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Oxidative stress (OS) is a keystone in the pathology of the ischemia reperfusion sequence (acute coronary syndromes, cardiac surgery, transplantation). In heart failure, the implication of OS is less understood. This study was intended to evaluate OS in acute heart failure. Criteria for inclusion were consecutive patients hospitalized in our cardiology department for a first pulmonary edema that revealed a dilated cardiomyopathy (DCM). Exclusion criteria included known cardiomyopathy, smoker, acute coronary syndrome, and treatment with angiotensin converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARAII). OS was evaluated in blood samples: thiobarbituric acid-reactive substances (TBARS), total antioxidant status (TAS), plasma alpha-tocopherol, vitamin A, and beta-carotene. Standard biochemical parameters including CRP, fibrinogen, lipid, and creatinine were assayed. Ten patients (80% men, mean age 55.3 +/- 7.9 years) were included and followed during a 6 month period. The etiologies of DCM were alcohol (n = 3), anti-cancer drugs (n = 2), valvulopathies (n = 2), or idiopathic (n = 3). In acute heart failure, TBARS were elevated (1.69 micromol/L; normal value 0.6-4.2 micromol/L) and TAS status was decreased (0.96 mmol/L; normal value 1.3-1.9 pmol/L). OS was more important when patients had atrial or ventricular arrhythmia. Nevertheless, liposoluble antioxidant parameters (beta-carotene, vitamin A, alpha-tocopherol) had a usual value. At the term of the follow-up, patients returned to a stable condition, OS markers revealed normal values, and every Holter ECG showed no supraventricular or ventricular arrhythmias. In acute heart failure, oxygen-free radicals are increased. We thus hypothetized that a modification in OS could be responsible for arrhythmias and complications of acute heart failure.

Aims: The benefits of cardiac resynchronization therapy (CRT) on functional status, left ventricular (LV) remodelling and survival in patients with drug-refractory congestive heart failure (CHF), LV systolic dysfunction, and wide QRS have been demonstrated in randomized trials. However, the impact of CRT on right ventricular (RV) function, an independent prognostic factor in CHF remains questionable. This study examined the acute effects of various pacing modes on RV function in recipients of CRT systems., Methods and Results: Echocardiographic examinations were performed in 15 patients (median age: 67 years, range 49-78), to compare RV function during atrial (AAI), RV and LV pacing, and biventricular (BiV) pacing, in random order. At baseline, the median LV ejection fraction was 20% (range 10-35) and the median LV end-diastolic diameter was 78 mm (range 62-85). Right ventricular function was impaired, with a median 36% fractional shortening of RV surfaces (7-59). Tissue Doppler systolic peak of velocity (Sa) recorded at the tricuspid annulus increased significantly from 9.9 cm/s (range 4.7-16.5) during AAI pacing, 10 cm/s (range 5.4-20.3) during RV pacing, and 11.7 cm/s (range 4.6-16.7) during LV pacing to 12.6 cm/s (range 6.6-19.1) during BiV pacing (P < 0.01). Trends toward improvements in other indices of RV function, particularly myocardial performance index and systolic excursion of the tricuspid annulus, were also observed., Conclusions: This short-term study showed a significant improvement in RV systolic function during BiV pacing compared with AAI, RV, or LV pacing in CRT recipients.

This study aimed at evaluating OS in an amyotrophic quadricipital syndrome with cardiac impairment in a family of 80 members with a mutation in lamin A/C gene. Twelve patients had cardiac involvement (5 cardiac and skeletal muscles impairment). OS was evaluated in blood samples (thiobarbituric acid-reactive substances (TBARS), carbonylated proteins (PCO)) 6 "affected patients" with phenotypic and genotypic abnormalities without heart failure and 3 "healthy carrier" patients. OS was higher in affected patients than in healthy, as shown by the higher TBARS and PCO values. Patients with cardiac and peripheral myopathy exhibited a higher OS than patients with only cardiac disease (TBARS: 1.73 ± 0.05 vs. 1.51 ± 0.04 mmol/l (p = 0.051), PCO: 2.73 ± 0.34 vs. 0.90 ± 0.10 nmol/mg protein (p = 0.47)), and with healthy carriers patients (TBARS: 1.73 ± 0.05 vs. 1.16 ± 0.14 mmol/l (p = 0.05), PCO: 2.73 ± 0.34 vs. 0.90 ± 0.20 nmol/mg protein (p = 0.47)). OS may thus contribute to the degenerative process of this laminopathy. ROS production occurs, prior to heart failure symptoms. We suggest that the extent activation may also promote the variable phenotypic expression of the disease. [ABSTRACT FROM AUTHOR]