Sudden death in tuberculous myocarditis

Amonkar, Gayathri; Rupani, Asha; Shah, Vinaya B; Parmar, Heena

doi:10.1016/j.carpath.2007.12.016

Cited by 19 publications

(8 citation statements)

References 3 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Most patients were young and asymptomatic prior to their fatal event. The proposed underlying mechanism leading to SCD was ventricular tachyarrhythmia, likely a consequence of aberrant conduction from extensive tuberculous septal involvement or ventricular wall necrosis [ 54 , 55 ]. Pulmonary tuberculosis without obvious direct mycobacterial involvement of the myocardium or coronary arteries has also been liked to SCD, but the exact mechanisms of death remain obscure [ 56 ].…”

Section: Reviewmentioning

confidence: 99%

Tuberculosis and cardiovascular disease: linking the epidemics

Huamán

Henson

Ticona

et al. 2015

Trop Dis Travel Med Vaccines

View full text Add to dashboard Cite

The burden of tuberculosis and cardiovascular disease (CVD) is enormous worldwide. CVD rates are rapidly increasing in low- and middle-income countries. Public health programs have been challenged with the overlapping tuberculosis and CVD epidemics. Monocyte/macrophages, lymphocytes and cytokines involved in cellular mediated immune responses against Mycobacterium tuberculosis are also main drivers of atherogenesis, suggesting a potential pathogenic role of tuberculosis in CVD via mechanisms that have been described for other pathogens that establish chronic infection and latency. Studies have shown a pro-atherogenic effect of antibody-mediated responses against mycobacterial heat shock protein-65 through cross reaction with self-antigens in human vessels. Furthermore, subsets of mycobacteria actively replicate during latent tuberculosis infection (LTBI), and recent studies suggest that LTBI is associated with persistent chronic inflammation that may lead to CVD. Recent epidemiologic work has shown that the risk of CVD in persons who develop tuberculosis is higher than in persons without a history of tuberculosis, even several years after recovery from tuberculosis. Together, these data suggest that tuberculosis may play a role in the pathogenesis of CVD. Further research to investigate a potential link between tuberculosis and CVD is warranted.

show abstract

Section: Reviewmentioning

confidence: 99%

Tuberculosis and cardiovascular disease: linking the epidemics

Huamán

Henson

Ticona

et al. 2015

Trop Dis Travel Med Vaccines

View full text Add to dashboard Cite

show abstract

“…Although the pericardium is most commonly involved and myocardial involvement is rare,23 TB myocarditis is a factor in the majority of TB-related sudden cardiac deaths 23 , 26 , 32 - 38. The mechanism of SD in TB myocarditis has been hypothesized to be ventricular tachyarrhythmias,23 , 26 , 32 - 34 , 37 , 38 although direct records of ventricular arrhythmia are lacking 23 , 26 , 30 , 39. When the pericardium is affected by TB, pericarditis and/or cardiac tamponade may develop, and they could be a cause of SD 31.…”

Section: Discussionmentioning

confidence: 99%

Sudden death caused by pulmonary fat embolism in a patient with miliary tuberculosis

Chinen

Ito

2019

Autops. Case Rep.

View full text Add to dashboard Cite

An 84-year-old Japanese woman with myelodysplastic syndrome was admitted with pyrexia and dyspnea, but died suddenly during diagnostic evaluation. The autopsy revealed miliary tuberculosis in addition to myelodysplastic syndrome in the bone marrow. The immediate cause of the patient’s sudden death was pulmonary fat embolism derived from bone marrow necrosis. This case shows that the infiltration of the myelodysplastic bone marrow by tuberculosis and consequent bone marrow necrosis and fat embolism can be the cause of sudden death. In this article, we report the autopsy results of this unusual cause of sudden death, and discuss tuberculosis-related sudden death with a review of the literature.

show abstract

“…Reasons for relative sparing of the myocardium include reference to the statement by Raviart regarding the protective effect of lactic acid produced by muscular activity of the myocardium [3,8]. According to Wallis et al, TB spreads to the myocardium by one of three methods: direct extension, retrograde spread via lymphatics from the mediastinal lymph nodes or by hematogenous route (from miliary disease) [11].…”

Section: Discussionmentioning

confidence: 99%