Herz
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In Germany, about 6,000 pregnancies in women with grown-up congenital heart disease or acquired valvular lesions are expected per year. The pregnancy-related physiology is characterized by a 50% increase in plasma volume and a 25% increase in erythrocyte volume. The cardiac output increases by 40% due to 30% increase in stroke volume and 10% increase in heart rate during the first half, and 10% increase in stroke volume but 30% increase in heart rate during the second half of pregnancy. As a consequence of the decrease of systemic vascular resistance, the systolic and, even more, the diastolic blood pressures are reduced during approximately the first 20 weeks of pregnancy. ⋯ With respect to anticoagulation during pregnancy, there is an ongoing debate about the potential risk and benefit of phenprocoumon, standard heparins, and low molecular heparins. Withdrawal of any anticoagulation results in the most favorable fetal outcome, oral anticoagulation throughout pregnancy in the best prognosis for the mother. An individual approach by an experienced center taking all therapeutic options into account is probably the best strategy.
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Hypertensive emergencies are acute, life threatening, and usually--but not necessarily--associated with severe increases in blood pressure. In pregnancy, this is the fact in eclampsia. Eclampsia refers to the occurrence of one or more generalized convulsions in the setting of preeclampsia with proteinuria, edema, and hypertension. ⋯ Preventive measures of preeclampsia and treatment of this specific hypertensive emergency in pregnancy are discussed.
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Inherited ventricular arrhythmias such as the long QT syndrome (LQTS), Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT), idiopathic ventricular fibrillation (VF), and arrhythmogenic right ventricular cardiomyopathy (ARVC) account for a relevant proportion of sudden cardiac death cases in young patients cohorts. The detailed pathogenetic mechanisms of inherited ventricular arrhythmias are still poorly understood because systematic investigations are difficult to perform due to low patient numbers and the lack of appropriate experimental models. However, recent advances in research and science have identified a genetic background for many of these diseases. ⋯ This review summarizes the current knowledge of the molecular mechanisms, including aspects of pathoanatomy, autonomic innervation, genetics, and genotype-phenotype correlations with their potential implications for diagnosis and treatment of inherited ventricular arrhythmias.
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Despite routine use of angiotensin-converting enzyme (ACE) inhibitors, beta-blockers and spironolactone in patients with heart failure due to dilated cardiomyopathy (DCM), these patients still have a considerable annual mortality rate of 5-10%. Sudden unexpected death accounts for up to 50% of all deaths and is most often due to rapid ventricular tachycardia or ventricular fibrillation and less often due to bradyarrhythmias or asystole. ⋯ This review describes potential arrhythmia mechanisms in DCM and summarizes the results of antiarrhythmic drug trials and of prophylactic ICD trials in patients with heart failure as well as our knowledge concerning arrhythmia risk stratification in patients with DCM.
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The beta-adrenergic receptors of the myocardium play an important role in the regulation of heart function. The beta-adrenergic receptors belong to the family of G-protein coupled receptors. Three subtypes have been distinguished (beta1-, beta2-, and beta3-adrenoceptors). The receptors consist of seven membrane-spanning domains, three intra- and three extracellular loops, one extracellular N-terminal domain, and one intracellular C-terminal tail. ⋯ In patients with dilated cardiomyopathy the beta-adrenergic responsiveness of the myocardium is diminished. It was shown that in these patients the expression of the beta1-adrenergic receptor is reduced on the mRNA and protein level. In these patients the expression of the inhibitory G-protein G(i) is increased. Furthermore, the expression of the G-protein receptor kinase is elevated. This kinase induces the uncoupling of the beta-adrenergic receptors. These alterations of the beta-adrenoceptor signal cascade may be induced by an elevated catecholamine release or by agonist-like autoantibodies directed against the beta1-adrenergic receptor found in patients with dilated cardiomyopathy. Both, permanent stimulation with catecholamines and chronic treatment with agonistic anti-beta1-adrenoceptor autoantibodies cause a reduction of the expression of the beta1-adrenoceptor on mRNA and protein level in "in vitro" experiments. Moreover, an over-expression of the beta1-adrenoceptor, the stimulatory G(s) protein, and the protein kinase A induce detrimental alterations of the cardiac function and morphology in transgenic animals. These animals developed heart failure accompanied by an increased mortality rate.