Circulation journal : official journal of the Japanese Circulation Society
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Heart failure is a condition in which the heart cannot supply enough blood to the body's organs, and is a final common consequence of various heart diseases. In the past 2 decades, much progress has been made in understanding the molecular and cellular processes that contribute to cardiac hypertrophy and heart failure, leading to the development of effective therapies. ⋯ These factors are closely related, and are considered to contribute to the pathogenesis of contractile dysfunction and heart failure in a cooperative manner. Elucidation of the molecular mechanisms underlying the transition of cardiac hypertrophy to heart failure will lead to the development of novel therapeutic strategies for heart diseases.
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It is well established that spiral wave reentry is the primary mechanism of ventricular tachyarrhythmias (ventricular fibrillation/tachycardia, VF/VT), but information is still limited concerning pharmacological modification of spiral waves by ion channel blockers. In this brief review, the antiarrhythmic and proarrhythmic actions of K(+)-channel blockade (I(Kr) and I (K1)) are discussed in terms of spiral wave dynamics, primarily based on recent experimental findings in ventricular preparations perfused in vitro with the aid of high-resolution optical mapping, as well as their related theoretical studies using computer simulation.
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The long and short QT syndromes are heterogeneous diseases characterized by abnormal ventricular repolarization and episodes of syncope and/or life-threatening cardiac arrhythmias. Several disease-causing genes have been identified, including those encoding cardiac ion channel-composing proteins. ⋯ Genetic testing is of special importance for the genotyped patient's family members to prevent unexpected cardiac death. By means of recently advanced methodology in molecular genetics and electrophysiology it is expected that novel genes responsible for these disease entities will be identified.