Cardiac resynchronization therapy produces a long-term improvement in the clinical symptoms of patients with HF who have a ventricular conduction delay. The differences between optimized biventricular and univentricular therapy appear to be small for short-term treatment.

When performed by experienced physicians, percutaneous dilatational tracheostomy under fiberoptic guidance is a safe method. The risks of early complications and of clinically relevant tracheal stenoses are low. Subclinical tracheal stenoses are found in about 40% of patients following PDT.

We suggest that total aponeurectomy is a promising alternative to partial fasciectomy with low risk for a recurrence and slightly increased risk for a nerve lesion.

The technique is simple and reliable giving consistent clinical results.

Abstract-In polygenetic disorders, such as ischemic heart disease, the investigation of gene-gene interactions rather than determination of single gene effects is crucial to better understand the contribution of genetic factors. The 825T allele of the G-protein ␤ 3 -subunit gene (GNB3) associated with enhanced G-protein signaling is a candidate to interact with the angiotensin-converting enzyme (ACE) deletion/insertion (D/I) polymorphism to increase the risk for myocardial infarction (MI Key Words: myocardial infarction Ⅲ genetics Ⅲ signal transduction Ⅲ G proteins Ⅲ angiotensin-converting enzyme A lthough coronary artery disease (CAD) and myocardial infarction (MI) are unlikely to be caused by single genetic polymorphisms, few studies have investigated the interaction of susceptibility genes with other genetic or conventional risk factors on MI. Insight into such interactions may result in a significant gain of knowledge about the pathogenesis of MI and may lead to novel risk stratification, prevention, and even therapeutic strategies.The DD genotype of a deletion/insertion (D/I) polymorphism in the angiotensin-converting enzyme (ACE) gene was initially reported to increase the risk for MI, 1 but subsequent studies yielded conflicting results potentially caused by the heterogeneity of the respective genetic background. 2 ACE mediates the conversion of angiotensin I to angiotensin II (AT-II), and, although this has not yet been rigorously proven, it is commonly assumed that the increased serum ACE levels associated with the ACE D allele 3 represent the main mechanism by which the ACE DD genotype increases the risk for MI. AT-II receptors are typical G-protein-coupled receptors 4 ; thus it appears plausible to assume that AT-II mediated effects are further enhanced in the presence of an increased responsiveness of G proteins. Enhanced G-protein reactivity is strictly correlated with the 825T allele of a C825T base exchange in the gene GNB3 encoding the G-protein ␤ 3 -subunit. 5 The 825T allele is also associated with essential hypertension [5][6][7][8] and with an enhancement of diverse cell functions that may play a role in mechanisms ultimately contributing to an increased risk for MI. 9 -12 Therefore, we investigated the hypothesis that the ACE gene D allele and the GNB3 825T allele significantly interact to increase the risk for MI. This analysis was conducted within a sample of thoroughly characterized patients with angiographically documented CAD with or without previous MI. MethodsThis study was conducted in accordance with the Helsinki Declaration, revised in 1983. Study PopulationA total of 585 patients with angiographically confirmed CAD were consecutively enrolled in this study. CAD was defined by a luminal narrowing with Ͼ50% diameter stenosis in at least 1 coronary artery. The following variables were assessed: current age, gender, body mass index, hypercholesterolemia, hypertension, diabetes, smoking, and previous MI. Previous MI was confirmed in 270 patients according to the American College of Car...