as well as an angioplasty; however, the patient had severe stenosis and stenting was not possible. Femoral popliteal bypass was planned. Due to the patient's acute kidney injury from renovacular hypertension, preoperative evaluation included a MRI abdomen w/wo contrast which showed a 1.4 cm right adrenal nodule with early contrast enhancement which appeared fairly avid and uniform. This nodule had been previously noted by CT scan three years prior. Previous outpatient labs showed elevated metanephrines of 543 pg/mL, which determined the adrenal nodule to be consistent with a pheochromocytoma. Subsequently, femoral popliteal bypass was postponed and the patient was started on an alpha blocker, doxazosin. Urology was consulted and right laproscopic adrenalectomy was planned. Preoperatively, patient developed chest pain due to ventricular tachycardia and NSTEMI was diagnosed by EKG. Patient then underwent a LHC which revealed severe left main 3 vessel coronary artery disease, postponing planned adrenalectomy. CABG was performed with pericardiectomy. After initial recovery, patient was discharged to in-patient rehabilitation, indefinitely delaying definitive pheochromocytoma therapy. Reference Jacques W. M. Lenders, Quan-Yang Duh, Graeme Eisenhofer, Anne-Paule Gimenez-Roqueplo, Stefan K. G. Grebe, Mohammad Hassan Murad, Mitsuhide Naruse, Karel Pacak, William F. Young, Jr, Pheochromocytoma and Paraganglioma: An Endocrine Society Clinical Practice Guideline, The Journal of Clinical Endocrinology &amp; Metabolism, Volume 99, Issue 6, 1 June 2014, Pages 1915–1942, https://doi.org/10.1210/jc.2014-1498 Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

PSAT033 Increased Risks of Atherosclerotic Heart Disease, Malignancy and Sleep Apnea with Primary Aldosteronism: A Case Report

Abstract Introduction Primary aldosteronism (PA) demonstrates an increased risk of atherosclerotic heart disease. A less commonly known fact is that PA is often associated with increased risks of malignancy, especially renal cell carcinoma (RCC) and sleep apnea. We are reporting a 51-year-old male with a long history of untreated PA caused by an adenoma (APA) who developed coronary artery disease (CAD), RCC, and sleep apnea during the course of his illness. Case presentation A 51-year-old male was evaluated in the endocrine clinic for secondary hypertension. Patient developed hypertension and hypokalemia at the age of 39 years and laboratory tests showed plasma renin activity PRA 0.06 ng/mL/hr, aldosterone 6 ng/dL, plasma metanephrines 79 pg/mL (ref 0–145), normetanephrine 22 pg/mL (ref 0-62), a serum cortisol value of 0.8 mcg/dL after 1 mg dexamethasone suppression. Despite using several anti-hypertensive medications, including quinapril, amlodipine, and potassium chloride, both his hypertension and hypokalemia remained poorly controlled. He also was diagnosed with sleep apnea at the age of 44 years, treated with CPAP. Abdominal CT showed normal adrenals and angiomyolipoma involving the right interior pole of the kidney. At the age of 47 years, a diagnosis of Liddle syndrome was considered, and the patient was placed on amiloride. At the age of 48 years, the patient developed chest pain and further diagnostic tests confirmed coronary artery disease, and a stent was placed in the left anterior descending artery. Due to the poor control of hypertension, carvedilol and eplerenone were also added to the regimen. Another abdominal CT done at the age of 50 years showed a left adrenal adenoma 1.2 cm, left kidney lower pole cyst 2.9 cm, and atherosclerotic calcification of aorta. Family history was negative for endocrine diseases. Physical examination: HR 62/min, BP 160/90 mmHg, normal examination of the heart, lungs, and abdomen. No clinical features of Cushing syndrome was observed. Repeat laboratory evaluations showed plasma renin activity &amp;lt; 0.167 ng/ml/hr, plasma aldosterone 111.4 ng/dL, concerning for PA. A follow-up CT of the abdomen confirmed left adrenal adenoma and a 1.8 cm left renal lesion suggestive of RCC. The patient underwent an adrenal venous sampling, which localized the left adrenal adenoma as the cause of PA. The patient underwent left adrenalectomy and left partial nephrectomy and pathology confirmed left adrenal adenoma and RCC. One week after surgery plasma aldosterone was 1.9 ng/dL and his hypertension was controlled with fewer medications and he did not require potassium supplements. Conclusion Our case illustrates that delayed diagnosis of PA (poorly treated PA) may be associated with an increased risk of CAD, malignancy and sleep apnea. Early diagnosis and surgical intervention are recommended for PA, especially caused by an adenoma. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

Temperature-related chest pain presentations and future projections with climate change

BackgroundClimate change has led to increased interest in studying adverse health effects relating to ambient temperatures. It is unclear whether incident chest pain is associated with non-optimal temperatures and how chest pain presentation rates might be affected by climate change. MethodsThe study included ambulance data of chest pain presentations in Melbourne, Australia from 1/1/2015 to 30/6/2019 with linkage to hospital and emergency discharge diagnosis data. A time series quasi-Poisson regression with a distributed lag nonlinear model was fitted to assess the temperature-chest pain presentation associations overall and according to age, sex, socioeconomic status, and event location subgroups, with adjustment for season, day of the week and long-term trend. Future excess chest pain presentations associated with cold and heat were projected under six general circulation models under medium and high emission scenarios. ResultsIn 206,789 chest pain presentations, mean (SD) age was 61.2 (18.9) years and 50.3 % were female. Significant heat- and cold-related increased risk of chest pain presentations were observed for mean air temperatures above and below 20.8 °C, respectively. Excess chest pain presentations related to heat were observed in all subgroups, but appeared to be attenuated for older patients (≥70 years), patients of higher socioeconomic status (SES), and patients developing chest pain at home. We projected increases in heat-related chest pain presentations with climate change under both medium- and high-emission scenarios, which are offset by decreases in chest pain presentations related to cold temperatures. ConclusionsHeat- and cold- exposure appear to increase the risk of chest pain presentations, especially among younger patients and patients of lower SES. This will have important implications with climate change modelling of chest pain, in particular highlighting the importance of risk mitigation strategies to minimise adverse health impacts on hotter days.

A Case Report of Sagittal Sinus Thrombosis and Pulmonary Embolism in an Asymptomatic SARS-CoV-2 Infection

Background: Vascular thrombotic events such as pulmonary embolisms have been frequently reported in the course of SARS-Cov-2 infection. However, sagittal sinus thrombus is extremely rare, and patients may lack other appealing Covid-19 infection symptoms. Case report: 46-year-old female with past medical history of Hyperlipidemia, Hypertension presented to Emergency room with headache, chest pain, vomiting. SARS-CoV-2 IgG Antibodies were reactive. Except for elevated PTT-Lupus Anticoagulant at 50 Sec, Hypercoagulable workup was negative. The MRI venogram findings were consistent with the Dural thrombus of superior sagittal sinus. Patient subsequently developed chest pain, and Computed tomography angiography found pulmonary emboli within segmental branches of the right lower lobe pulmonary artery. Patient was managed in the ICU with Heparin and switched to Coumadin for discharged. Conclusion: The incidence of Cerebral Venous Sinus thrombus (CVST) among Covid-19 patients is inferior to 0.02%. And most of the patients lack typical Covid-19 presentations such as pneumonia. The lack of symptoms may promote the insidious course of pre-thrombotic events that lead to CVST. However more Retrospective studies are necessary to established consistent odd ratios. Due to the higher mortality associated with CVST and the ongoing of Covid-19 pandemic, we recommend a higher level of clinical suspicion.

A Case Report of Spontaneous Coronary Artery Dissection

Atherothrombosis is the leading cause of acute coronary syndrome (ACS). Spontaneous coronary artery dissection (SCAD) refers to a nonatherosclerotic lesion involving the tearing and splitting of the coronary wall. The creation of a false lumen and blockage of the true lumen generates an oxygenation mismatch in the myocardial tissue. A middle-aged woman with unremarkable medical history developed chest pain. Uptrending cardiac enzymes and electrocardiogram changes prompted further testing. Coronary angiography showed a type 3 SCAD lesion in the left circumflex artery. SCAD lacks the average risk factors of ACS and its recognition can be delayed. On the other hand, it preserves the typical presentation of ACS.

P157 THE UNFORESEEABLE LINK: A CASE OF CORONARY–PULMONARY ARTERY FISTULA BRIDGING THE RIGHT CORONARY AND FIRST SEPTAL BRANCH OF THE LEFT ANTERIOR DESCENDING ARTERY

Abstract Coronary–pulmonary artery fistulas are a rare clinical entity with a variety of potential clinical manifestations. Albeit rare, such anomalies may in some instances involve multiple coronary arteries and go unnoticed until old age producing little to no clinical manifestations. We hereby present the case of an 83–year–old man, heavy smoker, with a history of cor pulmonale due to severe chronic obstructive pulmonary disease (COPD) who was recently diagnosed with metastatic lung adenocarcinoma. Incidentally, one of the ECGs performed revealed negative T waves in the precordial leads in the absence of symptoms and with a negative troponin curve. Echocardiography was thus performed and revealed severe left ventricular systolic dysfunction (EF 31%) with infero–postero–lateral akinesia. The patient underwent CT coronary angiogram, which ruled out any significant coronary stenosis but revealed a most surprising finding. An ectatic arterial branch running anteriorly and draining into the pulmonary artery connected the the proximal segment of the right coronary artery to the first septal branch of the left anterior descending (LAD) artery. Unfortunately, the severe left ventricular failure contraindicated any chemotherapy and the patient was discharged with a plan to start palliative radiotherapy. Three months later, the patient returned to our Hospital due to worsening weakness, cachexia and one episode of pre–sincope. During this hospital stay, he developed atypical chest pain with a significant troponin curve. A HRCT and pulmonary angiogram was performed, which revealed neoplastic progression with bilateral lung involvement and bone metastases, as well as bilateral segmental pulmonary emboli. Echocardiography demonstrated new segmental areas of akinesia (apical septum and mid–apical anteroseptal segment) suggestive of focal ischemic damage. Given the documented pulmonary embolism and the anomalous connection between pulmonary artery and coronary circulation, this event may have been caused by paradoxical embolism travelling from pulmonary to coronary circulation (most likely affecting the LAD artery territory). Due to the patient’s frailty however, this hypothesis could not be confirmed by coronary angiography. Despite their relative rarity, coronary–pulmonary artery fistulas involving multiple coronary arteries can occur in the elderly population with no previous clinical manifestations and may give rise to apparently unfathomable clinical constellations.

D-18 | High-Sensitivity Cardiac Troponin Concentrations in Patients with Chest Discomfort

We sought to assess the association with different Troponin levels and mortality in patients with chest pain in the Charleston Area Medical Center Emergency Department. Our study used Beckman Coulter assay and introduce novel cut offs that helps develop chest pain algorithms.

P048 A young girl with myocardial infarction

Abstract Background/Aims Takayasu arteritis is a chronic granulomatous inflammatory disease of the aorta and its major branches. It is commonly seen in young women but has been reported in children as young as 6 months. Acute myocardial infarction due to coronary artery involvement is a rare presentation in Takayasu’s arteritis. Methods A previously healthy 13-year-old girl presented with a history of five episodes of short lasting exertional tightening type chest pain with adrenergic symptoms over a week which was relieved by rest. She didn't have any history of shortness of breath, limb claudication or constitutional symptoms. However, on two of the occasions she felt faint. She denied any recreational drug use. There was no family history of cardiovascular disease, connective tissue diseases or sudden cardiac death. On examination she was of average build with no peripheral stigmata of connective tissue diseases or hypercholesterolemia. Apart from a tachycardia of 110 bpm, her cardiovascular examination was normal. There was no BP difference between the arms and no audible bruits. All her peripheral pulses were felt. Results Her ECG showed ST segment depressions in V1-V5. High sensitivity Troponin I was strongly positive. An urgent CT coronary angiogram revealed aortitis involving the ascending and arch of the aorta extending to the left subclavian artery with both coronary arteries showing smooth short segment narrowing at the origin. Doppler USS abdomen showed wall thickening of proximal and mid abdominal aorta. Blood investigations showed a leucocytosis of 14,100/µl and thrombocytosis of 532000/µl. Her ESR was raised at 31 mm/hr and CRP was 5 mg/l. While further awaiting investigations she was started on treatment as for non-ST elevation myocardial infarction according to standard guidelines. Screening for tuberculosis and VDRL were negative . A CT aortic angiogram showed wall thickening involving the aortic root, coronary arteries, ascending aorta and the abdominal aorta with involvement of the origins of coeliac axis and the superior mesenteric artery. Appearance were suggestive of Takayasu arteritis Type v. She was pulsed with intravenous methylprednisolone 30 mg/kg for 3 days followed by oral prednisolone 2 mg/kg. As a steroid sparing agent methotrexate was added. Despite treatment, while in hospital she developed chest pain with ECG showing new onset ST elevation in aVR. An urgent coronary angiogram done showed severe LMCA disease for which stenting was done. At this stage Tocilizumab was initiated. A year later she remains well controlled in terms of her disease activity. Conclusion Though rare, Takayasu’s arteritis should be considered in any adolescent female presenting with ischemic type symptoms and positive inflammatory response. High index of suspicion can lead to early imaging and aggressive immunosuppression that will reduce the morbidity and mortality of this disease. Disclosure S. Janagan: None. M.P.M.L. Gunathilaka: None. L. Rajagopala: None. J.D. Jagoda: None.

Atypical Takotsubo Cardiomyopathy Secondary to COVID-19 Presenting Late as Chest Pain with Subsequent Late Sudden Death

Background: Cardiac involvement at time of COVID-19, caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), is associated with poor prognosis. However, post-COVID-19, the recovery period might also be associated with lingering effects or predisposition to some cardiac manifestations including sudden death, which can not only be missed but which might also remain undefined. This is a report of 56-year man who developed chest pain diagnosed as atypical Takotsubo type cardiomyopathy presenting after recovery from COVID-19 pneumonia 12 days following confirmation of SARS-CoV-2 infection by real-time quantitative polymerase chain reaction (RT-qPCR) testing. Case Report: 56 years old male who re-presented after clinical recovery from COVID-19 pneumonia (diagnosed on 1st admission from a nasopharyngeal swab using RT-qPCR assay/test; Xpertâ Xpress SARS-CoV-2 in vitro diagnostic device), with new cardiac symptoms (3rd admission), which after appropriate investigations was diagnosed as non-coronary cardiac injury/atypical Takotsubo type cardiomyopathy leading to sudden fatal outcome. Plausible mechanisms include direct cardiac toxicity (myocarditis) and/or microthrombi/hypoxia. The precise timing of the cardiac injury was difficult to elucidate but the potential for lingering cardiac consequences was realistic with eventual negative prognostic outcome. Conclusions: This case presentation after full clinical recovery from COVID-19 pneumonia highlights the new challenges for such cases, including potential longer-term enduring impact on cardiovascular morbidity and late mortality. The implications on use/benefits from conventional cardio-protective therapies including duration remains unclear. Further studies to screen high-risk patients with elevated cardiac biomarkers or cardiac risk factors post COVID-19 recovery (if not all patients) might be helpful but at the expense of significant consequences on existing cardiac services and cardiologists.

Abstract 17059: Ocrelizumab Induced Kounis Syndrome

Kounis syndrome(KS), first described in 1991, is defined as concurrence of acute coronary syndrome and anaphylactic events. Primary mechanism of KS is interaction of mast cells with T-lymphocytes and macrophages via multidirectional stimuli leading to platelets activation. Case presentation: A 35 y.o. tennis coach with multiple sclerosis is admitted to the medical ICU with anaphylaxis after receiving Ocrelizumab infusion. Vital signs on presentation are significant for hypotension with blood pressure of 69/30 mm Hg, sinus tachycardia to 110 bpm and hypoxia with SatO2 88% on room air. Other investigations including chest x-ray, EKG and blood work are unrevealing for secondary pathological process outside of anaphylaxis. She undergoes fluid resuscitation followed by epinephrine drip for persistent hypotension. In addition methylprednisolone, famotidine and diphenhydramine are administered. She requires escalating doses of epinephrine and subsequently develops chest pain with troponin elevation to 0.29 ng/ml and EKG concerning for new ST depression and T wave inversion in II, III, aVF, V2 - V6 leads. Urgent echocardiography revealed normal biventricular function with no wall motion abnormalities and is only significant for moderate MR. Given excellent underlying functional capacity and no underlying cardiac risk factors, she was treated for Kounis syndrome by treating underlying anaphylaxis and weaning epinephrine as able with additional fluid resuscitation. Her chest pain resolved and EKG normalized with eventual discontinuation of epinephrine. Repeat echocardiography revealed preserved left ventricular (LV) function and mild MR. Discussion: KS is not a rare disease but easily overlooked and infrequently diagnosed. Our patient had the type I variant: endothelial dysfunction or microvascular angina in absence of cardiac risk factors. Inflammatory mediators can cause vasospasm and catecholamines used for treatment may potentiate it therefore requiring thoughtful dosing and appropriate duration of treatment. Prompt recognition is crucial for appropriate management of anaphylatic shock followed by that of ACS if LV function declines or risk factors for cardiac disease are present.

Abstract 9049: Masking the Bruce Protocol: Surgical Masks Decrease Exercise Duration

Introduction: Exercise stress echocardiography is a critical tool in the workup and assessment of angina, dyspnea, and cardiac disease. Due to the ongoing COVID-19 pandemic, the American Society of Echocardiography recommends that all patients wear surgical facemasks during exercise stress testing. Hypothesis: We hypothesized that masks decrease test duration, increase likelihood of test stoppage due to dyspnea, and increase likelihood of abnormal test results. Methods: We performed a retrospective chart review of 565 treadmill stress echocardiograms utilizing Bruce protocol between April 2019-July 2019 (without mask) and April 2020-July 2020 (with mask). Chi square and T testing were used for statistical analysis, controlling for age and gender. Results: Unmasked patients had a greater mean exercise duration than masked patients (8:12 min vs 7:35 min, p=.02), and were less likely to have dyspnea during the test than masked patients (odds ratio 0.58 [95% CI 0.39, 0.83], p=.003). Unmasked patients were twice as likely to develop chest pain during the test than masked patients (odds ratio 2.0 [95% CI 1.26, 3.22], p=.003). Lastly, unmasked patients were less likely to have an abnormal test result than masked patients, though the difference was not significant (odds ratio 0.81 [95% CI 0.43, 1.51], p=0.50). Conclusions: Surgical mask use during treadmill exercise stress tests associated with a significant decrease in test duration, increased dyspnea during the test, and a non-significant increase in likelihood of abnormal test result. Given the critical importance of stress testing in ischemia evaluation, further exploration is warranted to determine whether mask use during stress tests affects downstream testing, diagnoses, and outcomes.