Myocarditis with concomitant tuberculosis infection presenting with solitary ventricular tachycardia: a case report

Abstract

Background: Myocarditis is an infrequent extrapulmonary manifestation of tuberculosis that confers an unfavourable prognosis.

Case summary: A 36-year-old man presented to the hospital with palpitations and dyspnoea. Tests revealed the presence of non-sustained ventricular tachycardia, with mild elevation of troponin and C-reactive protein levels. Coronary angiography showed normal results. A cardiac magnetic resonance (CMR) showed moderate hypertrophy, preserved ejection fraction, and an extensive multi-segmental pattern of fibrosis and oedema. An ¹⁸F-fluorodeoxyglucose positron emission tomography-computed tomography (¹⁸F-FDG-PET-CT) scan revealed multiple hypermetabolic adenopathies and patchy cardiac uptake. A tuberculin skin test and interferon-gamma release assay were both positive. An endomyocardial biopsy (EMB) showed inflammation without granulomas; and microbiological stains were negative. Biopsy of an adenopathy revealed the presence of multiple necrotizing granulomas with Langhans cells. Based on the test results and clinical presentation, the suspected diagnosis was tuberculous myocarditis. Treatment with anti-tuberculosis drugs was started. One month later, the presence of mycobacterium tuberculosis (MT) was detected in the lymph node culture. At 7 months of follow-up, the patient remains asymptomatic, ventricular arrhythmias have ceased, and radiological signs of inflammation have resolved.

Discussion: Ventricular arrhythmia is one of the clinical manifestations of tuberculous myocarditis. Cardiac magnetic resonance and ¹⁸F-FDG-PET-CT imaging are an essential component of the non-invasive evaluation of inflammatory cardiomyopathy. However, a confirmatory biopsy may be required to identify potentially treatable aetiologies. Although the diagnosis of tuberculous myocarditis requires an isolation of MT by staining or culture in EMB, the diagnostic yield is very low. For this reason, extra-cardiac findings may provide the definitive diagnostic clue.

Keywords: Cardiac magnetic resonance; Case report; Myocarditis; Positron emission tomography; Tuberculosis; Ventricular tachycardia.

Figure 1

Initial electrocardiogram and electrocardiogram during tachycardia. (A) Electrocardiogram at admission showing negative T waves in the inferior leads. (B) Electrocardiogram on Day 7 shows a monomorphic non-sustained ventricular tachycardia with a superior axis, left bundle blanch block morphology, and transition at V5, suggesting an inferior-mid-apical septum origin. ECG, electrocardiogram.

Figure 2

Chest X-ray at admission. Anteroposterior supine chest X-ray performed with a portable machine on Day 0 showed normal results with no signs of vascular redistribution or notable alterations in the lung parenchyma.

Figure 3

Cardiac magnetic resonance findings performed on Day 7 of admission (acute phase). (A) The late gadolinium enhancement in short-axis view shows a non-ischaemic pattern with diffuse patchy hyper-enhancement in the anteroseptal basal wall (red arrows) and in the mid inferoseptal and septal apical wall (yellow arrows). (B) Quantitative T2 map in the basal, mid, and apical short axis, respectively. The T2 mapping sequence shows elevated values of T2 time in the anteroseptal (64 ms) and inferoseptal (77 ms) segments consistent with the presence of myocardial oedema (normal <55 ms). CMR, cardiac magnetic resonance.

Figure 4

Comparative ¹⁸F-fluorodeoxyglucose positron emission tomography–computed tomography findings (baseline and follow-up). (A) ¹⁸F-fluorodeoxyglucose positron emission tomography images (anterior view in the left, and right semilateral in the right) performed on Day 10 showing the distribution zones of uptake of the radiotracer ¹⁸F-fluorodeoxyglucose: multiple supra- and infra-diaphragmatic hypermetabolic adenopathies (blue arrows) and patchy cardiac uptake (green arrows). (B) In these ¹⁸F-fluorodeoxyglucose positron emission tomography–computed tomography images, we can identify one of the paratracheal hypermetabolic adenopathies (blue arrow) and the myocardial uptake in the septal region (green arrow). (C) ¹⁸F-fluorodeoxyglucose positron emission tomography performed after 7 months under anti-tuberculosis treatment shows a complete resolution of the uptakes. ¹⁸F-FDG-PET–CT, ¹⁸F-fluorodeoxyglucose positron emission tomography–computed tomography.

Figure 4

Comparative ¹⁸F-fluorodeoxyglucose positron emission tomography–computed tomography findings (baseline and follow-up). (A) ¹⁸F-fluorodeoxyglucose positron emission tomography images (anterior view in the left, and right semilateral in the right) performed on Day 10 showing the distribution zones of uptake of the radiotracer ¹⁸F-fluorodeoxyglucose: multiple supra- and infra-diaphragmatic hypermetabolic adenopathies (blue arrows) and patchy cardiac uptake (green arrows). (B) In these ¹⁸F-fluorodeoxyglucose positron emission tomography–computed tomography images, we can identify one of the paratracheal hypermetabolic adenopathies (blue arrow) and the myocardial uptake in the septal region (green arrow). (C) ¹⁸F-fluorodeoxyglucose positron emission tomography performed after 7 months under anti-tuberculosis treatment shows a complete resolution of the uptakes. ¹⁸F-FDG-PET–CT, ¹⁸F-fluorodeoxyglucose positron emission tomography–computed tomography.

Figure 5

Supraclavicular adenopathy biopsy. Lymph node with effacement of the node architecture at the expense of multiple granulomas and occasional multinucleated giant cells (Langhans cells).

Figure 6

Comparative CMR findings (baseline and follow-up). (A) Baseline: The LGE in short-axis view (A11) and A4C view (A12) show a non-ischaemic pattern with diffuse patchy hyper-enhancement in the anteroseptal basal wall (red arrows) and in the mid inferoseptal and septal apical wall (yellow arrows). Quantitative T2 map in the basal and mid short axis, respectively (A2). The T2 mapping sequence shows elevated values of T2 time in the anteroseptal (64 ms) and inferoseptal (77 ms) segments consistent with the presence of myocardial oedema (normal <55 ms). (B) Follow-up: after 7 months with anti-tuberculosis treatment, CMR shows a decrease in transmurality and extension of LGE in short-axis view (B11) and A4C view (B12) both in the anteroseptal basal wall (red arrows) and in the mid inferoseptal and septal apical wall (yellow arrows). A resolution of the myocardial oedema is also observed compared with the acute phase (B2). The T2 mapping sequence shows normal values of T2 time in the anteroseptal (48 ms) and inferoseptal (52 ms) segments (normal <55 ms). CMR, cardiac magnetic resonance; LGE, late gadolinium enhancement; A4C, apical four chamber view.

Figure 6

Comparative CMR findings (baseline and follow-up). (A) Baseline: The LGE in short-axis view (A11) and A4C view (A12) show a non-ischaemic pattern with diffuse patchy hyper-enhancement in the anteroseptal basal wall (red arrows) and in the mid inferoseptal and septal apical wall (yellow arrows). Quantitative T2 map in the basal and mid short axis, respectively (A2). The T2 mapping sequence shows elevated values of T2 time in the anteroseptal (64 ms) and inferoseptal (77 ms) segments consistent with the presence of myocardial oedema (normal <55 ms). (B) Follow-up: after 7 months with anti-tuberculosis treatment, CMR shows a decrease in transmurality and extension of LGE in short-axis view (B11) and A4C view (B12) both in the anteroseptal basal wall (red arrows) and in the mid inferoseptal and septal apical wall (yellow arrows). A resolution of the myocardial oedema is also observed compared with the acute phase (B2). The T2 mapping sequence shows normal values of T2 time in the anteroseptal (48 ms) and inferoseptal (52 ms) segments (normal <55 ms). CMR, cardiac magnetic resonance; LGE, late gadolinium enhancement; A4C, apical four chamber view.