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CASE SERIES
Year : 2017  |  Volume : 6  |  Issue : 1  |  Page : 111-115

Tuberculous myocarditis is not always fatal: Report of three confirmed cases with uneventful outcome


1 College of Medicine, King Saud University for Health Sciences, Riyadh, Saudi Arabia
2 Department of Medicine, Pulmonary Division, King Saud University for Health Sciences, Riyadh, Saudi Arabia

Date of Web Publication10-Mar-2017

Correspondence Address:
Hamdan AL-Jahdali
Professor of Medicine, King Saud University for Health Sciences, Adjunct Professor McGill University, Head of Pulmonary Division, Medical Director of Sleep Disorders Center, Medical Department, King Abdulaziz Medical City, PO Box 22490, Riyadh 11426
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijmy.ijmy_9_17

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  Abstract 

Tuberculosis (TB) is a leading cause of death worldwide. It can affect any organ. However, cardiac involvement is extremely rare. Anti-TB therapy has been proved to be effective and curative in majority of TB cases except TB myocarditis, where it is found to be fatal. We describe three cases with confirmed TB with impaired left ventricular systolic function and low ejection fraction. All three cases improved clinically and left ventricular function returned to normal within a few weeks after the commencement of TB therapy.

Keywords: Cardiomyopathy takotsubo cardiomyopathy, heart failure, myocarditis, tuberculosis


How to cite this article:
Al-Jahdali F, Al-Harbi A, Baharoon S, Al-Gamdi M, AL-Jahdali H. Tuberculous myocarditis is not always fatal: Report of three confirmed cases with uneventful outcome. Int J Mycobacteriol 2017;6:111-5

How to cite this URL:
Al-Jahdali F, Al-Harbi A, Baharoon S, Al-Gamdi M, AL-Jahdali H. Tuberculous myocarditis is not always fatal: Report of three confirmed cases with uneventful outcome. Int J Mycobacteriol [serial online] 2017 [cited 2020 Aug 4];6:111-5. Available from: http://www.ijmyco.org/text.asp?2017/6/1/111/201902


  Introduction Top


Tuberculosis (TB) remains one of the most prevalent infections around the world. In 2014, worldwide, 9.6 million people are estimated to be infected and 1.5 million death because of TB.[1] Although TB can affect any organ in the body, it is generally believed that involvement of myocardium and cardiomyopathy is extremely rare. Only 0.14%–2% of TB patients developed cardiac involvement, mainly pericardium.[2],[3],[4] The exact mechanism of myocardial involvement is not clear. However, the common proposed mechanisms include hematogenous or lymphatic spread or directly from the contagious structures.[5] Three distinct forms of myocardial involvement recognized are miliary tubercles of the myocardium, diffuse myocardial infiltration, and nodular tubercles (tuberculomas) of the myocardium.[3],[5] Recently, the predominant mechanism behind left ventricular systolic dysfunction was presumed to be loss of left ventricular torsion; however, this needs to be confirmed.[6]

Cardiac involvement may present with pericarditis, rhythm disturbances such as atrial fibrillation, supraventricular tachycardia, ventricular arrhythmias, or varying degrees of conduction blocks or even sudden cardiac death.[6],[7],[8],[9] Myocardial involvement if not diagnosed early, may lead to death.[2],[10] In one study, only one case survived from 19 cases of cardiac TB diagnosed antemortem.[4] Literature reported an isolated involvement of myocardium in 25% while concomitant organ involvement was reported in 75% of cases, 56% pulmonary, 56% extrapulmonary, and 43% pericarditis.[3] Reported mortality rate is approximately 30%.[3] Most of the reported cases were in young immunocompetent individuals.[2],[3],[11]

Herein, we describe the clinical presentation and management of three cases with left ventricular impairment and TB.


  Case Reports Top


All these three cases were young, presented with concomitant confirmed pulmonary-disseminated TB, have documented positive TB culture, and documented left ventricular impairment and low ejection fractions (EFs), which improved and returned to normal a few months post anti-TB therapy [Table 1].
Table 1: Patient's characteristics

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Case 1

A 21-year-old man with no significant medical history presented to the emergency department with 3 weeks history of fever, productive cough associated with shortness of breath, orthopnea, paroxysmal nocturnal dyspnea. He denied any history of chest pain, syncope, or palpitations. Medical and surgical history was insignificant. On physical examination, the patient looked unwell. He was febrile (38.5°C), with a pulse rate of 138 beats/min, blood pressure of 114/86 mmHg, and respiratory rate of 28/min. Chest examination revealed left lower lobe crackles and dullness. Electrocardiogram (EKG) showed sinus tachycardia [Figure 1]. Chest X-ray (CXR) [Figure 2]a showed left lower lobe consolidation and bilateral pleural effusion, which was more prominent on the left. Computed tomography (CT) scan of the chest [Figure 2]b revealed bilateral airspace disease more on the left lower lobe, bilateral pleural effusions more on the left side with pleural thickening, and minimal pericardial effusion.
Figure 1: Case 1: Electrocardiogram showed sinus tachycardia and T-wave abnormalities.

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Figure 2: (a) Chest X-ray: Left lower lobe infiltration with pleural effusion, (b) computed tomography scan of the chest showing left lower lobe airspace disease and bilateral pleural effusion more over the left side.

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Echocardiogram (ECHO) [Figure 3] revealed a normal left ventricular wall thickness and moderate global hypokinesis of left ventricle. EF was 35%–45%. Liver function test (LFT) revealed albumin 33 g/dl, total bilirubin 31.3 mg/dl, alkaline phosphate 249 mg/dl, and alanine transaminase (ALT) 21 U/L. Erythrocyte sedimentation rate (ESR) 33 mm/h, hemoglobin (Hb)-152 g/dl, and Pro-BNP 530 pg/mL.
Figure 3: Chest X-ray showing right upper lobe consolidation and cavitation.

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Sputum for acid-fast bacilli (AFB) was negative 3 times. Abdominal ultrasound showed moderate hepatomegaly and splenomegaly with no ascites. Pleural fluid analysis revealed exudative effusion, total protein 49, lactate dehydrogenase 238, white blood cell (WBC) – 4/mm 3, lymphocytes 86%.

QuantiFERON (QTF) was positive. HIV nonreactive. Bronchoscopy was done. Bronchoalveolar lavage (BAL) was negative for AFB, but polymerase chain reaction (PCR) was positive for Mycobacterium tuberculosis, transbronchial lung biopsy revealed multiple interstitial and subpleural noncaseating, nonnecrotizing granuloma.

The patient was diagnosed as disseminated TB involving lungs, pleura, liver, and spleen. Patient was started on the standard four anti-TB drugs. Follow-up BAL culture was positive for M. tuberculosis and pansensitive organism. ECHO was repeated after 2 months and revealed normal EF (EF > 55).

Case 2

A 21-year-old man previously healthy presented to the emergency department with a history of recurrent fever, progressive dyspnea, and cough with yellowish sputum for 2 months. He received several courses of antibiotics without improvement. The patient does not have chest pain or hemoptysis but reported loss of weight and appetite. He has no other medical problems, denied any contact with TB cases. On examination, his vital signs were as following: Temperature: 36.6°C, respiratory rate: 25 breaths/min, heart rate: 112 beats/min, and blood pressure: 133/82 mmHg. On examination, the patient generally looked stable but required oxygen of 4–5 L to keep oxygen above 90% and bronchial breathing was noted over the right upper lobe of the chest. Initial laboratory test revealed WBC: 8.2/mm 3, Hb: 109 g/dl, platelets: 237/mm 3, blood urea nitrogen (BUN): 3.5 mg/dL, creatinine: 75, Na: 130/mEq, K: 3.6/mEq, Cl: 96/mEq, CO2: 23, glucose: 6.3, total bilirubin: 18, alkaline phosphate: 297 U/L, ALT: 10 U/L, aspartate transaminase: 76 U/L, ESR: 75 mm/h, C-reactive protein: 108.

CXR [Figure 3] shows right upper lobe consolidation and cavitation. The patient was admitted to the hospital with suspected pulmonary TB. The second-day sputum for AFB stain was positive, confirming suspicion of pulmonary TB. The patient was started on the standard four anti-TB drugs. HIV test was negative. Hepatitis C and B were negative. The patient's liver enzymes returned to normal, but the patient continued to have fever and tachycardia despite the treatment. Several septic workups were done for the patient and all were negative. Abdomen and pelvic CT showed no abscesses or other abnormalities. Because of tachycardia, EKG and ECHO were done. EKG revealed sinus tachycardia, ECHO [Figure 4] showed small pericardial effusions, moderate global hypokinesis of the left ventricle with moderate reduction of left ventricular systolic function, EF was 45%–50%, Pro-BNP 650 pg/mL. Cardiology suggested starting heart failure treatment and he was started on lisinopril 20 mg and metoprolol 12.5 mg twice a day. Sputum culture confirmed M. tuberculosis that is resistant to isoniazid (INH). INH was replaced by moxifloxacin. Patient gradually improved and was seen as follow-up in outpatient clinics. ECHO repeated approximately 2 months later, left ventricle was normal in size and thickness, EF >55%. Anti-heart failure was thereby discontinued.
Figure 4: Echocardiogram showing severely dilated left ventricle.

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Case 3

A 34-year-old female admitted to our hospital with main complaints of fever, cough, lower abdominal pain, and weight loss for a few months. She was seen in another hospital and was diagnosed as Crohn's disease and was started on prednisone, mesalamine, and azathioprine. On examination, the patient was looking unwell but conscious and oriented. Temperature: 38°C, respiratory rate: 22 breaths/min, heart rate: 107 beats/min, blood pressure: 107/65 mmHg, O2 saturation: 93% on room air.

Chest examination revealed diffuse right side crackles, heart examination showed tachycardia but was otherwise unremarkable. Abdominal examination revealed mild periumbilical tenderness. Laboratory test revealed WBC: 4.5 mm 3, Hb: 82 g/dl, platelet: 770 mm 3, BUN: 3.8 mg/dL, creatinine: 37, Na: 131 mEq, K: 3.8, glucose: 5.2, and LFT: normal. ESR: 72. Her initial CXR [Figure 5]a demonstrated airspace disease in the right hemithorax. CT scan [Figure 5]b of the chest showed right hemithorax consolidation. Bronchoscopy was done; transbronchial biopsy revealed necrotizing caseation granuloma. BAL revealed positive AFB Ziehl–Nelson stain. Patient was started on the standard four anti-TB drugs.
Figure 5: (a) Chest X-ray showing right hemithorax consolidation, (b) chest computed tomography showing airspace disease and tree in bud opacity.

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A few days later, the patient developed acute abdomen and hypotension. Abdominal CT revealed thickening of the terminal ileum and cecum, lymphadenopathy, and perforated bowel secondary to ileitis. Patient underwent laparotomy with ilium resection.

The patient postoperatively was tachycardiac and hypotensive and CXR revealed pulmonary congestion and bilateral pleural effusion. Patient was admitted to the Intensive Care Unit and was started on broad-spectrum antibiotic and supportive treatment. EKG revealed sinus tachycardia. ECHO revealed that left ventricle was normal in size, moderate to severe global hypokinesis of left ventricular with low EF: 25%–35%, Pro-BNP-887 pg/mL. Patient was started on anti-heart failure therapy.

The patient gradually recovered, culture confirmed M. tuberculosis with pansensitive organism. Patient received anti-TB as per standard recommendation for 9 months.

Repeated ECHO after 12 weeks revealed normal left ventricle function and size and EF >55%. The gastroenterologist believed that she has no Crohn's disease and her initial diagnosis was missed TB-ileitis. Over the course of 1-year follow-up, she had good recovery and had no recurrence of her gastrointestinal symptoms. Pathology of resected bowel revealed noncaseating granuloma, AFB stain was negative.


  Discussion Top


Although global incidence of TB is declining, TB remains one of the most prevalent infectious etiologies around the world. In 2014, worldwide, 9.6 million people were estimated to be infected and 1.5 million deaths occurred because of TB.[1] TB can affect any organ in the body, but it is generally believed that cardiac involvement is less common and TB myocarditis and cardiomyopathy are extremely rare. Only 0.14%–2% of TB patients have cardiac involvement, mainly pericardium.[2],[3],[4] The exact mechanism of TB myocarditis is not clear; however, three possible mechanisms are proposed from hematogenous seeding, direct infection from infected pericardium, or by retrograde lymphatic drainage from the tuberculous mediastinal lymph node.[3],[4],[5],[12],[13]

Our three cases meet the definition of known clinical entity of a reversible acute left ventricular dysfunction (LVD) without any evidence of coronary artery obstruction but secondary to Mycobacterium myocarditis called takotsubo cardiomyopathy (TTC).[14]

All the patients from the cases we are reporting were very young from 20 to 32 years old. This is similar to many reported cases where it affects young individuals.[2],[4],[5],[8],[12],[13],[15],[16],[17] However, it has also been reported in older patients.[7],[18] Most of the reported cases were among immunocompetent patients.[2],[4] In our cases, only one patient was on immunosuppressive agent for presumed Crohn's disease developed acute pulmonary TB and acute bowel perforation. We believe she has TB ileitis that was misdiagnosed as Crohn's disease. We believe her presentation of disseminated TB and cardiomyopathy was the result of using immunosuppressive therapy and due to the delay in the diagnosis of TB. Endomyocardial biopsy for TB myocarditis is neither sensitive nor diagnostic even in cases with confirmed TB.[13],[18] Isolated involvement of myocardium is reported in 25% while concomitant organ involvement is reported in 75% of cases, 56% pulmonary, 56% extrapulmonary, and 43% pericarditis.[3] Mortality rate in almost 30%.[3] All of our cases have concomitant disseminated TB (involvement of at least two organs). All of our cases were diagnosed as LVD based on clinical confirmation of TB and reversibility of cardiac function to normal post anti-TB therapy. No endomyocardial biopsy performed. We believe in the right clinical context and when the diagnosis of TB is confirmed, endocardial biopsy may not be necessary. If TB is suspected as a cause of myocarditis, appropriate investigations such as chest CT, sputum for AFB stain, and culture should be performed and TB-PCR, QTF, bronchoscopy and BAL, transbronchial or endoscopic ultrasound-guided biopsies should be requested before considering endocardial biopsy.[13],[19] Cardiac magnetic resonance imaging (MRI) may help in the diagnosis of TB myocarditis. Several case reports demonstrated cardiac MRI's value in the diagnosis of TB myocarditis and endocarditis.[20],[21],[22],[23],[24]

TTC is a very serious disease and unfortunately if the diagnosis is missed or delayed, it can lead to fatal outcomes.[2],[4],[5],[7],[8],[10],[12],[17],[25] With increasing prevalence of TB, the possibility of potentially fatal myocardial TB must be considered. Two of our cases have short period of symptoms with a modest reduction of LVD while in the third case, the diagnosis was delayed for a few months, which may explain the severe LVD. None of our cases developed cardiac arrhythmias, and ECHO was requested to search for the cause of dyspnea and sinus tachycardia. Good response to antituberculosis therapy was reported in 68%.[3] The favorable outcome of LVD may be because the clinical presentations of our cases were highly suggestive of TB and diagnosis and initiation of treatment were rapid. Similar to our experiences, excellent outcome with complete reversibility of LVD has been reported with early commencement of anti-TB.[5],[13],[22],[23],[26] Paradoxical worsening post TB has been proposed as a possible cause of LVD in one case.[2] We could not confirm this in our cases as we do not have a baseline ECHO in all cases before the commencement of anti-TB.


  Conclusion Top


The clinician should have a high index of suspicion of myocarditis in any patient with unexplained tachycardia or signs of left ventricular failure or any arrhythmia in a patient with suspected or confirmed TB. Furthermore, in the right context where the patient is at high risk for TB and presents with an unexplained arrhythmia or congestive heart failure, TB should be suspected as the underlying cause. Misdiagnosis or delay in the diagnosis of TB myocarditis has portentous outcome.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
WHO. Global Tuberculosis Report 2. Saudi Arabia-Riyadh: WHO; 2015.  Back to cited text no. 1
    
2.
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Bansal M, Mehrotra R, Kasliwal RR. Loss of left ventricular torsion as the predominant mechanism of left ventricular systolic dysfunction in a patient with tubercular cardiomyopathy. Echocardiography 2012;29:E221-5.  Back to cited text no. 6
    
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Afzal A, Keohane M, Keeley E, Borzak S, Callender CW, Iannuzzi M. Myocarditis and pericarditis with tamponade associated with disseminated tuberculosis. Can J Cardiol 2000;16:519-21.  Back to cited text no. 9
    
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Rusev LR, Nikolov GS, Bindusov NI. Acute toxic myocarditis in pulmonary tuberculosis. Probl Tuberk 1961;39:23-8.  Back to cited text no. 11
    
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Behr G, Palin HC, Temperly JM. Myocardial tuberculosis. Br Med J 1977;1:951.  Back to cited text no. 12
    
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Farah Z, Beasley VE, Berry M, Coker RK, Kon OM. Two cases of culture proven Mycobacterium tuberculosis presenting with a broad-complex tachycardia and non-caseating granulomas. Respir Med Case Rep 2014;12:41-3.  Back to cited text no. 13
    
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Ha JH, Lee H, Park YJ, Kang HH, Lee SH, Moon HS. Takotsubo cardiomyopathy caused by pulmonary tuberculosis: A case report. Tuberc Respir Dis (Seoul) 2014;77:24-7.  Back to cited text no. 14
    
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Gupta MD, Yadav N, Palleda GM. Granulomatous tubercular myocarditis: A rare cause of heart failure in the young. Cardiol Young 2013;23:740-1.  Back to cited text no. 15
    
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Irdem A, Baspinar O, Küçükosmanoglu E. Dilated cardiomyopathy due to miliary tuberculosis. Anadolu Kardiyol Derg 2013;13:499-500.  Back to cited text no. 16
    
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Dada MA, Lazarus NG, Kharsany AB, Sturm AW. Sudden death caused by myocardial tuberculosis: Case report and review of the literature. Am J Forensic Med Pathol 2000;21:385-8.  Back to cited text no. 17
    
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Tanaka N, Takazawa K, Fujita M, Tamura S, Odani Y, Hirayama Y, et al. Adult case of isolated noncompaction of left ventricular myocardium revealed at hospitalization for tuberculous pleuritis. J Cardiol 1999;33:169-74.  Back to cited text no. 18
    
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Thachil A, Christopher J, Sastry BK, Reddy KN, Tourani VK, Hassan A, et al. Monomorphic ventricular tachycardia and mediastinal adenopathy due to granulomatous infiltration in patients with preserved ventricular function. J Am Coll Cardiol 2011;58:48-55.  Back to cited text no. 19
    
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Rodríguez E, Soler R, Juffé A, Salgado L. CT and MR findings in a calcified myocardial tuberculoma of the left ventricle. J Comput Assist Tomogr 2001;25:577-9.  Back to cited text no. 20
    
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Bhatia M. Myocarditis: Non invasive imaging of myocardial muscle in ventricular tachycardia by cardiac MRI. Indian Heart J 2014;66:731-2.  Back to cited text no. 21
    
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Syed FF, Aje A, Ntsekhe M, Mayosi BM, Moosa S, Tshifularo M, et al. Resolution of nodular myocardial tuberculosis demonstrated by contrast-enhanced magnetic resonance imaging. Cardiovasc J Afr 2008;19:198-9.  Back to cited text no. 22
    
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Breton G, Leclerc S, Longuet P, Leport C, Vildé JL, Laissy JP. Myocardial localisation of tuberculosis: The diagnostic value of cardiac MRI. Presse Med 2005;34:293-6.  Back to cited text no. 23
    
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Jagia P, Gulati GS, Sharma S, Goyal NK, Gaikwad S, Saxena A. MRI features of tuberculoma of the right atrial myocardium. Pediatr Radiol 2004;34:904-7.  Back to cited text no. 24
    
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Biedrzycki OJ, Baithun SI. TB-related sudden death (TBRSD) due to myocarditis complicating miliary TB: A case report and review of the literature. Am J Forensic Med Pathol 2006;27:335-6.  Back to cited text no. 25
    
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Everett RJ, Sheppard MN, Lefroy DC. Chest pain and palpitations: Taking a closer look. Circulation 2013;128:271-7.  Back to cited text no. 26
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
 
 
    Tables

  [Table 1]


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