Peripheral arterial tone during active standing.

Active standing test is clinically used to detect inadequate sympathetic nervous system response to the orthostasis. Peripheral arterial tone (PAT) is a recently developed technology whereby sympathetic activity can be measured through monitoring the digit arterial pulsatile volume. We aimed to determine the response of PAT to the orthostasis. The PAT and short-time frequency domain heart rate variability (HRV) were simultaneously measured during a 5.5-min active standing test in volunteers. The endpoints were changes in the PAT and ratio of low frequency to high frequency (LH/HF) before and after the postural changes: sitting→standing→sitting again. The blood pressure (BP) was constant throughout the test while the heart rate increased during standing in 54 participants. The natural logarithm of the mean LF/HF increased in the standing position (sitting, standing, and sitting again, mean±standard deviation, 1.3±1.04, 1.73±1.15, and 1.51±0.94; p=0.006), and the natural logarithm of its peak value was the highest also while standing (2.58±1.19, 3.08±1.2, and 2.85±1.05; p=0.007). The mean PAT (487.5±277.7, 314.5±180.4, and 458.1±244.3; p <0.001) and its nadir value (341.8±204.8, 189.4±119.2, and 264.3±157.6; p <0.001) declined during standing, and reascended after sitting again. The percent change before and after the standing in mean PAT was not correlated with that of the mean LF/HF. In conclusion, the PAT changed independently of and inversely with the LF/HF during the orthostatic test while the BP remained constant, possibly reflecting peripheral vasocontraction needed for the BP homeostasis.

Minor allele of GJA1 gene polymorphism is associated with higher heart rate during atrial fibrillation.

Atrial fibrillation (AF) tachycardia causes heart failure and requires more attention. The genetic background of individual heart rate (HR) variations during AF are unclear. We hypothesized that HR-associated single nucleotide polymorphisms (SNPs) reported in Genome-Wide Association Studies (GWAS) are also associated with HR during AF. We enrolled patients with persistent AF (311 for screening and 146 for replication) who underwent AF ablation and were genotyped for the 21 h-associated SNPs reported in GWAS. The patients underwent 24-h Holter monitoring before AF ablation and electrophysiological study after AF ablation during sinus rhythm. Only the GJA1 SNP rs1015451 (T>C) was significantly associated with total HR (TT 110,643 ± 17,542 beats/day, TC 116,350 ± 19,060 beats/day, CC 122,163 ± 25,684 beats/day, P = 8.5 × 10-4). We also confirmed this significant association in the replication set. The intra-atrial conduction was faster in AF patients with the GJA1 minor allele than in those without it. Multivariate analysis revealed the presence of a GJA1 SNP rs1015451 additive model, female gender, lower left ventricular ejection fraction, and higher 1:1 atrioventricular nodal conduction were independently associated with higher HR during AF. The GJA1 SNP might be a new genetic marker for AF tachycardia.

Cardiac electrophysiological characteristics of silent paroxysmal atrial fibrillation: What causes asymptomaticity?

BACKGROUND: A diagnosis of silent paroxysmal atrial fibrillation (AF) is highly challenging due to its asymptomatic and intermittent nature. The goal of the present study was to clarify its asymptomaticity with the use of a comprehensive electrophysiological approach. METHODS: We prospectively compared (a) 24-hour Holter monitoring data, (b) invasive cardiac electrophysiological properties, (c) AF inducibility, and (d) outcome of radiofrequency catheter ablation between patients with symptomatic paroxysmal AF and those with silent paroxysmal AF, defined as transient asymptomatic AF detected by chance. RESULTS: Patients with silent paroxysmal AF (N = 57) were more likely than patients with symptomatic paroxysmal AF (N = 282) to be male (75.4% vs 56.7%; P = .009), and to have a previous stroke (17.5% vs 6.7%; P = .008), more prolonged atrio-His interval (114.9 ± 29.1 vs 105.5 ± 24.1 ms; P = .01), longer atrioventricular nodal effective refractory period (352.3 ± 103 vs 318.2 ± 77.2 ms; P = .007), slower Wenckebach cycle length (488.5 ± 83.9 vs 443.3 ± 74.9 ms; P < .001), and lower maximum heart rate during AF (128.7 ± 31.9 vs 143.9 ± 29.6 beats/min; P = .02). Atrial ectopy (median [interquartile range], 385 [88, 2430] vs 207 [73.8, 870.8] beats/24 h; P = .02) and pharmacological AF induction (66.7% vs 43.2%; P = .02) were more common in silent paroxysmal AF patients. There was no difference in the 1-year freedom from AF following the ablation between the two patient groups. CONCLUSIONS: The more attenuated atrioventricular conduction properties in silent paroxysmal AF patients may explain their asymptomatic nature, and their higher likelihood of atrial arrhythmias may increase the chance to detect AF episodes. Whether or not they benefit from catheter ablation is uncertain.