This study was designed to determine the morphological correlate of chronic heart failure. Myocardial tissue from eight patients undergoing transplantation surgery because of end-stage dilated cardiomyopathy was investigated by electron microscopy and immunocytochemistry using monoclonal antibodies against elements of the cytoskeleton: desmin, tubulin, vinculin, and vimentin. The tissue showed hypertrophy, atrophy of myocytes, and an increased amount of fibrosis. Ultrastructural changes consisted of enlargement and varying shape of nuclei, numerous very small mitochondria, proliferation of T tubules, and accumulation of lipid droplets and glycogen. The most obvious ultrastructural alteration was the decrease of myofilaments, ranging from rarefication to complete absence of sarcomeres in cells filled with unspecified cytoplasm. Immunocytochemistry showed that desmin was localized at the Z lines. In diseased myocardium, the amount of desmin was increased, but it was disorderly arranged. Tubulin formed a fine network throughout the myocytes and was significantly increased in cardiomyopathic hearts. Vinculin, a protein closely associated with the cytoskeleton, occurred not only at the sarcolemma and the intercalated disc but also within the myocardial cells. Ultrastructural changes and alterations of the cytoskeleton were severe in about one third of all cells. About one third of all cells showed moderately severe changes, and the remaining cells were normal. Vimentin was present in the interstitial cells and was increased in relation to the increase of fibrosis. We conclude that the increase of fibrosis, the degeneration of hypertrophied myocardial cells, and the alterations of the cytoskeleton are the morphological correlates of reduced myocardial function in chronic heart failure.

No abstract

The prevalence of overweight including obesity was stable among Swedish children between 2003 and 2011. Gradients in the determinants of overweight persisted. There was some evidence of a less steep socio-economic gradient in overweight in eight-year-old girls over time.

The purpose of this randomized, prospective trial was to determine if Bachmann's bundle pacing reduces the incidence of AF after CABG. The study included 161 patients with no history of AF who were randomized to three groups. Group 1 included 50 patients as controls. Group 2 included 60 patients who had an epicardial wire placed at the lateral wall of the right atrium. In the 51 patients of group 3, the wire was placed at the Bachmann's bundle. In groups 2 and 3, atrial pacing (AAI 96 beats/min) was initiated immediately after CABG and continued for 5 days. The study endpoint was AF lasting > or = 1 minute. Baseline clinical parameters were similar in all three groups. The incidence of AF was not reduced by pacing (group 1: 42%; group 2:48%; group 3:37%; P = NS). The paced P wave duration was increased in group 2 (129 +/- 14 ms vs group 3: 96 +/- 21 ms; P < 0.05). Paced P wave duration was a risk factor for postoperative AF (odds ratio 1.015; 95% CI 1.0021-1.028; P < 0.05). Analysis comparing the pacing groups revealed a reduction in AF during Bachmann's bundle pacing (50 vs 29%; P < 0.01). Pacing thresholds were significantly better at Bachmann's bundle compared to group 2. In conclusion, an anatomically guided pacing at the Bachmann's bundle does not reduce the overall incidence of postoperative AF compared to controls. However, the Bachmann's bundle offers favorable capabilities for postoperative a trial pacing, and thus it is a preferable site for electrode placement if postoperative atrial pacing is required.

The results of cross-sectional studies addressing early preintrusive atherosclerosis in type 1 diabetic patients are conflicting. In an observational longitudinal study we determined the course of carotid artery intima-media thickness (IMT) over a period of 2.5 years in mean. A total of 102 patients with type 1 diabetes mellitus (age < or = 40 years, diabetes duration > or = 2 years at baseline examination) who were participants of the baseline examination was studied again in a follow-up. HbA1c, albumin excretion rate (AER), lipids, systolic and diastolic blood pressure, retinopathy, and current smoking status were assessed at baseline and follow-up. The IMT of the common carotid artery was measured by high-resolution ultrasound, the maximum IMT was evaluated. The annual progression rate (APR) was calculated from the difference between baseline and follow-up IMT reading and the time between both examinations. The follow-up IMT was significantly higher, compared to the baseline measurement: 0.65 +/- 0.18 vs. 0.57 +/- 0.14 mm (p < 0.001), the mean APR was 0.033 mm/year. The APR was correlated with age (r = 0.337, p < 0.01), diabetes duration (r = 0.252, p < 0.05), hypertension (r = 0.225, p < 0.05), and systolic blood pressure (r = 0.281, p < 0.05) at the baseline examination. Comparing subgroups, defined according to APR tertiles, with no IMT progression (first tertile, mean APR - 0.012 mm/year), mild progression (second tertile, mean APR 0.037 mm/year), and advanced progression (third tertile, mean APR 0.088 mm/year), patients with advanced progression significantly (p < 0.05) more often had hypertension and nephropathy than subjects with mild progression. In a multiple linear regression analysis, the changes of plaque frequency and of the nephropathy status between baseline and follow-up examinations were independent predictors of the APR.