Our data indicate that acupuncture treatment prevents arrhythmic recurrences after cardioversion in patients with persistent AF. This minimally invasive procedure was safe and well tolerated.

Endothelial dysfunction and underperfusion of exercising muscle contribute to exercise intolerance, hyperventilation, and breathlessness in atrial fibrillation (AF). Cardioversion (CV) improves endothelial function and exercise performance. We examined whether CV is equally beneficial in diabetes and hypertension, diseases that cause endothelial dysfunction and are often associated with AF. Cardiopulmonary exercise and pulmonary and endothelial (brachial artery flow-mediated dilation) function were tested before and after CV in patients with AF alone (n ϭ 18, group 1) or AF with hypertension (n ϭ 19, group 2) or diabetes (n ϭ 19, group 3). Compared with group 1, peak exercise workload, O2 consumption (V O2), O2 pulse, aerobic efficiency (⌬V O2/⌬WR), and ratio of brachial diameter changes to flow changes (⌬D/⌬F) were reduced in group 2 and, to a greater extent, in group 3; exercise ventilation efficiency (V E/V CO2 slope) and dead space-to-tidal volume ratio (VD/VT) were similar among groups. CV had less effect on peak workload (ϩ7% vs. ϩ18%), peak V O2 (ϩ12% vs. ϩ17%), O2 pulse (ϩ33% vs. ϩ50%), ⌬V O2/⌬WR (ϩ7% vs. ϩ12%), V E/V CO2 slope (Ϫ6% vs. Ϫ12%), ⌬D/⌬F (ϩ7% vs. ϩ10%), and breathlessness (Borg scale) in group 2 than in group 1 and was ineffective in group 3. The antioxidant vitamin C, tested in eight additional patients in each cohort, improved flow-mediated dilation in groups 1 and 2 before, but not after, CV and was ineffective in group 3, suggesting that the oxidative injury is least in lone AF, greater in hypertension with AF, and greater still in diabetes with AF. Comorbidities that impair endothelial activity worsen endothelial dysfunction and exercise intolerance in AF. The advantages of CV appear to be inversely related to the extent of the underlying oxidative injury.arrhythmias; endothelium; exercise ATRIAL FIBRILLATION (AF) impairs endothelial function and downregulates nitric oxide (NO) production (3, 10, 27). Exercise correlates of these dysfunctions are underperfusion of working muscle, hyperventilation, and breathlessness (10). These findings are consistent with the concept that, during exercise, an endothelium-mediated vasodilation modulates neurogenic vasoconstriction, increases arterial conductance, and upregulates muscle perfusion (6,12,16). Conversion to sinus rhythm [i.e., cardioversion (CV)] is beneficial in this respect (10). Irregular pulsatile blood flow in AF may impair the endothelial responsiveness to vascular shear stress, and loss of the cyclic stretch of atrial endocardial cells may decrease expression of NO synthase (3). Restoration of a regular flow regimen and atrial contactile activity with CV normalizes the endothelial physiology.Hypertension and diabetes cause endothelial dysfunction (13,20,23,26). Because AF is not uncommonly associated with high blood pressure and diabetes, we considered the pathophysiological and clinical significance of this association to investigate whether the improvement of endothelial function with CV, its exercise pathophysiological correlates, ...

Lone atrial fibrillation may be associated with daily life disability and exercise limitation. The extracardiac pathophysiology of these effects is poorly explored. In 35 subjects with lone atrial fibrillation (mean age 67 Ϯ 7 yr), we investigated pulmonary function, symptom-limited cardiopulmonary exercise performance, muscle ergoreflex (handgrip exercise) contribution to ventilation, and brachial artery flow-mediated dilation (as a measure of endothelial function) before and after (average interval 20 Ϯ 5 days) restoring sinus rhythm with external cardioversion. Respiratory volumes and lung diffusing capacity at rest were within normal limits during both atrial fibrillation and after restoring sinus rhythm. Cardioversion was associated with the following changes: a decrease of the slope of exercise ventilation vs. CO2 production (from 35 Ϯ 5 to 29 Ϯ 3; P Ͻ 0.01) and of dyspnea sensation (Borg score from 4 to 2) and an increase of peak oxygen uptake (V O2; from 16 Ϯ 4 to 20 Ϯ 5 ml⅐ min Ϫ1 ⅐ kg Ϫ1 ; P Ͻ 0.01), V O2 at anaerobic threshold (from 11 Ϯ 2 to 13 Ϯ 2 ml⅐ min Ϫ1 ⅐ kg Ϫ1 ; P Ͻ 0.05), and O2 pulse (from 8 Ϯ 3 to 11 Ϯ 3 ml/beat; P Ͻ 0.01). After cardioversion, the observed improvement in ventilatory efficiency was accompanied by a significant peak end-tidal CO2 increase (from 33 Ϯ 2 to 37 Ϯ 2 mmHg; P Ͻ 0.01) and no changes in dead space-to-tidal volume ratio (from 0.23 Ϯ 0.03 to 0.23 Ϯ 0.02; P ϭ not significant). In addition, the ergoreflex contribution to ventilation was remarkably attenuated, and the brachial artery flow-mediated dilatation was significantly augmented (from 0.32 Ϯ 0.07 to 0.42 Ϯ 0.08 mm; P Ͻ 0.01). Ten patients had atrial fibrillation relapse and, compared with values after restoration of regular sinus rhythm, invariably showed worsening of endothelial function, exercise ventilatory efficiency, and muscle ergoreflex contribution to ventilation. In subjects with lone atrial fibrillation, an impairment in ventilatory efficiency appears to be involved in the pathophysiology of exercise limitation, and to be primarily related with a demodulated peripheral control of ventilation. lone atrial fibrillation; exercise; ventilation; dyspnea LONE ATRIAL FIBRILLATION is the most common sustained arrhythmia encountered in clinical practice (11,39). A reduced maximal exercise oxygen uptake (V O 2 ; see Refs. 12, 21, and 23) is a frequent finding, and exercise intolerance is not an uncommon daily life disability factor (19,22). As to the pathophysiological bases of physical limitation, previous studies have extensively investigated the putative role of hemodynamic abnormalities associated with atrial fibrillation (3,8,10,36). Exercise performance, however, not only depends on the cardiovascular system function but on any organ system involved in O 2 transport, including the respiratory system, skeletal muscles, hormonal and neural feedback control system for breathing, cardiac output, blood pressure, and blood volume. A contribution of peripheral changes resulting from this arrhythmia to the pathogenes...

No abstract

No abstract

Bone marrow transplantation (BMT) is often complicated by acute graft‐versus‐host disease (aGVHD). In patients transplanted with an HLA‐matched donor the occurrence of this complication is believed to be favoured by disparities at the minor histocompatibility antigens (mHA). However, few of these polymorphic molecules have been identified. We sought to determine whether donor/recipient incompatibility for HPA‐1, HPA‐2, HPA‐3, HPA‐5 or CD31 (codon 125) antigens represented a risk factor for aGVHD and genotyped these antigens in 70 bone marrow donors and their HLA‐identical recipients. All patients were children who received BMT for haematological malignancies at a single institution according to well‐defined therapy protocols. Statistical analysis showed that incompatibility for CD31 (codon 125) was a risk factor for grade II–IV aGVHD in the overall patient population, whereas HPA‐3 incompatibility predicted aGVHD occurrence in HLA‐A2 patients only. The magnitude of the aGVHD risk was directly related to the number of HPA/CD31 incompatibilities. No correlation was found between non‐identity for HPA/CD31 and aGVHD. Since incompatibility but not non‐identity for CD31 or HPA‐3 was a risk factor for aGVHD, we suggest that allelic variants of these molecules can serve as mHA in BMT recipients from HLA‐identical donors.

No abstract

The present study demonstrates that in patients with persistent atrial fibrillation and preserved LVEF, CRP level is an independent predictor of atrial fibrillation subacute recurrence rate, whereas none of the indices of atrial dysfunction is associated with arrhythmic outcome. NT-proBNP levels reflect, instead, the hemodynamic alterations secondary to arrhythmia presence.