|
|
| (160 intermediate revisions by 10 users not shown) |
| Line 1: |
Line 1: |
| __NOTOC__
| |
|
| |
|
| {{CMG}} {{AE}} {{mitra}}{{MC}}
| |
|
| |
| ==Overview==
| |
|
| |
| ==Complications==
| |
|
| |
| ===Acute Coronary Syndromes===
| |
|
| |
| ===Heart Failure===
| |
|
| |
| ===Cardiogenic Shock===
| |
|
| |
| ===Myocarditis===
| |
|
| |
| ===Pericarditis===
| |
|
| |
| ===Arrhythmias ===
| |
|
| |
| ==== Pathophysiology: ====
| |
| Respiratory disease is the chief target of Coronavirus disease 2019 (COVID-19). One-third of patients with severe disease also reported other symptoms including [[Cardiac arrhythmia|arrhythmia]]. According to a study done in Wuhan, China, 16.7% of hospitalized and 44.4% of ICU patients with COVID-19 had arrhythmias.<ref name="WangHu2020">{{cite journal|last1=Wang|first1=Dawei|last2=Hu|first2=Bo|last3=Hu|first3=Chang|last4=Zhu|first4=Fangfang|last5=Liu|first5=Xing|last6=Zhang|first6=Jing|last7=Wang|first7=Binbin|last8=Xiang|first8=Hui|last9=Cheng|first9=Zhenshun|last10=Xiong|first10=Yong|last11=Zhao|first11=Yan|last12=Li|first12=Yirong|last13=Wang|first13=Xinghuan|last14=Peng|first14=Zhiyong|title=Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus–Infected Pneumonia in Wuhan, China|journal=JAMA|volume=323|issue=11|year=2020|pages=1061|issn=0098-7484|doi=10.1001/jama.2020.1585}}</ref> Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) utilizes S-spike to bind to angiotensin-converting enzyme 2 (ACE2) receptors to enter the cells. Type 1 and type 2 [[pneumocytes]] exhibit ACE 2 receptors in the lung. Studies report that coronary [[endothelial cells]] in the heart and intrarenal endothelial cells and renal tubular epithelial cells in the kidney exhibit ACE2. ACE2 is an inverse regulator of the [[renin-angiotensin system]].<ref name="XuShi2020">{{cite journal|last1=Xu|first1=Zhe|last2=Shi|first2=Lei|last3=Wang|first3=Yijin|last4=Zhang|first4=Jiyuan|last5=Huang|first5=Lei|last6=Zhang|first6=Chao|last7=Liu|first7=Shuhong|last8=Zhao|first8=Peng|last9=Liu|first9=Hongxia|last10=Zhu|first10=Li|last11=Tai|first11=Yanhong|last12=Bai|first12=Changqing|last13=Gao|first13=Tingting|last14=Song|first14=Jinwen|last15=Xia|first15=Peng|last16=Dong|first16=Jinghui|last17=Zhao|first17=Jingmin|last18=Wang|first18=Fu-Sheng|title=Pathological findings of COVID-19 associated with acute respiratory distress syndrome|journal=The Lancet Respiratory Medicine|volume=8|issue=4|year=2020|pages=420–422|issn=22132600|doi=10.1016/S2213-2600(20)30076-X}}</ref> The interaction between SARS-CoV2 and ACE2 can bring about changes in ACE2 pathways prompting intense injury to the lung, heart, and [[Endothelium|endothelial cells]]. [[Hypoxemia|Hypoxia]] and [[Electrolyte disturbance|electrolyte abnormalities]] that are common in the acute phase of severe [[COVID-19]] can potentiate [[Cardiac arrhythmia|cardiac arrhythmias]]. Binding of SARS-CoV-2 to ACE2 receptors can result into [[hypokalemia]] which causes various types of [[Cardiac arrhythmia|arrhythmia]]. Elevated levels of [[Cytokine|cytokines]] as a result of the [[Systemic inflammatory response syndrome|systemic inflammatory response]] of the severe [[COVID-19|Coronavirus disease 2019]] (COVID-19) can cause injury to multiple organs, including [[Cardiac muscle|cardiac myocytes]].<ref name="ChenPrendergast2020">{{cite journal|last1=Chen|first1=Mao|last2=Prendergast|first2=Bernard|last3=Redwood|first3=Simon|last4=Xiong|first4=Tian-Yuan|title=Coronaviruses and the cardiovascular system: acute and long-term implications|journal=European Heart Journal|volume=41|issue=19|year=2020|pages=1798–1800|issn=0195-668X|doi=10.1093/eurheartj/ehaa231}}</ref> According to the data based on studies on previous [[Severe acute respiratory syndrome]] ([[Severe acute respiratory syndrome|SARS]]) and the [[Middle East respiratory syndrome coronavirus infection|Middle East respiratory syndrome]] ([[Middle East respiratory syndrome coronavirus infection|MERS]]) epidemic and the ongoing [[COVID-19]] outbreak, multiple mechanisms have been suggested for cardiac damage.<ref name="ClerkinFried2020">{{cite journal|last1=Clerkin|first1=Kevin J.|last2=Fried|first2=Justin A.|last3=Raikhelkar|first3=Jayant|last4=Sayer|first4=Gabriel|last5=Griffin|first5=Jan M.|last6=Masoumi|first6=Amirali|last7=Jain|first7=Sneha S.|last8=Burkhoff|first8=Daniel|last9=Kumaraiah|first9=Deepa|last10=Rabbani|first10=LeRoy|last11=Schwartz|first11=Allan|last12=Uriel|first12=Nir|title=COVID-19 and Cardiovascular Disease|journal=Circulation|volume=141|issue=20|year=2020|pages=1648–1655|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.120.046941}}</ref>
| |
|
| |
| ==== Signs and Symptoms: ====
| |
| Arrhythmia or conduction system disease is the nonspecific clinical presentation of COVID-19. Patients may be tachycardic (with or without palpitations) in the setting of other COVID-19-related symptoms (eg, fever, shortness of breath, pain, etc).
| |
|
| |
| *'''Palpitations:''' According to a study done in Hubei province,[[Palpitation|palpitations]] were reported as a presenting symptom by 7.3 percent patients.
| |
| *'''Prolong QT Interval:''' According to a multicenter study done in New York that involved 4250 COVID-19 patients, 260 patients (6.1 percent) had [[QT interval|corrected QT interval]] (QTc) >500 milliseconds at the time of admittance. However, in another study that involved 84 patients who got [[hydroxychloroquine]] and [[azithromycin]], the baseline QTc interval was 435 milliseconds before receiving these medications.
| |
| *'''Atrial Arrhythmia:''' According to a study, among 393 patients with COVID-19, [[Cardiac arrhythmia|atrial arrhythmias]] were more common among patients requiring invasive [[mechanical ventilation]] than noninvasive [[mechanical ventilation]] (17.7 versus 1.9 percent)
| |
| *'''Ventricular Arrhythmia:''' According to a study done in Wuhan, China. among 187 hospitalized patients with [[COVID-19]], 11 patients (5.9 percent) developed [[Ventricular arrhythmias|ventricular tachyarrhythmias]].
| |
|
| |
| ==References ==
| |
| <references />
| |