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      Myocardial Infarction after ChAdOx1 nCoV-19 in a Young Male

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          Abstract

          Sir, Myocardial infarction rarely happens in young age.[1] Hereby, we report the case of a 21-year-old patient who presented with myocardial infarction 14 days after receiving the ChAdOx1 nCoV-19 COVID-19 (AstraZeneca/Vaxzevria) vaccine. Sometimes thrombotic events associated with thrombocytopenia after immunisation occurs known as vaccine-induced immune thrombotic thrombocytopenia (VITT) which manifests 3–30 days post vaccination. Thrombocytopenia, raised Platelet factor-4 antibodies, increased d-dimer, thrombi are common findings in VITT.[2 3] Possible etiological factors such as hyperhomocystenemia, vegetation, autoimmune, nephrotic syndrome, obesity, metabolic syndrome, stress, hypercoagulability, comorbidities were evaluated and excluded.[4] The presentation here is chest pain radiating to arms and vomiting for 5 days. He received vaccination 14 days prior to symptoms. The patient has no history of smoking, alcohol, and substance abuse. Electrocardiogram showing ST elevation Anterior wall Myocardial infarction [Figure 1a]. Echocardiography showed akinetic anterior and lateral wall, left ventricular apical thrombus, severe left ventricular dysfunction, regional wall motion abnormality present, dilated left atrium, left ventricle, left ventricular ejection fraction-35%, grade 1 diastolic dysfunction. Biochemical parameters reveal elevated cardiac markers troponin I 96000 pg/ml, antinuclear antibody-0.11, homocysteine 14.5micromol/l, HbA1C-5%. Patient was treated with anticoagulants, dual antiplatelets, statins, beta blockers, ACE inhibitors, antianginals and diuretics. Coronary angiography revealed occluded mid left anterior descending artery and proximal diagonal artery [Figure 1b]. Later reperfusion was achieved through percutaneous transluminal coronary angioplasty by placing three stents. Figure 1 (a) ECG suggestive of ST elevation in lead 1, aVL, V1-V6, pathological q-waves in V1-V6, poor R-wave progression, QRS > 0.12 s in V1, V2, tall R-wave in V1, wide S-wave in L1, V5, V6, suggestive of acute anterior wall and (b) coronary angiography It is the onus of responsibility for dispelling erroneous or exaggerated reports of COVID-19 vaccination dangers. Further research study could be vital. It is commonly acknowledged that vaccination benefits outweigh the risks and must be mindful to link negative outcomes to vaccine, anticipate patient queries and findings should not be overstated. Declaration of patient consent We certify that we have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed. Research quality and ethics statement We followed applicable EQUATOR Network (http://www. equator-network. org/) guidelines, notably the CARE guideline, during the conduct of this report. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

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          Myocardial infarction in young adults.

          Although myocardial infarction (MI) mainly occurs in patients older than 45, young men or women can suffer MI. Fortunately, its incidence is not common in patients younger than 45 years. However, the disease carries a significant morbidity, psychological effects, and financial constraints for the person and the family when it occurs at a young age. The causes of MI among patients aged less than 45 can be divided into four groups: (1) atheromatous coronary artery disease; (2) non-atheromatous coronary artery disease; (2) hyper-coagulable states; (4) MI related to substance misuse. There is a considerable overlap between all the groups. This article reviews the literature and highlights the practical issues involved in the management of young adults with MI.
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            Acute ST-segment elevation myocardial infarction secondary to vaccine-induced immune thrombosis with thrombocytopaenia (VITT)

            A 40-year-old man with no cardiac history presented with central chest pain 8 days after receiving the ChAdOx1 nCov-19 vaccine against COVID-19. Initial blood tests demonstrated a thrombocytopaenia (24×10 9  μg/L) and a raised d-dimer (>110 000 μg/L), and he was urgently transferred to our tertiary referral central for suspected vaccine-induced immune thrombocytopaenia and thrombosis (VITT). He developed dynamic ischaemic electrocardiographic changes with ST elevation, a troponin of 3185 ng/L, and regional wall motion abnormalities. An occlusion of his left anterior descending coronary artery was seen on CT coronary angiography. His platelet factor-4 (PF-4) antibody returned strongly positive. He was urgently treated for presumed VITT with intravenous immunoglobulin, methylprednisolone and plasma exchange, but remained thrombocytopaenic and was initiated on rituximab. Argatroban was used for anticoagulation for his myocardial infarction while he remained thrombocytopaenic. After 6 days, his platelet count improved, and his PF-4 antibody level, troponin and d-dimer fell. He was successfully discharged after 14 days.
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              Myocardial infarction in organophosphorus poisoning: Association or just chance?

              Dear Editor, Acute organophosphate poisoning (OPP) most often suicidal occurs very commonly in Vidarbha region of central India where farmers who are debt ridden use organophosphorus compounds as insecticides. Here, we report a case of a 40-years-old farmer admitted in the medicine intensive care unit with alleged history of pesticide consumption about 2 h prior at his home. The patient was hemodynamically stable with pulse rate of 60 per minute, regular and blood pressure of 110/76 mm of Hg. On evaluation the patient was drowsy with pinpoint pupil and bilateral crackles in the chest. Fasciculation were noticed over the thighs and arms. Management was done with atropine and pralidoxime along with mechanical ventilation. On investigations, his serum cholinesterase levels were 1048 IU/L (normal levels 4000-12000 IU/L). His hemogram, blood sugar, liver function, renal functions and lipid profile were within normal limits. On 3rd day, patient's ECG changes were noticed which were suggestive of inferolateral myocardial infarction [Figure 1]. The creatine kinase levels (CK-MB) done at that time was 154 IU/L (normal levels 15-35 IU/L). In view of ECG changes and raised enzymes levels, we made a diagnosis of myocardial infarction and was thrombolysed with injection Streptokinase 1.5 million units and managed conservatively afterwards. ECG became normal. His coronary angiography was planned but due to non-affordability this was deferred. Figure 1 ECG- ST elevation suggestive of inferolateral ischemia Cardiac complications are rare, serious and little known in OPP which include repolarization abnormalities like ST segment elevation and T wave inversion, prolongation of the QTc interval, rhythm abnormalities such as sinus tachycardia, sinus bradycardia, extra systoles, atrial fibrillation and ventricular tachycardia.[1] Acute myocardial infarction as a result of acute OPP though have been reported but are exceptionally rare.[2] The mechanism of toxicity of organophosphorus compounds is the irreversible binding of the compounds with the serum cholinesterase enzyme and converts this enzyme into a inactive protein complex with subsequent accumulation of increased amount of acetylcholine at the neuromuscular junction leading to persistent stimulation and subsequent disruption of the nerve transmission both in peripheral and central nervous system.[3] OPP are associated with the cardiac complications and most of them occur during the first few hours after exposure. However, in our case it was after three days. Possible mechanism of cardiac toxicity after OPP may include phase 1, a brief period of increased sympathetic tone; phase 2, a prolonged period of parasympathetic activity; and phase 3, in which Q-T prolongation followed by torsade de pointes ventricular tachycardia and then ventricular fibrillation occur.[4] This parasympathetic over activity plays a major role in the coronary artery spasm which is an important factor in pathogenesis of myocardial infarction. Also, pesticides release increased the amount of catecholamines and other vasoactive amines (histamines and neutral proteases) that penetrate the collagen matrix of plaque causing erosions and rupture which can lead to myocardial injury. These inflammatory mediators can cause coronary thrombosis, as well as spasm leading to myocardial infarction.[5] In our case this may be the pathogenesis as it happens after few days. But the exact pathophysiology behind organophosphorus compound leading to cardiac manifestations is not clearly understood. Apart from the direct toxic effect of the organophosphorus compounds on myocardium, over activity of cholinergic or nicotinic receptors, the increase in sympathetic and/or parasympathetic activity, hypoxemia, electrolyte abnormalities and acidosis have been hypothesized to play a role in the damage caused to myocardium along with the high dose of atropine. More studies are required to prove this hypothesis.
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                Author and article information

                Journal
                J Emerg Trauma Shock
                J Emerg Trauma Shock
                JETS
                Journal of Emergencies, Trauma, and Shock
                Wolters Kluwer - Medknow (India )
                0974-2700
                0974-519X
                Apr-Jun 2022
                27 June 2022
                : 15
                : 2
                : 112-113
                Affiliations
                [1]Department of General Medicine, Jawaharlal Nehru Medical College, Datta Meghe Institute of Medical Sciences, Wardha, Maharashtra, India
                Author notes
                Address for correspondence: Dr. V. V. S. S. Sagar, Department of General Medicine, Jawaharlal Nehru Medical College, Datta Meghe Institute of Medical Sciences, Wardha, Maharashtra, India. E-mail: vvsssagar@ 123456gmail.com
                Article
                JETS-15-112
                10.4103/jets.jets_20_22
                9336646
                35910317
                2190adef-5e46-43d0-b092-0a2e01d0f776
                Copyright: © 2022 Journal of Emergencies, Trauma, and Shock

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                History
                : 28 February 2022
                : 08 March 2022
                Categories
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                Emergency medicine & Trauma
                Emergency medicine & Trauma

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