Heart rate turbulence in adults with repaired tetralogy of Fallot.

BACKGROUND: Tetralogy of Fallot (ToF) patients face an increased risk of sudden cardiac death late after repair. Heart rate turbulence (HRT) indices are well-known predictors of sudden cardiac death. We aimed to estimate whether HRT is impaired in repaired ToF patients compared to healthy controls and relate those HRT parameters to already recognized prognostic markers. METHODS: Continuous ECG recordings were performed in 19 patients late after ToF repair (36.3+/-12.4 years, 26.6+/-7.1 years after repair) and 20 age-matched healthy controls (40.8+/-8.1 years). Turbulence slope (TS) and onset (TO), frequency and time domain heart rate variability parameters and QRS duration were estimated. Volumes of the right (RV) and left ventricle (LV) and ejection fraction (EF) were assessed by cardiovascular magnetic resonance imaging. Cardiopulmonary exercise testing was used to estimate peak oxygen consumption (VO(2)) and VE/VCO(2) slope. RESULTS: TS (15.95+/-9.41 vs 28.73+/-12.24 ms/RRI, p=0.0007) and TO (-0.98+/-2.06% vs -3.45+/-3.25%, p=0.007) were found to be significantly different between ToF patients and controls. TO correlated with LVEF (r=0.47, p<0.05), LVSVi (r=0.50, p=0.03), RVEF (r=0.53, p=0.02), peak VO(2) (r=0.50, p=0.05), VE/VCO(2) slope (r=-0.55, p=0.03) and with heart rate variability frequency domain indices (log LF, r=0.47, p=0.04, log HF, r=0.56, p=0.01). CONCLUSION: HRT indices are impaired in ToF patients late after surgical repair compared to healthy controls and relate to coexisting haemodynamic, ventilatory and autonomic impairment. A clinical prognostic role of HRT may be speculated, which warrants further investigation.

Psychological consequences among adults following the 1999 earthquake in Athens, Greece.

One year after the 7 September 1999 earthquake in Athens, Greece, we investigated the psychological consequences among 305 individuals (71 per cent female) residing in the settlements of Ano Liosia Municipality. Adaptability was difficult (63 per cent) due to limited space (50 per cent). Insecurity feelings were predictive of difficult adaptability (chi2= 29.8, p<0.0001) and were common (63 per cent) among married subjects, independent of age (chi2= 5.0, odds ratio (OR): 0.49, 95 per cent confidence interval (CI): 0.26-0.90). Eighty per cent expressed stress feelings, mainly nervousness/tension (60 per cent). Adaptability (chi2= 5.3, OR: 0.5, 95 per cent CI: 0.27-0.9), age (chi2= 6.5, OR: 1.03, 95 per cent CI: 1.01-1.06), and female gender (chi2= 4.7, OR: 0.48, 95 per cent CI: 0.25-0.90) were independent predictors of stress feelings. The majority (55 percent) developed sleep disorders, chiefly insomnia (60 percent). Adaptability problems were the only predictor of sleep disorders (chi2= 6.4, OR: 0.5, 95 per cent CI: 0.33-0.87). Psychiatric medication use increased after the earthquake.

Desmin mediates TNF-alpha-induced aggregate formation and intercalated disk reorganization in heart failure.

We explored the involvement of the muscle-specific intermediate filament protein desmin in the model of tumor necrosis factor alpha (TNF-alpha)-induced cardiomyopathy. We demonstrate that in mice overexpressing TNF-alpha in the heart (alpha-myosin heavy chain promoter-driven secretable TNF-alpha [MHCsTNF]), desmin is modified, loses its intercalated disk (ID) localization, and forms aggregates that colocalize with heat shock protein 25 and ubiquitin. Additionally, other ID proteins such as desmoplakin and beta-catenin show similar localization changes in a desmin-dependent fashion. To address underlying mechanisms, we examined whether desmin is a substrate for caspase-6 in vivo as well as the implications of desmin cleavage in MHCsTNF mice. We generated transgenic mice with cardiac-restricted expression of a desmin mutant (D263E) and proved that it is resistant to caspase cleavage in the MHCsTNF myocardium. The aggregates are diminished in these mice, and D263E desmin, desmoplakin, and beta-catenin largely retain their proper ID localization. Importantly, D263E desmin expression attenuated cardiomyocyte apoptosis, prevented left ventricular wall thinning, and improved the function of MHCsTNF hearts.