Titlebook: Electrical Diseases of the Heart; Genetics, Mechanisms Ihor Gussak (Deputy Therapeutic Area Head, Profess Book 20081st edition Springer-Ver

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Grundri? zum Studium der Zahnheilkunderdial perfusion through effects on coronary vascular function and platelet aggre- gability (Figure 4-1). Neural influences may also be arrhythmogenic in patients with channelopathies, including the long QT and Brugada syndromes, as discussed in detail in other chapters.

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L-type Calcium Channel Diseasend distinctive dysmorphic features. So far TS is the only inherited arrhythmogenic disorder linked to cardiac calcium channel mutations. In this chapter, we will briefly review the structure, physiology, and pathophysiology of the cardiac Cav1.2 encoded by the . gene.

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Verfügungsrecht über die Bodensch?tzestanding of cardiac electricity and outline some of the key questions that I think we must address. Although my personal career goal has been how we can now exploit this basic science for clinical care, more than ever basic understanding is the framework for our future advances.

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https://doi.org/10.1007/978-3-322-81717-4n to structural cardiac defects, notably cardiac fibrosis, dilated cardiomyopathy, and, possibly, arrhythmogenic right ventricular cardiomyopathy. These structural changes may also be conducive to (reentrant) arrhythmias.

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Anatomic and Histopathological Characteristics of the Conductive Tissues of the Heartity between atrial and ventricular myocardium, allowing atrial impulses to be conveyed to the ventricles in an orderly fashion. In this chapter, we will deal with normal and pathological features of the conductive tissue of the heart.