Myocarditis: The Dallas criteria

Myocardial infarction with nonobstructive coronary artery disease (MINOCA) is defined as acute myocardial infarction (AMI) with angiographically nonobstructive coronary artery disease. MINOCA represents 6% of all AMI cases and is associated with increased mortality and morbidity. However, the wide array of pathophysiological factors and causes associated with MINOCA presents a diagnostic conundrum. Therefore, we conducted a contemporary systematic review of the pathophysiology of MINOCA.

A comprehensive systematic review of MINOCA was carried out through the utilization of the PubMed database. All systematic reviews, meta-analyses, randomized controlled trials, and cohort studies available in English or French that reported on the pathophysiology of MINOCA published after January 1, 2013 were retained.

Of the 600 identified records, 80 records were retained. Central to the concept of MINOCA is the definition of AMI, characterized by the presence of myocardial damage reflected by elevated cardiac biomarkers in the setting of acute myocardial ischemia. As a result, a structured approach should be adopted to thoroughly assess and address clinically overlooked obstructive coronary artery disease, and cardiac and extracardiac mechanisms of myocyte injury. Once these options have been ruled out, a diagnosis of MINOCA can be established, and the appropriate multimodal assessment can be conducted to determine its specific underlying cause (plaque disruption, epicardial coronary vasospasm, coronary microvascular dysfunction, and coronary embolism and/or spontaneous coronary dissection or supply-demand mismatch).

Integrating a suitable definition of AMI and understanding the pathophysiological mechanisms of MINOCA are crucial to ensure an effective multimodal diagnostic evaluation and the provision of adequate tailored therapies.

L’infarctus du myocarde sans obstruction des artères coronaires (MINOCA) est défini comme un infarctus aigu du myocarde (IAM) en présence d’une coronaropathie non obstructive confirmée par angiographie. Le MINOCA représente 6 % de tous les cas d’IAM et est associé à une hausse des taux de mortalité et de morbidité. Cependant, le large éventail de facteurs physiopathologiques et de causes associés au MINOCA représente une énigme diagnostique. C’est pourquoi nous avons réalisé une analyse systématique des publications contemporaines sur la physiopathologie du MINOCA.

Une analyse exhaustive des publications sur le MINOCA a été menée au moyen de la base de données PubMed. L’ensemble des analyses systématiques, des méta-analyses, des essais contrôlés randomisés et des études de cohorte publiés en anglais ou en français après le 1^er janvier 2013 qui faisaient état de la physiopathologie du MINOCA ont été retenus.

Parmi les 600 dossiers relevés, 80 ont été retenus. La définition de l’IAM était centrale au concept de MINOCA et était caractérisée par la présence d’une lésion myocardique attestée par des taux élevés de biomarqueurs cardiaques en contexte d’ischémie myocardique aiguë. Par conséquent, une approche structurée devrait être adoptée pour évaluer pleinement et traiter les coronaropathies obstructives qui passent inaperçues en clinique ainsi que les mécanismes cardiaques et extracardiaques des lésions aux myocytes. Une fois ces options exclues, un diagnostic de MINOCA peut être établi et l’évaluation multimodale appropriée peut être menée pour déterminer la cause sous-jacente précise (rupture de plaque, vasospasme d’une artère coronaire épicardique, dysfonction microvasculaire coronarienne et embolie coronarienne et/ou dissection spontanée d’une artère coronaire ou déséquilibre entre apports et besoins).

Il est crucial d’intégrer une définition convenable de l’IAM et de comprendre les mécanismes physiopathologiques du MINOCA pour assurer une évaluation diagnostique multimodale efficace et une prestation de traitements adaptés et adéquats.

Myocarditis, and autoimmune heart disease, are classical examples of the interaction of infectious agents, particularly viruses, and the immune system in producing an autoimmune phenomena or disorder. Numerous components of the immune system are involved in the pathogenesis of autoimmune heart diseases, all are illustrated through this chapter. In addition, various infectious agents, including enteroviruses and SARS-CoV-2 among others, are discussed.

Iron overload cardiomyopathy (IOC) is a condition in which iron deposition in the heart causes cardiac dysfunction. We described a 21-year-old woman who presented with acute chest pain, dyspnea, and fever. The patient had a history of transfusion-dependent thalassemia (TDT) and secondary hemochromatosis with the latest serum ferritin ranging from 8000 to 15,000. Physical examinations revealed signs of anemia and heart failure. Electrocardiography showed diffuse ST-segment elevation with reciprocal ST-segment depression in aVR and complete atrioventricular block. Cardiac markers were markedly elevated. Echocardiography demonstrated the dilated size, impaired systolic function, global wall hypokinesia, restrictive filling pattern of the left ventricle, and a small amount of pericardial effusion. Coronary angiography showed normal coronary arteries. A cardiac magnetic resonance imaging showed multifocal early and late gadolinium enhancement involving mid-wall and subepicardial areas of biventricular myocardium suggestive of diffuse myocardial injury from an inflammatory process. She was provisionally diagnosed with acute myopericarditis. Ibuprofen and loop diuretic were prescribed; however, cardiogenic shock occurred. Thus, an endomyocardial biopsy was done and revealed diffuse myocardial hemosiderin deposition without evidence of inflammatory cell infiltration. Severe IOC mimicking acute myopericarditis was considered based on an endomyocardial biopsy result. An intravenous iron chelating agent was immediately administered. Unfortunately, cardiogenic shock was refractory resulting in death. This case demonstrated a rare manifestation of IOC, which can masquerade as acute myopericarditis, and emphasized that IOC should be differentially diagnosed, particularly in patients with TDT and hemochromatosis.

Myocarditis is frequently caused by viral infections, but animal models that closely resemble human disease suggest that virus-triggered autoimmune disease is the most likely cause of myocarditis. Myocarditis is a rare condition that occurs primarily in men under age 50. The incidence of myocarditis rose at least 15x during the coronavirus disease 2019 (COVID-19) pandemic from 1–10 to 150–400 cases/100 000 individuals, with most cases occurring in men under age 50. COVID-19 vaccination was also associated with rare cases of myocarditis primarily in young men under 50 years of age with an incidence as high as 50 cases/100 000 individuals reported for some mRNA vaccines. Sex differences in the immune response to COVID-19 are virtually identical to the mechanisms known to drive sex differences in myocarditis pre-COVID based on clinical studies and animal models. The many similarities between COVID-19 vaccine-associated myocarditis to COVID-19 myocarditis and non-COVID myocarditis suggest common immune mechanisms drive disease.

To evaluate the role of quantitative cardiac magnetic resonance imaging (CMRI) parameters in myocarditis, including acute and chronic myocarditis (AM and CM), for children and adolescents.

PRISMA principles were followed. PubMed, EMBASE, Web of Science, Cochrane Library, and grey literature were searched. The Newcastle-Ottawa Scale (NOS) and the Agency for Healthcare Research and Quality (AHRQ) checklist were utilised for quality assessment. Quantitative CMRI parameters were extracted and a meta-analysis was performed in comparison with healthy controls. The overall effect size was measured as the weighted mean difference (WMD).

Ten quantitative CMRI parameters of seven studies were analysed. Compared with the control group, the myocarditis group reported longer native T1 relaxation time (WMD=54.00, 95% confidence interval [CI]: 33.21,74.79, p<0.001), longer T2 relaxation time (WMD=2.13, 95% CI: 0.98, 3.28, p<0.001), increased extracellular volume (ECV; WMD=3.13, 95% CI: 1.34,4.91, p=0.001), elevated early gadolinium enhancement (EGE) ratio (WMD=1.47, 95% CI: 0.65,2.28, p<0.001), and increased T2-weighted ratio (WMD=0.43, 95% CI: 0.21,0.64, p<0.001). The AM group had longer native T1 relaxation times (WMD=72.02, 95% CI: 32.78,111.27, p<0.001), increased T2-weighted ratios (WMD=0.52, 95% CI: 0.21,0.84 p=0.001), and impaired left ventricular ejection fractions (LVEF; WMD=–5.84, 95% CI: -9.69, -1.99, p=0.003). Impaired LVEF (WMD=–2.24, 95% CI: -3.32, -1.17, p<0.001) was observed in the CM group.

Statistical differences can be observed in some CMRI parameters between patients with myocarditis and healthy controls; however, apart from native T1 mapping, there were no large differences in other parameters between two groups, which may reveal the limited benefit of CMRI in assessing myocarditis in children and adolescents.

Anteroseptal location of late gadolinium enhancement (LGE) in patients with acute myocarditis (AM) detected by cardiovascular magnetic resonance may indicate an independent marker of unfavorable outcomes according to recent data. We aimed to evaluate the clinical characteristics, management, and inhospital outcomes in patients with AM with positive LGE based on its presence in the anteroseptal location. We analyzed data from 262 consecutive patients hospitalized with a diagnosis of AM with positive LGE within 5 days of hospitalization (n = 425). Patients were divided into 2 groups: those with anteroseptal LGE (n = 25, 9.5%) and those with non–anteroseptal LGE (n = 237, 90.5%). Except for age that was higher in patients with anteroseptal LGE, the demographic and clinical characteristics did not differ significantly between both groups including past medical history, clinical presentation, electrocardiogram parameters, and lab values. Moreover, patients with anteroseptal LGE were more likely to present with reduced left ventricular ejection fraction and to receive congestive heart failure treatments. Although univariate analysis showed that patients with anteroseptal LGE were more likely to have inhospital major adverse cardiac events (28% vs 9%, p = 0.003), there was no difference inhospital outcomes on multivariable analysis between both groups (hazard ratio, 1.17 [95% confidence interval, 0.32 to 4.22], p = 0.81). A higher left ventricular ejection fraction in either echocardiography or cardiovascular magnetic resonance corresponded to better inhospital outcomes regardless of the presence or absence of anteroseptal LGE. In conclusion, the presence of anteroseptal LGE did not confer additional prognostic value for inhospital outcomes.