Search

BACKGROUND The respiratory instability frequently observed in advanced heart failure (HF) is likely to mirror the clinical status of worsening HF. The present multicenter study was conducted to examine whether the noble respiratory stability index (RSI), a quantitative measure of respiratory instability, reflects the recovery process from HF decompensation. Methods and Results: Thirty-six of 44 patients hospitalized for worsening HF completed all-night measurements of RSI both at deterioration and recovery phases. Based on the signs, symptoms, and laboratory data during hospitalization, the Central Adjudication Committee identified 22 convalescent patients and 14 patients with less extent of recovery in a blinded manner without any information on RSI or other respiratory variables. The all-night RSI in the convalescent patients was increased from 27.8±18.4 to 34.6±15.8 (P

Background: Recognizing the relative location of the esophagus to the left atrial posterior wall (LAPW) is required to avoid esophageal injury during atrial fibrillation ablation. Methods and Results: The 24 patients undergoing circumferential pulmonary vein isolation (CPVI) each had the geometry of their left atrium (LA) and esophagus constructed by a noncontact mapping system with EnSite version 6.0J. The esophageal course relative to the LAPW was found to be to the left in 12, middle in 8, right in 2, and obliquely left-to-right in 2 patients, and in 13 patients (54%) it was located on or near either the left or right CPVI line. The mean distance between the esophagus and LAPW was shorter at the bottom line of the LAPW connecting both inferior pulmonary veins (3 ±3 mm) than at the LA roof line connecting both superior pulmonary veins (6 ±6 mm, P

To determine whether L-arginine, a precursor of nitric oxide, can improve exercise-induced vasodilation of the forearm in patients with heart failure, we measured forearm blood flow in 9 patients with heart failure and in 7 age-matched control subjects before and after intra-arterial infusion of L-arginine. Resting forearm blood flow was significantly lower in patients with heart failure than in control subjects (2.34 +/- 0.85 (SD) vs 4.76 +/- 0.77 ml/min per 100 ml, p < 0.001). Endothelium-dependent vasodilation induced by acetylcholine was attenuated in patients with heart failure (p < 0.05). Exercise-induced vasodilation after handgrip exercise was significantly lower in patients with heart failure (p < 0.05). Intra-arterial infusion of L-arginine did not change basal forearm blood flow but significantly augmented acetylcholine-induced vasodilation in both patients with heart failure and control subjects (p < 0.05). Although L-arginine did not affect maximum forearm blood flow after handgrip exercise in control subjects (before, 26.2 +/- 13.5; after, 25.7 +/- 14.3; p = NS), it was increased in patients with heart failure (from 15.2 +/- 4.9 to 24.7 +/- 14.6, p < 0.01). The finding that L-arginine increased both acetylcholine- and exercise-induced vasodilation in patients with heart failure suggests that endothelial dysfunction might play an important role in impaired exercise-induced vasodilation in patients with heart failure.