Coronavirus disease 2019 (COVID-19) caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection has become a pandemic. Patient with cardiovascular comorbidity has a higher risk of suffering more severe manifestation of COVID-19 associated with a higher mortality. Although dominated by respiratory clinical manifestation, COVID-19 may also cause severe cardiovascular disorders. Angiotensin converting enzyme 2 (ACE2) acts as a receptor of SARS-CoV-2. Patients of COVID-19 with cardiovascular comorbidities may experience more severe clinical manifestations, presumably due to higher ACE2 expression in this population. Cardiovascular complications in COVID-19 may include myocardial injury, myocarditis, acute myocardial infarction, acute heart failure, thromboembolism, and arrhythmias. Therefore, optimization of conservative medical therapy needs to be prioritized in patients with cardiovascular comorbidities. Emergency intervention can be considered in certain cases with hemodynamic instability.Keywords: cardiovascular system, COVID-19, SARS-CoV-2, ACE2 Abstrak: Coronavirus disease 2019 (COVID-19) telah merupakan pandemi yang disebabkan oleh infeksi Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2). Pasien dengan komorbid kardiovaskular berisiko lebih tinggi untuk mengalami manifestasi yang lebih berat jika terinfeksi COVID-19 dan berhubungan dengan mortalitas yang lebih tinggi. Meskipun didominasi oleh manifestasi klinis respiratorik, COVID-19 juga dapat menyebabkan gangguan kardiovaskular yang berat. Angiotensin converting enzyme 2 (ACE2) berperan sebagai reseptor SARS-CoV-2. Diduga pasien dengan penyakit kardiovaskular dapat bermanifestasi klinis lebih berat karena ekspresi ACE2 yang lebih tinggi pada populasi ini. Komplikasi kardiovaskular pada COVID-19 dapat meliputi jejas miokardium, miokarditis, infark miokard akut, gagal jantung akut, tromboemboli, dan aritmia. Pada pasien dengan komorbid kardiovaskular, optimalisasi terapi medis konservatif perlu diprioritaskan. Tindakan intervensi darurat dapat dipertimbangkan pada kasus tertentu dengan instabilitas hemodinamik.Kata kunci: sistem kardiovaskular, COVID-19, SARS-CoV-2, ACE2
Background: Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). COVID-19 has spread globally and become a new pandemic. Although the clinical manifestation of COVID-19 mainly affected the respiratory system, coagulopathy often occurs in the severe cases and is associated with increased mortality. This literature review aims to provide a review of coagulopathy in COVID-19.Methods: This literature review involved 52 relevant literature about coagulopathy and COVID-19. Different data sources or manual literature search methods used to find articles related to the topic of literature.Results: COVID-19 can trigger cytokine storms and systemic hyperinflammation which cause increased activation of coagulation and resulting in hypercoagulability. Hypercoagulability state in COVID-19 increases the risk of thrombosis and thromboembolism, particularly venous thromboembolism. Prophylactic anticoagulants can prevent thromboembolic events and improve the prognosis of COVID-19 patients with coagulopathy.Conclusion: The hypercoagulation state in COVID-19 can increase the risk of complications from thrombosis and thromboembolism, especially venous thromboembolism. Increased D-dimers are a marker of coagulopathy that is often found in patients with severe COVID-19 and is associated with disease severity. Latar Belakang: Coronavirus disease 2019 (COVID-19) merupakan penyakit infeksi akibat severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). COVID-19 telah menyebar secara global dan menjadi pandemi baru. Walaupun manifestasi klinis COVID-19 terutama mengenai sistem respirasi, koagulopati seringkali terjadi pada kasus berat dan berhubungan dengan peningkatan mortalitas. Tinjauan pustaka ini bertujuan untuk memberikan ulasan mengenai koagulopati pada COVID-19.Metode: Tinjauan pustaka ini melibatkan 52 literatur yang relevan tentang koagulopati dan COVID-19. Sumber data yang berbeda atau metode pencarian literatur manual digunakan untuk mencari artikel yang berkaitan dengan topik literatur.Hasil: COVID-19 dapat memicu terjadinya badai sitokin dan hiperinflamasi sistemik yang menyebabkan terjadinya peningkatan aktivasi koagulasi dan mengakibatkan hiperkoagulasi. Keadaan hiperkoagulasi pada COVID-19 meningkatkan risiko terjadinya trombosis dan tromboemboli, terutama tromboemboli vena. Antikoagulan profilaksis dapat mencegah kejadian tromboemboli dan meningkatkan prognosis pada pasien COVID-19 dengan koagulopati.Kesimpulan: Keadaan hiperkoagulasi pada COVID-19 dapat meningkatkan risiko terjadinya komplikasi trombosis dan tromboemboli, terutama tromboemboli vena. Peningkatan D-dimer merupakan penanda koagulopati yang sering ditemukan pada pasien COVID-19 berat dan berhubungan dengan keparahan penyakit.
Congenital heart disease is a structural defect due to the malformation of the heart, aorta, and or great blood vessels. It is the most frequent congenital malformation in newborn babies. Tetralogy of Fallot is one of the congenital heart diseases (CHD) with central cyanosis, and covers 5-10% of all CHD. We reported a boy of one year old with Tetralogy of Fallot and pulmonal atresia (ToF-PA), associated with bronchopneumonia. The diagnosis was based on anamnesis, physical examination, and other supporting examinations. The chest X-ray showed a normal sized heart (CTR 57%) with coer-en-sabot shape, and right and left parahilar infiltration, which resulted in bronchopneumonia and ToF. The electrocardiography showed a right deviation of axis and a hypertrophy of the right ventricle; the echocardiography showed a right ventricle hypertrophy, an over-riding aorta, a large malalignment of the ventricular septal defect, no visualization of pulmonar artery, and no visualization of patent ductus arteriosus (PDA). Conclusion: Based on all the tests performed, the diagnosis of this patient was Tetralogy of Fallot and pulmonal atresia (ToF-PA), associated with bronchopneumonia. The prognosis related to bronchopneumonia in this case was good due to the use of antibiotics. Keywords: tetralogy of Fallot, pulmona atresia, bronchopneumonia. Abstrak: Penyakit jantung bawaan (PJB) ialah kelainan struktural akibat malformasi jantung, aorta dan atau pembuluh darah besar, dan merupakan kelainan kongenital tersering pada bayi baru lahir. Tetralogi Fallot merupakan salah satu PJB dengan sianosis sentral, dan mencakup 5-10% dari seluruh PJB. Kami melaporkan kasus seorang anak laki-laki berusia satu tahun dengan Tetralogi Fallot dan atresia pulmonal (ToF-PA) disertai bronkopneumonia. Diagnosis ditegakkan melalui anamnesis, pemeriksaan fisik, dan pemeriksaan penunjang. Hasil ekspertisi foto toraks AP memperlihatkan ukuran jantung normal (CTR 57%) berbentuk coer-en-sabot, dan pada paru-paru terlihat infiltrat parahilar kanan dan kiri serta corakan vaskular paru berkurang yang menunjukkan suspek bronkopneumonia dan ToF. Elektrokardiografi memperlihatkan deviasi aksis ke kanan dan hipertrofi ventrikel kanan, dan pada ekokardiografi tampak right ventricle hypertrophy, overriding aorta, VSD malalignment besar, tidak tampak visualisasi arteri pulmonal, dan tidak tampak patent ductus arteriosus (PDA) dengan hasil Tetralogi Fallot dan atresia pulmonal. Simpulan: Berdasarkan hasil pemeriksaan yang dilakukan, diagnosis pasien ini ialah Tetralogi Fallot dan atresia pulmonal (ToF-PA) disertai bronkopneumonia. Prognosis bronkopenumonia pada kasus ini baik yang dapat diatasi dengan antibiotika.Kata kunci: tetralogi Fallot, atresia pulmonal, bronkopneumonia.
Critical congenital heart disease (CHD) is a type of CHD that requires early intervention in the first year of life to survive. Morbidity and mortality increases significantly if newborns with critical CHD experience delay in the initial diagnosis and management. The infants may develop cyanosis, systemic hypoperfusion, or respiratory distress as the main manifestations of critical CHD. Pulse oximetry screening for early detection of critical CHD must be performed in newborns after 24 hours of age or before discharge from hospital. Generally, infants with critical CHD require patency of the ductus arteriosus with infusion of prostaglandin to maintain pulmonary or systemic blood flow. After initial management, the infants must be immediately referred to tertiary care center for definitive intervention. Keywords: congenital heart disease, duct-dependent circulation, ductus arteriosus, prostaglandin
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