The effects of HIV/AIDS on the clinical profile and outcomes post pericardiectomy of patients with constrictive pericarditis: a retrospective review.

OBJECTIVE: The clinical profile and surgical outcomes of patients with constrictive pericarditis were compared in HIV-positive and -negative individuals. METHODS: This study was a retrospective analysis of patients diagnosed with constrictive pericarditis at Inkosi Albert Luthuli Central Hospital, Durban, over a 10-year period (2004-2014). RESULTS: Of 83 patients with constrictive pericarditis, 32 (38.1%) were HIV positive. Except for pericardial calcification, which was more common in HIV-negative subjects (n = 15, 29.4% vs n = 2, 6.3%; p = 0.011), the clinical profile was similar in the two groups. Fourteen patients died preoperatively (16.9%) and three died peri-operatively (5.8%). On multivariable analysis, age (OR 1.17; 95% CI: 1.03-1.34; p = 0.02), serum albumin level (OR 0.63; 95% CI: 0.43-0.92; p = 0.016), gamma glutamyl transferase level (OR 0.97; 95% CI: 0.94-0.1.0; p = 0.034) and pulmonary artery pressure (OR 1.49; 95% CI: 1.07-2.08; p = 0.018) emerged as independent predictors of pre-operative mortality rate. Peri-operative complications occurred more frequently in HIV-positive patients [9 (45%) vs 6 (17.6%); p = 0.030]. CONCLUSIONS: Without surgery, tuberculous constrictive pericarditis was associated with a high mortality rate. Although peri-operative complications occurred more frequently, surgery was not associated with increased mortality rates in HIV-positive subjects.

A prospective investigation into the effect of colchicine on tuberculous pericarditis.

INTRODUCTION: Tuberculous (TB) pericarditis carries significant mortality and morbidity rates, not only during the primary infection, but also as part of the granulomatous scar-forming fibrocalcific constrictive pericarditis so commonly associated with this disease. Numerous therapies have previously been investigated as adjuvant strategies in the prevention of pericardial constriction. Colchicine is well described in the treatment of various aetiologies of pericarditis. The aim of this research was to investigate the merit for the use of colchicine in the management of tuberculous pericarditis, specifically to prevent constrictive pericarditis. METHODS: This pilot study was designed as a prospective, double-blinded, randomised, control cohort study and was conducted at a secondary level hospital in the Northern Cape of South Africa between August 2013 and December 2015. Patients with a probable or definite diagnosis of TB pericarditis were included (n = 33). Study participants with pericardial effusions amenable to pericardiocentesis underwent aspiration until dryness. All patients were treated with standard TB treatment and corticosteroids in accordance with the South African Tuberculosis Treatment Guidelines. Patients were randomised to an intervention and control group using a web-based computer system that ensured assignment concealment. The intervention group received colchicine 1.0 mg per day for six weeks and the control group received a placebo for the same period. Patients were followed up with serial echocardiography for 16 weeks. The primary outcome assessed was the development of pericardial constriction. Upon completion of the research period, the blinding was unveiled and data were presented for statistical analysis. RESULTS: TB pericarditis was found exclusively in HIV-positive individuals. The incidence of pericardial constriction in our cohort was 23.8%. No demonstrable benefit with the use of colchicine was found in terms of prevention of pericardial constriction (p = 0.88, relative risk 1.07, 95% CI: 0.46-2.46). Interestingly, pericardiocentesis appeared to decrease the incidence of pericardial constriction. CONCLUSION: Based on this research, the use of colchicine in TB pericarditis cannot be advised. Adjuvant therapy in the prevention of pericardial constriction is still being investigated and routine pericardiocentesis may prove to be beneficial in this regard.

Tuberculous constrictive pericarditis complicated with tuberculous mediastinitis - case report.

Constrictive pericarditis is a rare and severe disease. A 37-year-old patient was admitted in the hospital for dyspnea, precordial pain, right-sided cardiac failure. Chest X-ray showed cardiac enlargement and an opacity suggestive for pleural effusion. Echocardiography revealed an adhesive-effusive-constrictive pericarditis, a very thickened pericardium and bilateral pleural effusion. After a pericardiectomy done to restore cardiac compensation and to identify etiological factors, a tuberculous pericarditis (TBP) was diagnosed. After surgery and starting anti-TB treatment, the patient presented altered clinical status, dyspnea, dry cough, fever and delayed callus formation at sternum level. Thoracic scan revealed mediastinal air collections, pericarditis and pleurisy. Thus, the TBP diagnosis was extended to mediastinal TB and anti-TB therapy was continued. After four months of treatment, another thoracic scan showed disappearance of the mediastinal air-leakage bubbles, multiple new micronodules in both lungs and lymph nodes of up to 15 mm; also increasing pericardial and pleural effusions. This case was interpreted as a TB treatment failure situation. A retreatment regimen was started, resulting in a slow favorable outcome. Pericardial TB is a rare condition, usually with delayed diagnosis and poor treatment benefits. Whenever possible, earlier diagnostic can contribute to better management of these cases.

Tuberculous constrictive pericarditis and atrial septal defect: Surgical challenge.

Tuberculous constrictive pericarditis with atrial septal defect is very rare. A 23-year-old man required pericardiectomy and atrial septal defect closure under cardiopulmonary bypass by cannulating the aorta and right atrium because femoral cannulation was not possible and the venae cavae could not be visualized. He was discharged in a satisfactory condition on the 15th postoperative day, but returned one month later with swelling all over his body and dyspnea on exertion. Echocardiography showed atrial septal defect patch dehiscence and a bidirectional shunt with a collection or mass compressing the right ventricle. Subxiphoid exploration was carried out, and the swelling subsided.

[An uncommon detection of Mycobacterium tuberculosis in pericardial effusion]. / Ojedinelý prípad izolovaného výskytu Mycobacterium tuberculosis v perikardiálním výpotku.

Pericardial tuberculosis is a specific pericarditis which is rarely reported in the absence of pulmonary tuberculosis. A case history is presented of a 74-year-old patient, immunocompromised as a result of kidney and liver cancer therapy. Mycobacterium tuberculosis was repeatedly recovered from pericardial effusion but not from other clinical specimens. Despite the early treatment of specific pericarditis, the patient died.

Diagnostic accuracy of quantitative PCR (Xpert MTB/RIF) for tuberculous pericarditis compared to adenosine deaminase and unstimulated interferon-γ in a high burden setting: a prospective study.

BACKGROUND: Tuberculous pericarditis (TBP) is associated with high morbidity and mortality, and is an important treatable cause of heart failure in developing countries. Tuberculous aetiology of pericarditis is difficult to diagnose promptly. The utility of the new quantitative PCR test (Xpert MTB/RIF) for the diagnosis of TBP is unknown. This study sought to evaluate the diagnostic accuracy of the Xpert MTB/RIF test compared to pericardial adenosine deaminase (ADA) and unstimulated interferon-gamma (uIFNγ) in suspected TBP. METHODS: From October 2009 through September 2012, 151 consecutive patients with suspected TBP were enrolled at a single centre in Cape Town, South Africa. Mycobacterium tuberculosis culture and/or pericardial histology served as the reference standard for definite TBP. Receiver-operating-characteristic curve analysis was used for selection of ADA and uIFNγ cut-points. RESULTS: Of the participants, 49% (74/151) were classified as definite TBP, 33% (50/151) as probable TBP and 18% (27/151) as non TBP. A total of 105 (74%) participants were human immunodeficiency virus (HIV) positive. Xpert-MTB/RIF had a sensitivity and specificity (95% confidence interval (CI)) of 63.8% (52.4% to 75.1%) and 100% (85.6% to 100%), respectively. Concentration of pericardial fluid by centrifugation and using standard sample processing did not improve Xpert MTB/RIF accuracy. ADA (≥35 IU/L) and uIFNγ (≥44 pg/ml) both had a sensitivity of 95.7% (88.1% to 98.5%) and a negative likelihood ratio of 0.05 (0.02 to 0.10). However, the specificity and positive likelihood ratio of uIFNγ was higher than ADA (96.3% (81.7% to 99.3%) and 25.8 (3.6 to 183.4) versus 84% (65.4% to 93.6%) and 6.0 (3.7 to 9.8); P = 0.03) at an estimated background prevalence of TB of 30%. The sensitivity and negative predictive value of both uIFNγ and ADA were higher than Xpert-MT/RIF (P < 0.001). CONCLUSIONS: uIFNγ offers superior accuracy for the diagnosis of microbiologically confirmed TBP compared to the ADA assay and the Xpert MTB/RIF test.

Uncommon cause of left ventricular pseudoaneurysm: case report and review of literature.

We report a case of an 18-year-old man without tuberculosis history who presented with chest distress, dyspnea, and fever. Chest computed tomography scan and echocardiography showed left ventricular posterior wall pseudoaneurysm and perforation. Unfortunately, the patient died shortly after surgery. On the basis of surgical pathology, we made a final diagnosis of tuberculous pericarditis complicated with left ventricular pseudoaneurysm. This has not been reported before in the published literature.

Presentation of tuberculosis as isolated massive pericardial effusion in a patient with rheumatoid arthritis.

The case of a 60 year old male patient, diagnosed with rheumatoid arthritis presenting with recurrent massive pericardial effusion, and unresponsive to treatment of rheumatoid arthritis is documented. Pericardial biopsy proved Tuberculous pericarditis with positive fluid culture for Mycobacterium Tuberculosis. Anti-tuberculous treatment was started along with corticosteroids. Follow up after three months showed no evidence of pericardial effusion.

Medical therapy of pericardial diseases: part I: idiopathic and infectious pericarditis.

The treatment of pericardial diseases is largely empirical because of the relative lack of randomized trials compared with other cardiovascular diseases. The main forms of pericardial diseases that can be encountered in the clinical setting include acute and recurrent pericarditis, pericardial effusion with or without cardiac tamponade, and constrictive pericarditis. Medical treatment should be targeted at the cause of the disease as much as possible. However, the cause of pericardial diseases may be varied and depends on the prevalence of specific diseases (especially tuberculosis). The search for an etiology is often inconclusive, and most cases are classified as idiopathic in developed countries where tuberculosis is relatively rare, whereas a tuberculous etiology is often presumed in developing countries where tuberculosis is endemic. The aim of the present article is to review current medical therapy for pericardial diseases, highlighting recent significant advances in clinical research, ongoing challenges and unmet needs. Following a probabilistic approach, the most common causes are considered (idiopathic, viral, tuberculous, purulent, connective tissue diseases and neoplastic pericardial disease). In this article, the therapy of idiopathic and more common forms of infectious pericarditis (viral and bacterial) is reviewed.

[Tuberculous pericarditis: still a relevant disease]. / La péricardite tuberculeuse: un diagnostic qui reste d'actualité

Vaccination against tuberculosis is not an obligation anymore in France, except for children at risk, but this disease remains not so rare, including its extrapulmonary forms. The authors report the case of a 27-year-old Madagascan HIV seronegative patient, who developed a pericardial effusion when coming back from a long stay in Madagascar. An anti-inflammatory treatment and then a probabilistic antibiotic treatment were ineffective, and at the same time echocardiographic signs of tamponade appeared. As a consequence, it was decided to perform a surgical pericardial drainage and a biopsy, and to introduce an antituberculosis chemotherapy, given the epidemiologic status. The course was then quickly favorable. The presence of granulomatous inflammation on the biopsy and an elevated pericardial adenosine deaminase activity level retrospectively supported the diagnosis of tuberculous pericarditis.

Constriction infection.

Chronic constrictive pericarditis (CCP) is a clinical syndrome caused by compression of the heart due to a thickened or rigid pericardium. In the affluent West, the majority of cases of CCP are neither tuberculous nor calcific. In an American cohort undergoing pericardectomy for the condition, only 27% had calcification and under 10% had TB [1]. As a result, pericardial calcification (PC) as a marker of CCP has become neglected. We present a 48-year-old male admitted with atrial flutter, acute chest infection and signs of right heart congestion. PC was documented one year previously on a non-contrast CT chest. On this occasion, cardiac catheterisation confirmed hemodynamically significant CCP and cardiac magnetic resonance (cMR) study showed contiguous mass lesions in the pericardium, compression of the right ventricle, enlargement of the right atrium, hepatic enlargement and a pneumonic process in the left lung. He was commenced on antibiotics and anti-tuberculous therapy with a diagnosis of bacterial super-infection of tuberculous CCP. This was confirmed at pericardectomy along with an infected fistula into the left lung. Any finding of PC should be followed up with a thorough haemodynamic and anatomical assessment using any of a wide range of non-invasive imaging modalities.

Pericarditis por Mycobacterium tuberculosis multiresistente en un paciente con infección por VIH: Reporte de un caso clínico y revisión de la literatura / Pericarditis due to multidrug resistant Mycobacterium tuberculosis in an HIV infected patient: Case report and review of literature

Multidrug resistant Mycobacterium tuberculosis infection represents a new clinical challenge and it burdens threat. The association with HIV/AIDS makes very hard to treat these two co-infections. We present a patient of 30 years oíd whose HIV infection was diagnosed 4 years before, and acquired M. tuberculosis pericarditis without response to initial treatment because of a multidrug resistant TB strain. We describe the clinical management, outcome and final recovery of the patient. The epidemiology, diagnosis and treatment of TB pericarditis in HIV positive patients are reviewed.

La infección por Mycobacterium tuberculosis multi-resistente representa una nueva y grave amenaza. La asociación con infección por VIH/SIDA vuelve muy complejo el tratamiento exitoso de ambas infecciones. Presentamos el caso de un paciente de 30 años de edad, con cuatro años de diagnóstico de infección por VIH, que desarrolló una pericarditis por M tuberculosis sin una respuesta favorable inicial al tratamiento debido a que se trataba de una cepa multi-resistente. Se describe el manejo médico, evolución y recuperación final del paciente. Se revisa la epidemiología, diagnóstico y tratamiento de la pericarditis TBC en pacientes con infección por VIH.

The role of histopathology in establishing the diagnosis of tuberculous pericardial effusions in the presence of HIV.

AIMS: To establish the influence of human immunodeficiency virus (HIV) infection on the histopathological features of patients presenting with tuberculous pericarditis. METHODS AND RESULTS: A prospective study was carried out at Tygerberg Academic Hospital, South Africa; 36 patients with large pericardial effusions had open pericardial biopsies under general anaesthesia and were included in the study. Patients underwent pericardiocentesis, followed by daily intermittent catheter drainage; a comprehensive diagnostic work-up (including histopathology of the pericardial tissue) was also performed. Histological tuberculous pericarditis was diagnosed according to predetermined criteria. Tuberculous pericarditis was identified in 25 patients, five of whom were HIV+. The presence of granulomatous inflammation (with or without necrosis) and/or Ziehl-Neelsen positivity yielded the best test results (sensitivity 64%, specificity 100% and diagnostic efficiency 75%). CONCLUSIONS: Co-infection with HIV impacts on the histopathological features of pericardial tuberculosis and leads to a decrease in the sensitivity of the test. In areas which have a high prevalence of tuberculosis, the combination of a sensitive test such as adenosine deaminase, chest X-ray and clinical features has a higher diagnostic efficiency than pericardial biopsy in diagnosing tuberculous pericarditis.

Detection of Mycobacterium tuberculosis complex DNA in pericardial fluid, bone marrow and peripheral blood in a patient with pericardial tuberculosis. A case report.

Definitive diagnosis of tuberculous pericarditis requires identification of bacilli in pericardial fluid or tissue. Conventional diagnostic methods are time-consuming and have a low sensitivity making bacteriological confirmation of the disease very difficult. Hereby, we report the case of molecular detection of Mycobacterium tuberculosis in pericardial fluid, bone marrow and peripheral blood from a 63-year-old woman with pericardial tuberculosis, using a nested PCR assay specific for IS6110 insertion element of M. tuberculosis complex. The patient had an excellent response to a three-drug combination anti-tuberculous regimen and 1 year later was asymptomatic, without evidence of constrictive pericarditis.

Tuberculous pericarditis: optimal diagnosis and management.

Pericarditis is a rare manifestation of tuberculous disease. The appropriate diagnostic workup and optimal therapeutic management are not well defined. We present 10 new cases of tuberculous pericarditis and review the relevant literature. The specific topics addressed are (1) the importance of tissue for diagnosis, (2) the optimal surgical management, (3) the role of corticosteroids, and (4) the impact of human immunodeficiency virus (HIV) on the management of this disease. The cases and the literature suggest that the optimal management includes an open pericardial window with biopsy, both for diagnosis and to prevent reaccumulation of fluid. Corticosteroids probably offer some benefit in preventing fluid reaccumulation as well. The data are inconclusive regarding whether open drainage or corticosteroid use prevents progression to constrictive pericarditis. No studies have addressed these issues specifically in HIV-positive patients, but the 3 HIV-positive patients in our series had an excellent response to drainage and antituberculous therapy.

Pancardiac tuberculosis--a case report.

The authors report a very unusual and unique case of pancardiac tuberculosis in a 25-year-old man who presented initially with atrial flutter with 1:1 conduction. Echocardiographic findings, computerized tomography images, and pathology specimens are presented. After initiation of antituberculous therapy, the patient converted to normal sinus rhythm.

Comparison of PCR, culture, and histopathology for diagnosis of tuberculous pericarditis.

Nucleic acid amplification techniques for the diagnosis of tuberculosis (TB) are rapidly being developed. Scant work, however, has focused on pericardial TB. Using cryopreserved specimens from a prior study of pericarditis, we compared PCR to culture and histopathology for the diagnosis of tuberculous pericarditis in 36 specimens of pericardial fluid and 19 specimens of pericardial tissue from 20 patients. Fluid and tissue were cultured on Lowenstein-Jensen and Middlebrook solid media and in BACTEC radiometric broth. Tissue specimens were stained with hematoxylin-eosin, Ziehl-Neelsen, auramine O, and Kinyoun stains and were examined for granuloma formation and acid-fast bacilli. PCR was performed with both fluid and tissue with IS6110-based primers specific for the Mycobacterium tuberculosis complex by published methods. Sixteen of the 20 patients had tuberculous pericarditis and 4 patients had other diagnoses. TB was correctly diagnosed by culture in 15 (93%) patients, by PCR in 13 (81%) patients, and by histology in 13 of 15 (87%) patients. PCR gave one false-positive result for a patient with Staphylococcus aureus pericarditis. Considering the individual specimens as the unit of analysis, M. tuberculosis was identified by culture in 30 of 43 specimens (70%) from patients with tuberculous pericarditis and by PCR in 14 of 28 specimens (50%) from patients with tuberculous pericarditis (P > 0.15). The sensitivity of PCR was higher with tissue specimens (12 of 15; 80%) than with fluid specimens (2 of 13; 15%; P = 0.002). In conclusion, the overall accuracy of PCR approached the results of conventional methods, although PCR was much faster. Therefore, PCR merits further development in this regard. The sensitivity of PCR with pericardial fluid was poor, and false-positive results with PCR remain a concern.