Patients with Brugada syndrome exhibited enhanced presynaptic norepinephrine recycling compared to healthy controls (92.9 vs 69.1 mL/g; P<0.05), with preserved postsynaptic beta-adrenoceptor density.
Case-Control (n=9)
Does myocardial presynaptic and postsynaptic sympathetic function differ in patients with Brugada syndrome compared to healthy controls?
Patients with Brugada syndrome exhibit enhanced presynaptic norepinephrine recycling with preserved beta-adrenoceptor density, supporting the hypothesis of an underlying autonomic dysfunction.
Absolute Event Rate: 92.9% vs 69.1%
p-value: p=<0.05
BACKGROUND: Life-threatening ventricular tachyarrhythmias can occur in young patients without structural heart disease (idiopathic forms). In many patients, these are typically triggered by an increased sympathetic tone, eg, by physical or mental stress. In contrast, in Brugada syndrome, ventricular tachyarrhythmias more often occur during rest or sleep when the vagal tone is predominant. Furthermore, adrenergic agonists can reduce the level of ST-segment elevation, whereas it is increased by parasympathetic agonists or adrenergic antagonists. The aim of this study was to investigate presynaptic and postsynaptic myocardial sympathetic function in patients with Brugada syndrome. METHODS AND RESULTS: Nine patients with Brugada syndrome (6 male, 3 female; age, 41+/-13 years) were enrolled in this study. The cardiac autonomic nervous system was assessed noninvasively, quantifying myocardial presynaptic and postsynaptic sympathetic function by means of positron emission tomography with the norepinephrine analogue 11C-Hydroxyephedrine (11C-HED) and the nonselective beta-blocker 11C-CGP 12177 (11C-CGP). Presynaptic sympathetic norepinephrine recycling, assessed by 11C-HED, was globally increased in patients with Brugada syndrome compared with a group of age-matched healthy control subjects (92.9+/-16.2 mL/g versus 69.1+/-14.2 mL/g; P<0.05), whereas postsynaptic beta-adrenoceptor density, assessed by 11C-CGP, was similar in patients and control subjects (10.4+/-6.7 pmol/g versus 10.2+/-2.9 pmol/g; P=NS). CONCLUSIONS: The present study on autonomic innervation in Brugada syndrome describes an enhanced presynaptic norepinephrine recycling with preserved beta-adrenoceptor density, further supporting the hypothesis of an autonomic dysfunction in Brugada syndrome. This is a further step toward the understanding of the pathophysiology of the disease with potential future impact on therapeutic strategies.
Kies et al. (2004) conducted a case-control in Brugada syndrome (n=9). Brugada syndrome vs. Age-matched healthy control subjects was evaluated on Presynaptic sympathetic norepinephrine recycling assessed by 11C-HED (p=<0.05). Patients with Brugada syndrome exhibited enhanced presynaptic norepinephrine recycling compared to healthy controls (92.9 vs 69.1 mL/g; P<0.05), with preserved postsynaptic beta-adrenoceptor density.