Myocarditis Publications (17716)
Gallium-67 SPECT/CT images helped understanding the disease condition that temporary inflammation in the left atrium caused atrial fibrillation.
The global signal intensity ratio (heart muscle in relation to skeletal muscle) was calculated (global STIR+ ratio) to evaluate edema. All patients had repeat examinations at follow-up (mean interval 4.9 months, 1-12 months).
The mean global STIR+ ratio was 2.15 ± 0.4 in the initial examination of patients as compared to 1.78 ± 0.3 in controls (p < 0.0001) and 1.89 ± 0.3 in patients at follow-up (p = 0.0001 vs. first visit). Left ventricular ejection fraction did not differ between patients and controls at baseline and at follow-up.
We could identify a significantly higher global STIR+ ratio in patients with suspected myocarditis compared to controls, and a dynamic change during follow-up. The global STIR+ ratio may, therefore, be useful for the diagnosis of myocarditis and should be further explored.
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.
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.
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.
Although is usually mild, AV block can fluctuates rapidly and progress from a prolonged P-R interval to a His-Purkinje block within minutes to hours and days. Rarely, Lyme disease may be the cause of endocarditis, while some studies and reports, based on serological and/or molecular investigations, have suggested possible influence of Borrelia burgdorferi on degenerative cardiac valvular disease. Myocarditis, pericarditis, pancarditis, dilated cardiomyopathy, and heart failure have also been described as possible manifestations of Lyme carditis. The clinical course of Lyme carditis is generally mild, short term, and in most cases, completely reversible after adequate antibiotic treatment.
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.
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.
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.