Myocarditis Publications (17716)

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Myocarditis Publications

2016Jan
Case Rep Radiol
Case Rep Radiol 2016 20;2016:6374584. Epub 2016 Dec 20.
Department of Nuclear Medicine, Graduate School of Medicine, Osaka City University, 1-4-3 Asahi-machi, Abeno-ku, Osaka 545-8585, Japan.

Gallium-67 scintigraphy is useful for detecting active inflammation. We show a 66-year-old female patient with atrial fibrillation and diffuse thickening of the left atrial wall due to acute myocarditis, who presented diffuse abnormal accumulation of gallium-67 in the left atrium on single photon emission computed tomography/computed tomography (SPECT/CT) fusion images. In the second gallium-67 scan 2 months after the first scintigraphy, the abnormal accumulation in the heart was no longer visible. Read More

Gallium-67 SPECT/CT images helped understanding the disease condition that temporary inflammation in the left atrium caused atrial fibrillation.

2017Jan
J Cardiovasc Med (Hagerstown)
J Cardiovasc Med (Hagerstown) 2017 Jan 13. Epub 2017 Jan 13.
Bristol Heart Institute, University of Bristol, Bristol, UK.
2017Jan
MAGMA
MAGMA 2017 Jan 16. Epub 2017 Jan 16.
Department of Cardiology, Friedrich-Alexander-Universität Erlangen-Nürnberg, 91054, Erlangen, Germany.
2017Jan
Intern. Med.
Intern Med 2017 15;56(2):157-161. Epub 2017 Jan 15.
Department of Cardiovascular Medicine, Saitama Medical Center, Jichi Medical University, Japan.

Eosinophilic myocarditis is a rare form of myocardial inflammation that is characterized by the infiltration of eosinophilic cells into the myocardium. The clinical symptoms of eosinophilic myocarditis are similar to those of acute coronary syndrome, and eosinophilic myocarditis sometimes occurs in combination with bronchial asthma. We herein present a case of eosinophilic myocarditis in which additional time was required to make a definitive diagnosis because the patient received steroid therapy. Read More

The diagnosis of eosinophilic myocarditis is challenging, especially when a patient has other inflammatory diseases, such as bronchial asthma. We should pay attention to the possibility that steroid therapy may mask the presentation of eosinophilic myocarditis.

2017Jan
Int. J. Cardiol.
Int J Cardiol 2017 Jan 7. Epub 2017 Jan 7.
Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands; ICaR-VU, Institute for Cardiovascular Research, VU University Medical Center, The Netherlands.

Although lymphocytic myocarditis (LM) clinically can mimic myocardial infarction (MI), they are regarded as distinct clinical entities. However, we observed a high prevalence (32%) of recent MI in patients diagnosed post-mortem with LM. To investigate if LM changes coronary atherosclerotic plaque, we analyzed in autopsied hearts the inflammatory infiltrate and stability in coronary atherosclerotic lesions in patients with LM and/or MI. Read More


The three main coronary arteries were isolated at autopsy of patients with LM, with MI of 3-6h old, with LM and MI of 3-6h old (LM+MI) and controls. In tissue sections of atherosclerotic plaque-containing coronary segments inflammatory infiltration, plaque stability, intraplaque hemorrhage and thrombi were determined via (immuno)histological criteria.
In tissue sections of those coronary segments the inflammatory infiltrate was found to be significantly increased in patients with LM, LM+MI and MI compared with controls. This inflammatory infiltrate consisted predominantly of macrophages and neutrophils in patients with only LM or MI, of lymphocytes in LM+MI and MI patients and of mast cells in LM+MI patients. Moreover, in LM+MI and MI patients this coincided with an increase of unstable plaques and thrombi. Finally, LM and especially MI and LM+MI patients showed significantly increased intraplaque hemorrhage.
This study demonstrates prevalent co-occurrence of LM with a very recent MI at autopsy. Moreover, LM was associated with remodeling and inflammation of atherosclerotic plaques indicative of plaque destabilization pointing to coronary spasm, suggesting that preexistent LM, or its causes, may facilitate the development of MI.

2017Jan
Eur. J. Clin. Microbiol. Infect. Dis.
Eur J Clin Microbiol Infect Dis 2017 Jan 12. Epub 2017 Jan 12.
Department of Infectious Diseases, C5P-40, Leiden University Medical Center, Albinusdreef 2, 2333 ZA, Leiden, The Netherlands.

While postnatal toxoplasmosis in immune-competent patients is generally considered a self-limiting and mild illness, it has been associated with a variety of more severe clinical manifestations. The causal relation with some manifestations, e.g. Read More

myocarditis, has been microbiologically proven, but this is not unequivocally so for other reported associations, such as with epilepsy. We aimed to systematically assess causality between postnatal toxoplasmosis and epilepsy in immune-competent patients. A literature search was performed. The Bradford Hill criteria for causality were used to score selected articles for each component of causality. Using an arbitrary but defined scoring system, the maximal score was 15 points (13 for case reports). Of 704 articles, five case reports or series and five case-control studies were selected. The strongest evidence for a causal relation was provided by two case reports and one case-control study, with a maximal causality score of, respectively, 9/13, 10/13 and 10/15. The remaining studies had a median causality score of 7 (range 5-9). No selection bias was identified, but 6/10 studies contained potential confounders (it was unsure whether the infection was pre- or postnatal acquired, or immunodeficiency was not specifically excluded). Based on the evaluation of the available literature, although scanty and of limited quality, a causal relationship between postnatal toxoplasmosis and epilepsy seems possible. More definite proof requires further research, e.g. by performing Toxoplasma serology in all de novo epilepsy cases.

2016Dec
Int. J. Cardiol.
Int J Cardiol 2016 Dec 27. Epub 2016 Dec 27.
Center of Microbiology and Parasitology, Public Health Institute Niš, Serbia, Blvd Zorana Djindjica 81, 18000 Niš, Serbia; Department of Microbiology and Immunology, Faculty of Medicine, University of Niš, Serbia, Blvd Zorana Djindjica 81, 18000 Niš, Serbia.

The delayed Gadolinium Myocardium Enhancement (DGE) extent on Cardiac Magnetic Resonance (CMR) correlates with biomarkers of myocardial injury in patients with acute viral myocarditis and is an independent predictor of adverse cardiovascular outcome. Ventriculoarterial Coupling (VAC) is related to both the cardiovascular work output and energy efficiency and can be noninvasively assessed. In this work, we aimed to evaluate alterations in VAC indices in correlation with DGE in patients with acute myocarditis. Read More


Fifty-seven patients (mean age 42 (18) years old, 58% male, 19% had hypertension, 9% coronary artery disease and 2% diabetes mellitus) with diagnosed acute myocarditis were enrolled. All patients underwent comprehensive echocardiographic evaluation with a VAC value calculation and CMR imaging within a 24-hour period.
The mean ejection fraction was 42±18%; 49% had preserved systolic function. DGE was noted in 56% of patients. When stratified by EF (preserved or reduced), those with an EF>50% had significantly smaller ventricles and a lower VAC, closer to the values that maximize the stroke work and energy efficiency (p=0.002 for end diastolic diameters, 0.001 for VAC, 0.01 for distance from 0.7 and 0.5 and 0.056 for distance from 1). No difference in DGE prevalence was noted (p=0.34). DGE-based stratification did not reveal any difference in the EF or VAC values between groups. Multi-adjusted regression analysis showed that EF was a significant predictor of VAC alterations.
In acute myocarditis patients, DGE is related to neither EF nor VAC; however, EF significantly affects the VAC status. Further studies are needed to investigate the potential quantitative, rather than qualitative, relationships between these variables.

2017Jan
Intervirology
Intervirology 2017 Jan 13;59(3):143-151. Epub 2017 Jan 13.
Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.

The meaning of viral nucleic acids in the myocardium in many cases is difficult for clinical interpretation, whereas the presence of viral nucleic acids in the serum is a marker of active infection. We determined the diagnostic value of viral nucleic acids in ventricular serum and peripheral serum samples in comparison with endomyocardial biopsy (EMB) specimens in patients with clinically suspected myocarditis.
The viral nucleic acid evaluation was performed in serum samples and EMB specimens by real-time PCR in 70 patients (age: 47 ± 16 years). Read More

The biopsy specimens were examined by histo- and immunohistochemistry to detect inflammatory response.
The viral nucleic acids were detected in ventricular and peripheral serum, and EMB samples of 10 (14%), 14 (20%), and 32 (46%) patients, respectively. Notably, viral nucleic acids of the same virus as in the EMB sample were present more often in ventricular than in peripheral serum (60 vs. 7%, p = 0.01). A significant concurrence was observed between the positive and the negative results of viral nucleic acids present in EMB and ventricular serum (p = 0.0001).
The detection of the same viral nucleic acid type in the myocardium and in ventricular serum being significantly more frequent than in the peripheral serum may suggest that the site of the blood collection is important for more precise and reliable confirmation of the active viral replication in the heart.

2017Jan
Radiol Med
Radiol Med 2017 Jan 9. Epub 2017 Jan 9.
Department of Surgical Sciences, Radiology Institute, University of Turin, Via Genova 3, 10126, Turin, Italy.

To analyse the clinical and magnetic resonance evolution of myocarditis in patients with an "infarct-like" presentation pattern.
The study is a retrospective analysis of 52 patients with clinical diagnosis of "infarct-like" myocarditis confirmed by CMR as acute myocarditis according to Lake Louise criteria and 6 months follow-up. The CMR protocol included T2-weighted (oedema), early (hyperaemia) and late (fibrosis/necrosis) gadolinium enhancement sequences, according to Lake Louise criteria. Read More

Clinical and radiological follow-up by CMR was performed after a median time interval of 6 months (interquartile range 5-8). Quantitative outcomes were checked for normality and compared with the non-parametric Wilcoxon's test for matched data.
At the clinical follow-up all patients were free of symptoms and reported no cardiac complications. The CMR follow-up evidenced a significant increase of the ejection fraction (from 53 ± 6 to 55 ± 4%, p = 0.03), a decrease of the ventricular mass [from 67.0 (58.8-79.0) to 61.0 (54.0-67.0), p < 0.0001] without significant modification of the cardiac volume index (p = 0.26). No patient had residual oedema or capillary leakage: the T2 ratio decreased from 3.94 (3.00-4.86) to 0.98 (0.75-1.17) with p < 0.0001 and the Early gadolinium enhancement (EGE) ratio from 5.7 (4.8-6.5) to 2.9 (2.4-3.2) with p < 0.0001. Late gadolinium enhancement (LGE) persisted over the course of the follow-up in 48/52 patients, but with a significant reduction in every patient (LGE % from 34.3 ± 9.1 to 19.4 ± 6.6%; p < 0.0001).
Patients diagnosed with "infarct-like" myocarditis, according to both clinical and CMR examinations may look forward to a positive evolution with a good prognosis.