2021
DOI: 10.1007/s11886-021-01551-x
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SARS-CoV-2 Myocarditis: Insights Into Incidence, Prognosis, and Therapeutic Implications

Abstract: Purpose of Review In coronavirus disease 2019 (COVID-19), myocardial injury occurs frequently in severe or critically ill hospitalized patients, yet myocarditis is much less common. In this context, revisiting the definition of myocarditis is appropriate with a specific focus on diagnostic and management considerations in patients infected with SARS-CoV-2. Recent Findings Pathologic cardiac specimens from patients with COVID-19 suggest a mixed inflammatory response invo… Show more

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Cited by 20 publications
(15 citation statements)
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“…Around 10%–35% of hospitalized COVID-19 patients have acute cardiac injury defined as an elevated high-sensitivity troponin I or troponin T above the 99 th percentile upper reference range. [ 13 ] Myocarditis and the associated systemic inflammation can be delayed up to a month after initial SARS-CoV-2 infection. [ 14 ] However, pathologic myocarditis is rare.…”
Section: Discussionmentioning
confidence: 99%
“…Around 10%–35% of hospitalized COVID-19 patients have acute cardiac injury defined as an elevated high-sensitivity troponin I or troponin T above the 99 th percentile upper reference range. [ 13 ] Myocarditis and the associated systemic inflammation can be delayed up to a month after initial SARS-CoV-2 infection. [ 14 ] However, pathologic myocarditis is rare.…”
Section: Discussionmentioning
confidence: 99%
“…However, as COVID-19 is a polymorphic disease characterised by great variability in clinical presentation, non-respiratory complications may sometimes occur [ 19 , 20 , 21 ]. In humans, cardiac involvement during SARS-CoV-2 infection has been documented by many authors and represents a source of great concern [ 22 , 23 , 24 ]. The mechanisms that lead to cardiac involvement in the setting of COVID-19 include direct injury caused by direct viral entry to cardiomyocytes, which is possible by direct viral binding to the angiotensin-converting enzyme 2 present on these cells, hypoxia-induced myocardial ischaemia, and exaggerated inflammatory response characterised by endothelial overactivation and microvascular thrombi [ 22 , 23 , 24 ].…”
Section: Discussionmentioning
confidence: 99%
“…In humans, cardiac involvement during SARS-CoV-2 infection has been documented by many authors and represents a source of great concern [ 22 , 23 , 24 ]. The mechanisms that lead to cardiac involvement in the setting of COVID-19 include direct injury caused by direct viral entry to cardiomyocytes, which is possible by direct viral binding to the angiotensin-converting enzyme 2 present on these cells, hypoxia-induced myocardial ischaemia, and exaggerated inflammatory response characterised by endothelial overactivation and microvascular thrombi [ 22 , 23 , 24 ]. Histologically, this may trigger non-myocarditis inflammatory infiltrates, acute myocardial infarction, and, rarely, myocarditis [ 47 , 48 ], which represent the anatomical prerequisites for the development of clinical complications, such as LV systolic dysfunction, congestive heart failure and arrhythmias [ 22 , 23 , 24 ].…”
Section: Discussionmentioning
confidence: 99%
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“…With the increase in clinical cases [13,14] and reported deaths [15] of SARS-CoV-2 associated respiratory and cardiac complications, people increased interest in COVID-19 Myocarditis. However, in clinical practice, the diagnosis of COVID-19 Myocarditis is not well established, and the biological pathways associated with the two are not fully understood, which has caused widespread concern in the medical community [16,17].…”
Section: Introductionmentioning
confidence: 99%