Sustained quality-of-life improvement post-cryoballoon ablation in patients with paroxysmal atrial fibrillation: Results from the STOP-AF Post-Approval Study.
Patients with PAF were more likely to receive treatment with amiodarone (31.6% vs 13.8%, p < 0.001) and antiplatelet agents (54.1% vs 42.5%, p = 0.041) but less likely to receive treatment with renin-angiotensin system blockers (52.3% vs 64.9%, p = 0.021) and anticoagulants (33.3% vs 50%, p = 0.003) compared with patients with N-PAF at discharge.
Parkinson disease (PD), pure autonomic failure (PAF), and multiple system atrophy (MSA) are characterized by intra-cerebral deposition of the protein alpha-synuclein and are termed synucleinopathies.
While patients with PD, DLB, and MSA show both central and peripheral nervous system involvement of α-synuclein pathology, pure autonomic failure (PAF) is a condition characterized by generalized dysregulation of the autonomic nervous system with neuronal cytoplasmic α-synuclein inclusions in the peripheral autonomic small nerve fibers.
Patients with TIMP-1 < 107 ng/mL and no variant allele (GG) at rs10033464 had lower recurrence rates compared with other groups in those with paroxysmal AF (logrank; P = .007), whereas there was no significant difference among those patients with persistent forms of AF.
There were significant differences in MFAP4 levels based on clinical group, with a gradient from control (1.71 ±0.53 ng/ml) to PAF (1.98 ±0.53 ng/ml) to PersAF (2.09 ±0.76 ng/ml) (<i>p</i> < 0.01).
Among 1514 patients with AF on warfarin therapy (75±10 years; 42% women; CHA <sub>2</sub> DS <sub>2</sub>- VAS c 3.9±1.7), those most burdened with warfarin therapy were younger and more likely to be women, have paroxysmal AF , and to be treated with antiarrhythmic drugs.
In addition, p-AF can induce cardiomyocyte fibrosis remodeling and increase MMP-9 expression, and p-AF also increases atrial intracardiac waveform activity by prolonging P<sub>max</sub>, P<sub>min,</sub> PWD, and AERPd and shortening AERP.
This study could neither confirm that EAT-V was predictive of recurrence of supraventricular arrhythmias in patients undergoing a hybrid AF ablation, nor that EAT-V was different between patients with paroxysmal AF and persistent and long-standing persistent AF.
Paroxysmal atrial fibrillation (AF) can be caused by gain-of-function mutations in genes, encoding the cardiac potassium channel subunits KCNJ2, KCNE1, and KCNH2 that mediate the repolarizing potassium currents I<sub>k1</sub>, I<sub>ks</sub>, and I<sub>kr</sub>, respectively.
We genotyped ZFHX3 SNP rs2106261 and compared the minor (T) allele frequency between 362 paroxysmal AF (PAF) patients underwent pulmonary vein isolation (PVI) and 627 non-AF controls.