- StatPearls [BOOK]
- BOOKStatPearls Publishing: Treasure Island (FL)
- According to European Society of Cardiology, American College of Cardiology Foundation, American Heart Association, and World Health Federation Expert consensus document on the third universal defini...
According to European Society of Cardiology, American College of Cardiology Foundation, American Heart Association, and World Health Federation Expert consensus document on the third universal definition of myocardial infarction, acute myocardial infarction can be diagnosed in several ways, one of which depends on cardiac enzymes. The pertinent definition is: "Detection of a rise and/or fall of cardiac biomarker values (preferably cardiac troponin) with at least one value above the 99 percentile upper reference limit and with at least one of the following: Symptoms of ischemia. New or presumed new significant ST segment-T wave changes or new left bundle branch block. Development of pathological Q waves on ECG. Imaging evidence of a new loss of viable myocardium or new regional wall motion abnormality. Identification of an intracoronary thrombus by angiography or autopsy.” The morbidity and mortality associated with acute myocardial infarction are well understood and discussed elsewhere. Given the known morbidity and mortality associated with acute myocardial infarction and the importance of early diagnosis and management, the above definition places a heavy burden on cardiac enzymes as their elevation alone along with symptoms of ischemia is enough to make the diagnosis of acute myocardial infarction. The ideal cardiac enzyme or biomarker needs to be highly specific, highly sensitive, and easily detectable as early as possible in the disease process. Several biomarkers have been developed in the past and will be discussed in this article. "Cardiac enzymes" is a broad term encompassing several intracellular myocyte components that can be found in serum and measured under certain circumstances such as myocardial ischemia, trauma, myocarditis. In the proper clinical setting, elevation in the level of enzymes present in serum is key in the diagnosis of myocardial infarction. While troponin is the most commonly used cardiac enzyme for diagnosis of myocardial infarction, others exist and may be helpful in some situations.
- Expression of tenascin C in cardiovascular lesions of Kawasaki disease. [Journal Article]
- CPCardiovasc Pathol 2018 Oct 24; 38:25-30
- CONCLUSIONS: The findings suggest a correlation between the degree of inflammation and TN-C expression in the cardiovascular lesions of acute-stage Kawasaki disease.
- Tyrosine Kinase Inhibitor-Induced Acute Myocarditis, Myositis, and Cardiogenic Shock. [Journal Article]
- MDMethodist Debakey Cardiovasc J 2018 Jul-Sep; 14(3):e5-e6
- TRIM21 Restricts Coxsackievirus B3 Replication, Cardiac and Pancreatic Injury via Interacting With MAVS and Positively Regulating IRF3-Mediated Type-I Interferon Production. [Journal Article]
- FIFront Immunol 2018; 9:2479
- Tripartite motif-containing 21 (TRIM21) is a regulator of tissue inflammation and pro-inflammatory cytokine production, and has been implicated in negative regulation of IRF3-dependent type I interfe...
Tripartite motif-containing 21 (TRIM21) is a regulator of tissue inflammation and pro-inflammatory cytokine production, and has been implicated in negative regulation of IRF3-dependent type I interferon signaling. However, the antiviral activity of TRIM21 varies among diverse viruses and its role on regulation of type I interferon remains inconsistent in different microbial infections. Here, we investigate the potential role for TRIM21 in controlling Coxsackievirus B3 (CVB3) replication and susceptible organ pathology. We found that CVB3 infection up-regulated the expression of TRIM21 in hearts of mice and cardiomyocytes at early phase of infection. Knock-down of TRIM21 resulted in increased viral replication, while overexpression led to increased phosphorylation and dimerization of IRF3, increased IFN-β transcription and reduced viral replication in vitro. We demonstrate that TRIM21 promotes the activation of IRF3 in CVB3-infected cells via interacting with MAVS and catalyzing the K27-linked polyubiquitination of MAVS, thereby enhancing type I interferon signaling. The RING domain of ubiquitin ligase activity and PRY-SPRY domain of TRIM21 are critical for its anti-viral effect. In vivo overexpression of TRIM21 significantly protected mice against viral myocarditis by suppressing CVB3 replication and reducing cardiac inflammatory cytokine production. While TRIM21 deficient mice exhibited a decreased IFN-β production, an increased cardiac and pancreatic CVB3 replication, and aggravated pancreatic injury as well as myocarditis during acute infection. Thus, our results demonstrate TRIM21 as a positive regulator of IFN-β signaling by targeting MAVS during CVB3 infection and suggest it as a potent host defense against CVB3 infection and viral-induced injury in hearts and pancreas.
- Cardiac involvement in critically ill patients with leptospirosis: A prospective study using myocardial deformation imaging. [Journal Article]
- EHEur Heart J Acute Cardiovasc Care 2018 Nov 08; :2048872618809319
- CONCLUSIONS: Cardiac involvement in leptospirosis appears to be similar to that of sepsis syndrome, with myocardial systolic dysfunction being common. As such, clinical vigilance pertaining to cardiac status is paramount in these high-risk patients.
- Evidence of aldosterone synthesis in human myocardium in acute myocarditis. [Journal Article]
- IJInt J Cardiol 2018 Oct 24
- CONCLUSIONS: In this proof-of-concept study, myocardium from patients with acute myocarditis demonstrates evidence and high prevalence of local aldosterone synthesis by immunohistochemistry that showed high accuracy, specificity, and sensitivity. Aldosterone warrants consideration as a specific target for therapy in patients with myocardial damage due to inflammation towards strategies that reduce downstream complications.
- Fasudil exerts a cardio-protective effect on mice with coxsackievirus B3-induced acute viral myocarditis. [Journal Article]
- CTCardiovasc Ther 2018 Oct 31; :e12477
- To investigate whether there exists a cardio-protective effect of Fasudil, a selective Rho kinase (ROCK) inhibitor, in an experimental murine model of acute viral myocarditis.
To investigate whether there exists a cardio-protective effect of Fasudil, a selective Rho kinase (ROCK) inhibitor, in an experimental murine model of acute viral myocarditis.
- Acute lymphocytic myocarditis. [Journal Article]
- JGJ Geriatr Cardiol 2018; 15(7):517-518
- Influenza Myocarditis Treated With Antithymocyte Globulin. [Journal Article]
- PedPediatrics 2018; 142(5)
- Influenza is a cause of significant morbidity and mortality worldwide. Myocarditis is a rare complication of the virus and can vary widely in severity. The published cases of influenza B myocarditis ...
Influenza is a cause of significant morbidity and mortality worldwide. Myocarditis is a rare complication of the virus and can vary widely in severity. The published cases of influenza B myocarditis in children tend to be severe with a high mortality rate. Current standard treatment of viral myocarditis is supportive care, although immunomodulatory therapies, such as steroids and intravenous immunoglobulin, are often used. T cells have been implicated in causing significant myocyte damage in myocarditis by leading to the downstream production of antibodies against viral and myocyte antigens; this has created a theoretical basis for the use of antithymocyte globulin to target T cells in these patients. We present a case of acute fulminant influenza B myocarditis in a pediatric patient that required mechanical circulatory support and improved only after treatment with antithymocyte globulin.
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- Innate Immunity Evasion by Enteroviruses Linked to Epidemic Hand-Foot-Mouth Disease. [Review]
- FMFront Microbiol 2018; 9:2422
- Enterovirus (EV) infections are a major threat to global public health, and are responsible for mild respiratory illness, hand, foot, and mouth disease (HFMD), acute hemorrhagic conjunctivitis, asept...
Enterovirus (EV) infections are a major threat to global public health, and are responsible for mild respiratory illness, hand, foot, and mouth disease (HFMD), acute hemorrhagic conjunctivitis, aseptic meningitis, myocarditis, severe neonatal sepsis-like disease, and acute flaccid paralysis epidemic. Among them, HFMD is a common pediatric infectious disease caused by EVs of the family Picornaviridae including EV-A71, coxsackieviruses (CV)-A2, CV-A6, CV-A10, and CV-A16. Due to lack of vaccines and specific antiviral therapeutics, millions of children still suffer from HFMD. Innate immune system detects foreign invaders by means of a relatively limited number of sensors, such as pattern recognition receptors (PRRs) [e.g., retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), Toll-like receptors (TLRs), and NOD-like receptors (NLRs)] and even some secreted functional proteins. However, a range of research, highlighted in this review, suggest that EV-associated with HFMD have evolved different strategies to avoid detection by innate immunity via different proteases (e.g., 2A, 3C, 2C, and 3D). Ongoing efforts to better understand virus-host interactions that control innate immunity and then distill how that influences HFMD development promises to have real-world significance. In this review, we address this complex topic in nine sections including multiple proteins associated with PRR and type I interferon (IFN) signaling. Recognizing how EVs linked to HFMD evade host innate immune system, we also describe the interactions between them and, finally, suggest future directions to better inform drug development and public health.