Ventricular Tachycardia as the Initial Presentation of Tuberculous Myocarditis

Figures

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  Visual Summary. Tuberculous Myocarditis Presenting With Sustained Monomorphic Ventricular Tachycardia Multimodality imaging with cardiac magnetic resonance and [18F]FDG PET/CT demonstrated active granulomatous myocardial inflammation with extracardiac lymphadenopathy. Delayed lymph node culture confirmed Mycobacterium tuberculosis, allowing definitive diagnosis and targeted therapy. CMR = cardiac magnetic resonance; LGE = late gadolinium enhancement; [18F]FDG PET/CT = fluorodeoxyglucose positron emission tomography–computed tomography; ICD = implantable cardioverter-defibrillator; MMVT = monomorphic ventricular tachycardia.

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  Figure 1. Admission Electrocardiogram 12-lead electrocardiogram on admission showing a regular wide-complex tachycardia at 150 beats/min with right bundle branch block morphology, superior right-axis deviation, negative precordial transition (R to S) in lead V3, and atrioventricular dissociation, consistent with sustained monomorphic ventricular tachycardia of inferolateral-apical origin.

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  Figure 2. Chest Radiography at Presentation Chest radiography showing normal cardiothoracic index and marked bilateral mediastinal widening. No pleural effusion or signs of pulmonary vascular redistribution are present.

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  Figure 3. Postconversion Electrocardiogram Electrocardiogram after pharmacologic cardioversion showing sinus rhythm at 100 beats/min, PR interval of 160 ms, narrow QRS complexes (80 ms), flattened T waves in leads V4 to V6, normal R-wave progression, normal corrected QT interval (QTc 430 ms, Bazett), and frequent monomorphic premature ventricular complexes with an inferolateral axis.

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  Figure 4. Cardiac Magnetic Resonance During the Acute Phase (A) Late gadolinium enhancement images in short-axis views demonstrating a nonischemic pattern with intramyocardial septal and inferoseptal enhancement forming the characteristic “hook sign” (red arrow), as well as subepicardial enhancement in the anterior, anterolateral, lateral, and inferolateral mid-ventricular segments. (B) Native T1 mapping (top) in basal, mid, and apical short-axis slices showing globally (1,099 ms) and septally (1,190 ms) increased values, consistent with myocardial fibrosis (normal <1,050 ms). T2 mapping (bottom) demonstrates patchy myocardial edema with increased T2 values (up to 70 ms; normal <55 ms).

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  Figure 5. [18F]FDG PET/CT During the Acute Phase Fused [18F]FDG PET/CT images in coronal (top left), axial (top right), and short-axis (bottom) planes demonstrating extensive heterogeneous myocardial uptake involving the anterior, anterolateral, mid-septal, and basal septal regions (SUVmax = 12). Additional focal uptake is observed in the right ventricular outflow tract and pulmonary infundibulum. Hypermetabolic supraclavicular, right paratracheal, and subcarinal lymphadenopathy are present (SUVmax = 28). No pulmonary, pleural, or pericardial uptake is observed. [18F]FDG PET/CT = fluorodeoxyglucose positron emission tomography–computed tomography.

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  Figure 6. Supraclavicular Lymph Node Biopsy Hematoxylin and eosin–stained section of a right supraclavicular lymph node demonstrating nonnecrotizing granulomatous lymphadenitis (red arrow) with multinucleated giant cells of Langhans type (green arrow).

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  Figure 7. Catheter Ablation of Ventricular Tachycardia (A) Endocardial activation map of the right and left ventricles during sustained monomorphic ventricular tachycardia showing a focal activation pattern with earliest activation in the apical septal region of the right ventricle. The earliest endocardial electrogram precedes QRS onset by only 5 ms, suggesting an intramyocardial focus or re-entry. Radiofrequency applications delivered from this region and the opposing left ventricular aspect successfully terminated the arrhythmia (red circle). Additional ablation was performed targeting late potentials in the septal right ventricular outflow tract adjacent to the basal septal intramyocardial scar identified on cardiac magnetic resonance (green circle). A second ventricular tachycardia was inducible but was nonsustained and not reproducibly mappable. (B) ECG of the induced ventricular tachycardia during the electrophysiology study, showing a morphology slightly different from the clinical tachycardia, characterized by a superior axis, left bundle branch block pattern, and negative precordial concordance, consistent with a different exit site from the same septoapical arrhythmic substrate.

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  Figure 8. Follow-Up Cardiac Magnetic Resonance at 12 Months Late gadolinium enhancement images in short-axis views demonstrating a marked reduction in the extent, thickness, and intensity of both intramyocardial and subepicardial enhancement compared with the acute phase (red arrow).

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  Figure 9. Follow-Up [18F]FDG PET/CT at 12 months (A) Maximum intensity projection (left) and fused coronal images (right) demonstrating the absence of significant myocardial or lymph node uptake. (B) Fused axial image showing near-complete resolution of myocardial hypermetabolic activity (SUVmax = 1.84) and marked reduction of lymphadenopathy (SUVmax = 3.7). Myocardial metabolic activity is comparable to blood pool activity measured in the left atrium. [18F]FDG PET/CT = fluorodeoxyglucose positron emission tomography–computed tomography.