A case report: pause and consider the late complications of heart transplantation.

BACKGROUND: A 75-year-old woman with a past medical history significant for non-ischaemic cardiomyopathy status post orthotopic heart transplant, type II diabetes mellitus, hypertension, chronic kidney disease stage III, chronic anaemia, and chronic diarrhoea presented with nausea, vomiting, and an unexplained fall 23 years after original transplantation. CASE SUMMARY: During her hospital stay, she had multiple episodes of sinus arrest with syncope, preceded by seizure like activity. She was stabilized, and broad work up revealed an occult brain mass that was ultimately resected and consistent with post-transplant lymphoproliferative disease. DISCUSSION: Features that make this case study unique include the late onset and location of the malignancy, the absence of Epstein-Barr virus involvement, and asystole that was potentially neurologically mediated and induced by a brain space occupying mass. This case offers insight into potential late parasympathetic reinnervation of transplanted hearts, adds to the growing literature regarding the connection between the brain and the heart, and reviews potential complications in patients with a remote history of heart transplantation.

Lifestyle Therapy for the Management of Atrial Fibrillation.

Atrial fibrillation (AF) is a common arrhythmia associated with increased risk of morbidity and mortality. There is evidence that lifestyle interventions may serve as complementary treatments to reduce AF burden. The objective of this review was to summarize the efficacy of lifestyle interventions for the management of AF. Studies which included patients with systolic heart failure (ejection fraction ≤40%), and those limited to an examination of vigorous physical activity were excluded from our search. Studies were identified through a search of the following databases: MEDLINE, EMBASE, CINAHIL, and PubMed, run from inception through August 2016. All studies were graded for quality using the Oxford Centre for Evidence-based Medicine recommendations. Meta-analyses of the studies were not performed due to the heterogeneity of the studies. From a total of 1,811 publications, 10 articles were identified and included. Selected publications included 1 study on yoga, 2 studies on acupuncture, 3 studies that examined weight loss programs, and 4 studies that evaluated the impact of moderate physical activity. Yoga was associated with less symptomatic AF episodes and improved quality of life. Acupuncture was associated with reduced AF occurrence in patients with persistent and paroxysmal AF. Weight loss was associated with a significant reduction AF burden and symptoms. Moderate exercise resulted in greater arrhythmia free survival and a mean reduction in AF burden. In conclusion, evidence exists to suggest that yoga, weight loss, and moderate exercise are associated with reductions in AF burden and symptoms. Evidence is greatest for weight loss and moderate exercise.

Sex-specific differential in risk of diabetes-related macrovascular outcomes.

Reports from recent studies suggest that diabetes confers a higher risk of cardiovascular disease in women compared to men. Larger studies, including meta-analyses, report that women with diabetes have a 44 % greater risk of incident coronary heart disease and a 27 % greater risk of incident stroke compared to men with diabetes. In this article, we summarize results from longitudinal studies that examine sex differences in risk factors for and rates of macrovascular complications from diabetes. We also discuss possible mechanisms for increased cardiovascular risk associated with diabetes in women compared to men, including the clustering of hypertension, obesity, and elevated triglycerides, the possible contribution of hormonal differences, and sex differences in the prescription of and adherence to pharmacologic treatment. In conclusion, diabetes is associated with a slightly higher risk of cardiovascular disease in women compared to men. Future studies should further explore the reasons underlying imperfect use of medications that lower cardiovascular risk in both women and men with diabetes.

Inflammatory response to liver fluke Opisthorchis viverrini in mice depends on host master coregulator MTA1, a marker for parasite-induced cholangiocarcinoma in humans.

UNLABELLED: Based on the recently established role for the master coregulator MTA1 and MTA1-containing nuclear remodeling complexes in oncogenesis and inflammation, we explored the links between parasitism by the carcinogenic liver fluke Opisthorchis viverrini and this coregulator using both an Mta1(-/-) mouse model of infection and a tissue microarray of liver fluke-induced human cholangiocarcinomas (CCAs). Intense foci of inflammation and periductal fibrosis in the liver and kidneys of wild-type Mta1(+/+) mice were evident at 23 days postinfection with O. viverrini. In contrast, little inflammatory response was observed in the same organs of infected Mta1(-/-) mice. Livers of infected Mta1(+/+) mice revealed strong up-regulation of fibrosis-associated markers such as cytokeratins 18 and 19 and annexin 2, as determined both by immunostaining and by reverse-transcription polymerase chain reaction compared with infected Mta1(-/-) mice. CD4 expression was up-regulated by infection in the livers of both experimental groups; however, its levels were several-fold higher in the Mta1(+/+) mice than in infected Mta1(-/-) mice. Mta1(-/-) infected mice also exhibited significantly higher systemic and hepatic levels of host cytokines such as interleukin (IL)-12p70, IL-10, and interferon-γ compared with the levels of these cytokines in the Mta1(+/+) mice, suggesting an essential role of MTA1 in the cross-regulation of the Th1 and Th2 responses, presumably due to chromatin remodeling of the target chromatin genes. Immunohistochemical analysis of ≈ 300 liver tissue cores from confirmed cases of O. viverrini-induced CCA showed that MTA1 expression was elevated in >80% of the specimens. CONCLUSION: These findings suggest that MTA1 status plays an important role in conferring an optimal cytokine response in mice following infection with O. viverrini and is a major player in parasite-induced CCA in humans.

The metastasis-associated protein-1 gene encodes a host permissive factor for schistosomiasis, a leading global cause of inflammation and cancer.

UNLABELLED: Schistosoma haematobium is responsible for two-thirds of the world's 200 million to 400 million cases of human schistosomiasis. It is a group 1 carcinogen and a leading cause of bladder cancer that occurs after years of chronic inflammation, fibrosis, and hyperproliferation in the host liver. The coevolution of blood flukes of the genus Schistosoma and their human hosts is paradigmatic of long-term parasite development, survival, and maintenance in mammals. However, the contribution of host genes, especially those discrete from the immune system, necessary for parasite establishment and development remains poorly understood. This study investigated the role of metastasis-associated protein-1 gene (Mta1) product in the survival of S. haematobium and productive infection in the host. Using a Mta-1 null mouse model, here we provide genetic evidence to suggest that MTA1 expression positively influences survival and/or maturation of schistosomes in the host to patency, as we reproducibly recovered significantly fewer S. haematobium worms and eggs from Mta1-/- mice than wild-type mice. In addition, we found a distinct loss of cytokine interdependence and aberrant Th1 and Th2 cytokine responses in the Mta1-/- mice compared to age-matched wild-type mice. Thus, utilizing this Mta1-null mouse model, we identified a distinct contribution of the mammalian MTA1 in establishing a productive host-parasite interaction and thus revealed a host factor critical for the optimal survival of schistosomes and successful parasitism. Moreover, MTA1 appears to play a significant role in driving inflammatory responses to schistosome egg-induced hepatic granulomata reactions, and thus offers a survival cue for parasitism as well as an obligatory contribution of liver in schistosomiasis. CONCLUSION: These findings raise the possibility to develop intervention strategies targeting MTA1 to reduce the global burden of schistosomiasis, inflammation, and neoplasia.