Author + information
- Alladi Mohan, MD,
- Ajit Thachil, MD, DM,
- Gomathi Sundar, PG, PA,
- B.K.S. Sastry, MD, DM,
- Ashfaq Hasan, MD,
- C. Sridevi, MD, DNB and
- Calambur Narasimhan, MD, DM∗ ()
- ↵∗CARE Hospital, Department of Cardiac Electrophysiology, Road No. 1, Banjara Hills, Hyderabad, Telangana, India 500 034
Myocardial tuberculosis (TB) is an exceptionally rare form of extrapulmonary TB (1). It is a serious illness with varied clinical manifestations (conduction blocks, ventricular failure, malignant ventricular arrhythmias, and sudden cardiac death) and has been occasionally documented in case reports (2,3). In this report, we describe our experience in the clinical recognition and management of myocardial TB, associated with mediastinal and/or peripheral lymphadenopathy in 13 patients presenting with unexplained ventricular tachycardia (VT) or heart failure. None of these patients manifested constitutional symptoms or clinical features that were suggestive of TB. We believe that this entity is an under-recognized cause of ventricular arrhythmia and ventricular dysfunction that can be treated successfully.
The predominant symptom seen in 10 of the 13 patients was palpitations with or without pre-syncope. Eleven patients presented with sustained VT, and 2 patients presented with congestive heart failure. Electrocardiogram revealed right bundle branch block in 2 patients and nonspecific T-wave changes in 1 patient. The chest radiograph was normal in all patients. Echocardiogram revealed left ventricular dysfunction in 6 patients with no other significant abnormality evident. Coronary artery disease was ruled out in all adult patients. Mid-myocardial scar was present in 8 of the 10 patients in whom delayed enhancement cardiac magnetic resonance imaging was performed. Positron emission tomography/computed tomography (PET/CT) of the chest with 18-fluorodeoxyglucose revealed increased fluorodeoxyglucose uptake in the myocardium and lymph nodes in all patients.
Tuberculin skin test (5 tuberculin units) result was positive in 11 patients. Baseline erythrocyte sedimentation rate (first hour) was elevated in 10 patients. All patients were seronegative for human immunodeficiency virus. Serum angiotensin-converting enzyme levels were within normal limits in all patients. Biopsy specimens were sampled from those lymph nodes showing the highest metabolic activity on PET/CT scan. Histopathology revealed epithelioid granulomas in all patients and caseating necrosis in 8 patients. The diagnosis of TB was made by lymph node biopsy based on a positive Ziehl–Neelsen stain for acid-fast bacilli, Lowenstein–Jensen culture for Mycobacterium tuberculosis, and/or a positive TB polymerase chain reaction. Right ventricular endomyocardial biopsy was negative in all 5 patients in whom it was performed.
All patients received daily self-supervised standard anti-TB treatment comprising rifampicin, isoniazid, pyrazinamide, and ethambutol for the first 2 months (intensive phase), followed by rifampicin and isoniazid for the subsequent 7 to 10 months (continuation phase). The patients also received oral prednisolone (1 mg/kg/day) that was tapered over 3 months. All patients also received antiarrhythmic drugs and/or drugs for heart failure. An implantable cardioverter defibrillator was recommended in all patients who presented with VT. Radiofrequency catheter ablation was completed in 4 patients with incessant VT: before the diagnosis of TB in 1 patient and during anti-TB treatment in the remaining 3 patients. Patients were followed up at 1, 3, and 6 months after the initiation of anti-TB treatment and when clinically warranted. The response was assessed after the intensive phase of anti-TB treatment in terms of clinical improvement, change in ejection fraction by echocardiography, and change in 18-fluorodexoyglucose uptake by PET/CT.
There was significant improvement in ejection fraction (mean 46.7 ± 14.4% to 50.8 ± 16.1%; p = 0.009). All patients but 1 became free of VT. In a follow-up PET/CT (n = 11), abnormal metabolic activity resolved completely in the myocardium in 4 patients and in the lymph nodes in 9 patients (Table 1). There were no deaths.
Our observations suggest that TB can present as idiopathic VT or unexplained ventricular dysfunction; patients may not have constitutional symptoms. Biopsy targeting fluorodeoxyglucose-avid lymph nodes rather than endomyocardial biopsy is more useful in making a clinical diagnosis. It may be prudent to investigate all patients with unexplained VT or left ventricular dysfunction and lymphadenopathy for myocardial TB, especially in those areas where the prevalence of TB is high. By subjecting the biopsy specimen to mycobacterial culture, TB polymerase chain reaction and histopathologic examination will help in distinguishing between TB and sarcoidosis—another granulomatous condition that may present in a similar fashion (4). This report serves to highlight the fact that myocardial TB may be more common than believed. Early diagnosis is important to prevent morbidity and mortality.
Please note: Dr. Narasimhan has received research grants from Biosense Webster, Inc., Medtronic, Inc., and St. Jude Medical, Inc.; and a fellowship grant from Medtronic, Inc. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. The authors thank John G. Cleland, Foundation Chair of Cardiology at the University of Hull, for useful suggestions.
- American College of Cardiology Foundation