The heart rate turbulence (HRT) parameters were introduced for risk stratification of ventricular arrhythmias in postmyocardial infarction patients. However, the relationship of these parameters with other risk stratificators such as heart rate variability (HRV), repolarization parameters or left ventricular function is unknown. Furthermore, the influence of age and medication on HRT remains to be evaluated. Holter ECG's of 509 post-MI patients (1-10 years after MI) were screened for single ventricular extrasystole. In 196 patients the parameters' turbulence onset (TO) and turbulence slope (TS) could be computed. A pathological TO (>0%) and TS (<2.5 ms) was found in 58 and 54 patients, respectively. HRT was not related to gender, but was correlated with age (TS: r = 0.209, P < 0.01). No relationship was observed between QT interval, QTc interval or QT dispersion and HRT parameters. Individuals with a pathological HRT showed decreased HRV values (e.g., PNN50: 2.8 vs. 11.5; P < 0.001). Of all MI patients with systolic left ventricular dysfunction (EF < 45%, n = 46), 18 showed a pathological TO (39%) compared to 34 out of 142 patients (24%) with an EF > 45%. In contrast, the percentage of pathological HRT was not different between patients with left ventricular hypertrophy (16 out of 59, 27%) compared to patients without LVH (38 out of 133, 28%). The HRT was pathological in 14 out of 24 patients with diabetes mellitus (58%) compared to 40 out of 172 (23%) normoglycemic patients (TO: -0.6 +/- 3.1 vs. -2.5 +/- 5.5, P < 0.02). HRT was similar in patients with ss-blockers (n = 96) as in patients without ss-blockers (n = 100). In stable post-MI patients, HRT is influenced by age and left ventricular function and correlates with heart rate variability. Therapy with ss-blockers has no influence on HRT, while diabetic patients may have an increased likelihood of pathological HRT.
Novel silencer elements were cloned, localized to two AP-2 binding sites in the upstream ANP promoter, and functionally characterized. Given that the putative upregulation of left ventricular ANP by the extensively studied 3.6 kb proximal promoter region is substantially diminished by the newly cloned segment, the functional significance of regulatory elements within the proximal promoter region should be re-evaluated. The molecular mechanism causing ANP mRNA induction in left ventricular hypertrophy remains obscure.
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