Key result
Patients with LQTS or CPVT had significantly higher levels of CD3+ and CD8+ T cells/mm2 in their stellate ganglia compared to healthy controls (P=0.0018 and P=0.0009, respectively).
Why the study?
Is there T-cell-mediated inflammatory activity in the stellate ganglia of patients with LQTS and CPVT compared to healthy controls?
Case-Control (n=22)
Is there T-cell-mediated inflammatory activity in the stellate ganglia of patients with LQTS and CPVT compared to healthy controls?
The presence of T-cell-mediated ganglionitis in the stellate ganglia of LQTS and CPVT patients suggests that local inflammation may boost adrenergic activity and trigger arrhythmias in genetically predisposed individuals.
Answers are grounded in this paper and cite their sources.
May indicate T-cell ganglionitis in LQTS/CPVT; hypothesis-generating and requires prospective validation before any clinical role.
BACKGROUND: Long QT syndrome (LQTS) and catecholaminergic polymorphic ventricular tachycardia (CPVT) are electric diseases characterized by catecholamine-induced ventricular arrhythmias. Unbalanced autonomic innervation of the heart may trigger arrhythmic events and stellectomy is a treatment option for patients who are resistant to pharmacological drugs. We analyzed left stellectomy specimens of LQTS and CPVT patients for signs of inflammatory activity. METHODS AND RESULTS: Stellate ganglia were retrieved from 12 consecutive patients (8F; 4 mol/L; mean age, 23.4±17 years) with either LQTS (n=8) or CPVT (n=4) and serious arrhythmias. Control stellate ganglia were obtained from 10 accidently deceased patients (6F; 4 mol/L; mean age, 35±17.6 years). Sections were immunostained with antibodies against T cells (CD3, CD4, CD8, CD20, Granzyme B), CD68 (macrophages), and HLA-DR (human leukocyte antigen-DR) antigens (activation marker). Immunopositive cells were quantified as cells/mm2. Polymerase chain reaction (PCR) and reverse transcription PCR were performed to screen for herpes virus DNA. Stellate ganglia of all 12 LQTS/CPVT patients revealed mild but distinct inflammatory infiltrates composed of T lymphocytes and macrophages, which were diffusely spread, but also clustered in small foci opposed to ganglion cells, interpreted as T-cell-mediated ganglionitis. Morphometric analysis showed that CD3+ and CD8+ T cells/mm2 were significantly higher in the ganglia of LQTS/CPVT cases than in healthy controls (P=0.0018 and P=0.0009, respectively). Molecular analyses were negative for neurotropic viruses. CONCLUSIONS: T-cell-mediated cytotoxicity toward ganglion cells may boost adrenergic activity as to trigger or enhance electric instability in LQTS/CPVT patients who are already genetically predisposed to arrhythmias.
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Rizzo et al. (2014) conducted a case-control in Long QT syndrome (LQTS) and catecholaminergic polymorphic ventricular tachycardia (CPVT) (n=22). LQTS or CPVT vs. Accidently deceased patients (healthy controls) was evaluated on CD3+ and CD8+ T cells/mm2 in stellate ganglia (p=P=0.0018 and P=0.0009). Patients with LQTS or CPVT had significantly higher levels of CD3+ and CD8+ T cells/mm2 in their stellate ganglia compared to healthy controls (P=0.0018 and P=0.0009, respectively).
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