Patterns and clinical manifestations of tuberculous myocarditis: a systematic review of cases

Michira, Brian N.; Alkizim, Faraj O.; Matheka, Duncan Mwangangi

doi:10.11604/pamj.2015.21.118.4282

Cited by 30 publications

(35 citation statements)

References 20 publications

(6 reference statements)

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“…Infiltration of the myocardium by TB can occur by haematogenous seeding from a remote focus, direct spread from the pericardium or, as seems likely in this case, via lymphatic spread from mediastinal lymph nodes ( 4 ). A predilection for the right-sided mediastinal lymph nodes has been described in TB thus allowing direct spread to the myocardium with the right side of the heart being most commonly affected in this situation, as seen in the post-mortem of this patient ( 5 , 6 ). Three different types of myocardial involvement in TB have been described pathologically: diffuse infiltrative, caseating nodular and miliary.…”

Section: Discussionmentioning

confidence: 71%

Acute myocarditis secondary to cardiac tuberculosis: a case report

Cowley¹,

Dobson²,

Kurian³

et al. 2017

Echo Res Pract

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Isolated myocardial involvement in tuberculosis is exceedingly rare but there are reports it can present with sudden cardiac death, atrioventricular block, ventricular arrhythmias or congestive cardiac failure. We report the case of a 33-year-old male, of South Asian descent, who presented with chest pain, shortness of breath and an abnormal ECG. The patient had no significant past medical history and coronary angiogram showed no evidence of coronary artery disease. Of note, the patient had recently been discharged from a local district hospital with an episode of myocarditis. The patient was found to be severely hypoxic with evidence of severe biventricular failure on echocardiography. Computed tomography of the chest demonstrated hilar lymphadenopathy, and the differential diagnosis was thought to be tuberculosis or sarcoidosis. A TB Quantiferon gold test performed at the district hospital was positive; however, fine needle aspiration was negative for acid-fast bacilli. Despite aggressive diuresis, the patient became increasingly hypoxic and suffered a cardiac arrest. Post-mortem confirmed a diagnosis of myocardial tuberculosis – a rare case of acute decompensated heart failure.Learning points:Tuberculosis myocarditis is a rare diagnosis but should be considered in at risk individuals presenting with acute fulminant myocarditis.Cardiac failure can occur even in the absence of disseminated tubercular disease.TB myocarditis is not just a disease of the immunocompromised.Definitive diagnosis of cardiac tuberculosis during life requires a myocardial biopsy.Echocardiography is a vital tool for the assessment of cardiac function, filling pressures and fluid status in the critically unwell patient.

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Section: Discussionmentioning

confidence: 71%

Acute myocarditis secondary to cardiac tuberculosis: a case report

Cowley¹,

Dobson²,

Kurian³

et al. 2017

Echo Res Pract

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“…Bacterial infections such as those caused by Staphylococcus aureus, Neisseria meningitidis, Streptococcus pyogenes, brucellosis, salmonellosis, Haemophilus influenzae, tuberculosis, syphilis and Lyme disease are less frequent as causes of myocarditis; severe myocarditis is reported in severe systemic Chlamydia pneumophila infection and in fatal Streptococcus pneumoniae sepsis [51e53]. Reports of tubercular myocarditis, though rare, show a high rate of sudden cardiac deaths [54].…”

Section: Myocarditismentioning

confidence: 99%

Cardiac arrest among patients with infections: causes, clinical practice and research implications

Leoni

Rello

2017

Clinical Microbiology and Infection

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The incidence of sepsis is increasing, and the condition is now the leading cause of death in general intensive care units. Our review failed to identify studies of the causes of cardiac arrest among infected patients, even though non-cardiac causes represent 15% of out-of-hospital cardiac arrests and though one-third of events have positive blood cultures. Sudden cardiac arrest is the result of local damage to the heart and of the impact of systemic and pulmonary conditions on cardiac performance, and its danger is underestimated. Necropsy findings in sudden death often identify myocarditis as an unexpected cause. The role of hypoxaemia, severe pulmonary thromboembolism with subsequent pulseless cardiac activity, alterations of electrolytes and hydrogen concentrations, distort fluid distribution with reduced pre-load, direct myocyte damage and adverse cardiac effects related to antibiotic use need to be defined. Many cardiac arrests might be preventable. Because cardiopulmonary resuscitation is challenging and usually unsuccessful in patients with sepsis, research is needed to help predict which patients are at risk. Only half of pneumonia patients with cardiac arrest in the ward receive prior ECG monitoring. Telemedicine and non-invasive monitoring in the ward, avoidance of antibiotics associated with prolonged QT syndrome, and adequate haemodynamic resuscitation might be important in preventing in-hospital arrests among patients with infections.

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“…However, a large number of patients are completely asymptomatic. Anti-tuberculosis therapy is usually effective; nevertheless, it does not reduce the risk of sudden cardiac death [72].…”

Section: Mycobacterium Tuberculosismentioning

confidence: 99%

Infective Cardiomyopathy

Pawlak¹,

Gil²

2017

Cardiomyopathies - Types and Treatments

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Both the infectious agent and development of inflammatory response to infection can lead to irreversible myocardial injury, which affects the outcome of short-and long-term prognosis. In the case of the rapid elimination of the infectious agent and rapid withholding of inflammatory process, changes in myocardium are small. If the immune response does not lead to complete elimination of infectious agent or inflammation progresses after removing the virus, chronic myocardial damage may develop. Persistence of the virus in myocardium, postinfectious immune reaction, autoimmunity, and primary cardiac damage may result in the development of progressive ventricular dysfunction, development of cardiac arrhythmias, and exacerbation of symptom. Because of the long-term consequences, it is important to diagnose infective cardiomyopathy (IC) quickly and start appropriate treatment. However, IC is still a diagnostic challenge. Infective cardiomyopathy is often underdiagnosed because of a wide spectrum of factors causing IC-infectious, toxic, immunologic, and various clinical manifestation. The processes responsible for the development of IC take place at the cellular level, which is why it is important to make the diagnosis not only based on clinical symptoms and imaging but also to confirm it with the use of histological, immunohistochemical, and molecular studies. Progress in the diagnosis and understanding of the pathomechanisms responsible for the development of IC contributed to the use of new therapeutic options. Immunosuppresive and immunomodulative treatment is still of limited use. However, in some cases of viral IC, targeted antiviral treatment can be added to the standard heart failure therapy resulting in improvement of the prognosis.Infective cardiomyopathy may be caused by many etiological factors including viruses, bacteria, rickettsiae, fungi, protozoa, and parasites. However, the spectrum of pathogens has changed over the decades and also varies geographically as, for example, Trypanosoma cruzi [4]. Moreover, it can result from noninfectious agents, such as allergic agents, autoimmunity, toxins, and drugs [5]. Etiological factors that could cause IC are presented in Table 1. The most popular infective agents VirusesRNA viruses:

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Patterns and clinical manifestations of tuberculous myocarditis: a systematic review of cases

Cited by 30 publications

References 20 publications

Acute myocarditis secondary to cardiac tuberculosis: a case report

Acute myocarditis secondary to cardiac tuberculosis: a case report

Cardiac arrest among patients with infections: causes, clinical practice and research implications

Infective Cardiomyopathy

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