Nihon rinsho. Japanese journal of clinical medicine
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Survival of patients with heart failure has improved over the past decade due to advances in medical therapy. However, sudden cardiac death continues to cause 35 to 65% of death. Ventricular arrhythmias are important causes of sudden cardiac death in patients with heart failure. ⋯ Therefore, in the absence of a clear indication, antiarrhythmic drug therapy should be avoided. A number of recent randomized trials have provided evidence that beta-adrenergic blockers, angiotensin-converting enzyme(ACE) inhibitors and angiotensin II receptor blockers(ARB) significantly reduces the risk of sudden death in patients with chronic congestive heart failure. For patients who have a history of sustained ventricular tachycardia(VT) or ventricular fibrillation(VF) amiodarone or an implantable cardioverter defibrillator(ICD) should be considered, and these therapy may benefit some high risk patients who have nonsustained VT.
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In the past decade, molecular genetics has revealed that some life-threatening arrhythmogenic disorders, such as long QT syndrome, are due to mutated genes encoding ion channels that generate the cardiac action potential. Great efforts made in various fields have partly solved problems caused by unforeseen genetic diversity of these congenital arrhythmogenic disorders, while the genetics of these disorders has recently proved to be applicable to very wide-ranging conditions associated with sudden cardiac death, and increased knowledge about the human genome will revolutionize researches into arrhythmic diseases in future. The purpose of this review is to outline the recent advances and problems in the molecular genetics in long QT syndrome.