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Tuberculosis and the Heart

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Tuberculosis and the Heart Tuberculosis and the Heart Arthur K. Mutyaba, MBChB, MMed, FCP(SA), Mpiko Ntsekhe, MD, PhD* KEYWORDS Tuberculosis Tuberculous pericarditis Tuberculous myopericarditis Tuberculous myocarditis Tuberculous aortitis KEY POINTS Tuberculosis remains an important health problem of the developing world. Tuberculous heart dis- ease is an important extrapulmonary manifestation of the disease. Tuberculous pericarditis occurs with higher frequency in individuals infected with the human immu- nodeficiency virus (HIV) and is characterized by differences in immune and clinical responses compared with HIV-negative individuals. A biomarker-based approach that uses pericardial fluid unstimulated interferon-g, adenosine deaminase, and polymerase chain reaction offers a fast and reliable way of establishing the diagnosis. Four-drug antituberculous therapy is the mainstay of management for tuberculous pericarditis. Adjunctive steroid therapy has been shown to reduce hospitalization and progression to constric- tive pericarditis, but not mortality; in HIV-positive patients, adjunctive steroids are associated with a higher incidence of malignancy. Video content accompanies this article at http://www.cardiology.theclinics.com. INTRODUCTION (Fig. 1). Autopsy studies performed in the pre- HIV/AIDS era suggest that the heart is involved in Recognized since antiquity, tuberculosis (TB) still approximately 2% of cases of patients who died contributes significantly to the global burden of from TB.3 Similar studies of patients who died of disease, with an estimated 9.6 million new cases 1 TB and were coinfected with HIV demonstrate of the disease worldwide in 2014. This is espe- multisystemic dissemination in up to 80% of pa- cially true in the developing world where human tients.4,5 Of all the extrapulmonary manifestations immunodeficiency virus (HIV) infection and AIDS, of TB, involvement of the heart is second only to socioeconomic deprivation, and poor health sys- central nervous system TB in terms of its devas- tems infrastructure interact to make TB a signifi- 2 tating morbidity and mortality. cant public health problem. Although it remains It has been almost a decade since there was a primarily a disease of the lungs, the classic lesion comprehensive review of the main form of tuber- Mycobacterium tuberculosis of TB—the acid fast culous heart disease.6 That review focused on (Mtb) bacilli in a necrotic core bound by aggre- the pathogenesis, diagnosis, and management of gates of various inflammatory cells (granuloma)— tuberculous pericarditis and concluded by noting can be found in virtually any part of the body that there remained major gaps in our The authors have nothing to disclose. Division of Cardiology, Department of Medicine, Groote Schuur Hospital, University of Cape Town, E17 Cardiac Clinic, New Groote Schuur Hospital, Anzio Road, Observatory 7925, Cape Town, South Africa * Corresponding author. E-mail address: [email protected] Cardiol Clin 35 (2017) 135–144 http://dx.doi.org/10.1016/j.ccl.2016.08.007 0733-8651/17/Ó 2016 Elsevier Inc. All rights reserved. cardiology.theclinics.com Downloaded from ClinicalKey.com at SA Consortium - University of Cape Town February 17, 2017. For personal use only. No other uses without permission. Copyright ©2017. Elsevier Inc. All rights reserved. 136 Mutyaba & Ntsekhe Fig. 1. Mycobacterium tuberculosis. Tuberculous granuloma (A) showing an aggregation of lymphocytes, mono- cytes, multinucleate giant cells with a central area of caseous necrosis. Ziehl-Neelsen stain (B) demonstrating acid-fast M tuberculosis (arrow). (Courtesy of Dr Craig Jamieson, formerly of Anatomical Pathology Department, University of Cape Town, Observatory, Cape Town, South Africa.) understanding of the subject. The identified gaps The IMPI immunotherapy trial was a double- included the need for improved diagnostic tools, blind, randomised control trial of 1400 patients a better understanding of the impact of HIV, and with definite or probable TB pericarditis who determination of the effectiveness of adjuvant were randomised to receive adjunctive corticoste- therapy on clinical outcomes.6 Since then, much roids or Mycobacterium indicus pranii versus pla- data, predominantly from sub-Saharan Africa, cebo in a 2 Â 2 factorial design.19 These studies, have been generated to address some of these which were conducted between 2004 and 2015, gaps. An updated comprehensive overview of TB form the backbone of new insights gained since and the heart with a summary of the new insights 2005. is therefore timely and hopefully of value to the There are 3 predominant clinical manifestations general physician and cardiologist on the front of tuberculous heart disease. In descending order lines of patient care. of frequency, these include TB pericarditis, The search strategy for this review involved a myocardial TB with or without aneurysm forma- comprehensive search of MEDLINE, EMBASE tion, and TB aortitis with or without mycotic aneu- and the Cochrane library of systematic reviews rysms and pseudoaneurysms involving the aortic with the MeSH terms: “tuberculosis and the heart,” valve and/or sinuses of Valsalva. Important clin- “cardiac tuberculosis,” “cardiovascular tubercu- ical, diagnostic, and management aspects of losis,” “myopericarditis and tuberculosis,” “tuber- each are reviewed. culous pericarditis,” “tuberculous aortitis,” and “HIV and the heart’’ from January 2005 to TUBERCULOUS PERICARDITIS December 2015. The reference lists of selected ar- ticles were searched for articles deemed to be of Tubercle bacilli access the pericardium via 3 main relevance to the subject. Appropriate English lan- mechanisms. These include retrograde lymphatic guage studies were retrieved and reviewed. spread from mediastinal, paratracheal and peri- There have been a number of important ad- bronchial lymph nodes,20 hematogenous spread vances in our understanding of tuberculous peri- (dominant in immunocompromised hosts),21 and, carditis over the last decade. Most of the new rarely, direct contiguous spread from adjacent information has been generated from sub- structures such as the lungs, pleura, and spine.20 Saharan Africa and Asia, where TB is endemic, In the presence of a competent immune system, HIV is epidemic, and the majority of patients with tuberculous pericardial disease is usually localized TB are also coinfected with HIV.2 The Investigation to the pericardial space. It is typically a paucibacil- of the Management of Pericarditis in Africa (IMPI) lary condition; tubercle proteins trigger a vigorous registry was a prospective observational cohort cell-mediated hypersensitivity response with of consecutive patients with suspected TB peri- T-helper cell (subtype 1) predominant cytokine carditis across multiple sites in sub-Saharan Af- release, leading to an inflammatory exudative effu- rica. Important questions related to the sion and its hemodynamic sequelae.6 In patients immunopathogenesis, clinical manifestations, with dysfunctional immunity as occurs in HIV/ diagnosis, and outcomes of TB pericarditis in the AIDS, there is evidence that mycobacterial replica- HIV era were investigated in the registry.7–18 tion is active, bacillary loads are high, and the Downloaded from ClinicalKey.com at SA Consortium - University of Cape Town February 17, 2017. For personal use only. No other uses without permission. Copyright ©2017. Elsevier Inc. All rights reserved. Tuberculosis and the Heart 137 clinical manifestations of tuberculous pericarditis Effusive pericarditis is the commonest form of are related to the impact of the infectious and viru- pericardial TB in patients with and without HIV.6 lent nature of the Mtb itself in addition to the hemo- In the developing world, 40% to 70% of large peri- dynamic sequelae.13,21 Tuberculous pericarditis cardial effusions are tuberculous in origin.18,23,24 typically presents as 1 of 4 clinical syndromes, This is in contrast with the developed world, where namely, acute pericarditis, effusive pericarditis less than 4% of cases are tuberculous.25 The clin- and its complications, myopericarditis, and ical presentation of this group of patients is deter- constrictive pericarditis. Although it is convenient mined by the rate of fluid accumulation, magnitude to review them as distinct clinical entities, it is of pericardial fluid-induced cardiac compression, important to understand that there is much overlap and the severity of the inflammation, edema, and in the clinical manifestations. loss of visceral pericardial compliance.14,26 The triad of severe pericarditic chest pain, a peri- Where cardiac compression is significant or rapid, cardial friction rub, widespread ST-segment and T cardiac filling and stroke volume can be compro- wave abnormalities and PR segment depression mised significantly. If hemodynamic compensa- typical of acute pericarditis is an uncommon clinical tory mechanisms are adequate, the symptoms presentation of tuberculous pericarditis, account- are usually those of congestive heart failure ing for only 3% to 8% of patients who present without hypotension, and the clinical signs those with tuberculous pericarditis.7,19 The syndrome is of a large pericardial effusion24,27 (Table 2). Where thought to occur soon after inoculation of tubercle pericardial fluid accumulation is relatively quick bacilli into the pericardium, and is characterized and compensatory mechanisms are inadequate, pathologically by polymorphonuclear leukocytosis patients present with evidence of hypotension with abundant
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