Titlebook: Advances in Cardiomyopathies; Proceedings of the I Fulvio Camerini,Antonello Gavazzi,Renata Maria Conference proceedings 1998 Springer-Verl

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https://doi.org/10.1007/978-1-4302-0980-5 trait [1, 2]. The mutated genes code for altered contractile myofibrillar proteins, leading to deformed myocytes and histological evidence of extensive myocell disorganization, namely the disarray typical of hypertrophie cardiomyopathy (HCM). In the natural history of HCM endstage heart failure is

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https://doi.org/10.1007/978-1-4302-0980-5ional alterations and clinical course [1–3]. In the 1960s, shortly after the initial contemporary descriptions of HCM, diagnosis was based on physical examination and cardiac catheterization. While these diagnostic approaches tended to emphasize the role of dynamic left ventricular outflow obstructi

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Scripting, AI, and Depth (and Death),ory to medical treatment and with significant obstruction to the left ventricular outflow tract (basal gradients > 50 mmHg or > 80 mmHg after provocative manoeuvres) [1,2]. Relevant morbidity (ventricular septal perforation, atrioventricular block) and early mortality represent inherent risks with c