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Congenital long QT syndrome is an uncommon disease that is characterized by recurrent syncope, a long QT interval (usually 05 07 second), documented ventricular arrhythmias, and sudden death It may occur in the presence (JervellLange-Nielsen syndrome) or absence (Romano-Ward syndrome) of congenital deafness Inheritance may be autosomal recessive or autosomal dominant (Romano-Ward) Specific genetic mutations affecting membrane potassium and sodium channels have been identified and help delineate the mechanisms of susceptibility to arrhythmia Because this is a primary electrical disorder, usually with no evidence of structural heart disease or LV dysfunction, the long-term prognosis is excellent if arrhythmia is controlled Long-term treatment with -blockers, permanent pacing, or left cervicothoracic sympathectomy has been shown to be effective ICD implantation is recommended for patients in whom recurrent syncope, sustained ventricular arrhythmias, or sudden cardiac death occurs despite drug therapy The ICD should be considered as primary therapy in certain patients, such as those in whom aborted sudden cardiac death is the initial presentation of the long-QT syndrome, when there is a strong family history of sudden cardiac death, or when compliance or intolerance to drugs is a concern Acquired long QT interval secondary to use of antiarrhythmic agents or antidepressant drugs, electrolyte abnormalities, myocardial ischemia, or significant bradycardia may result in ventricular tachycardia (particularly torsades de pointes, ie, twisting about the baseline into varying QRS morphology) Notably, many drugs that are in some settings effective for the treatment of ventricular arrhythmias prolong the QT interval Prudence dictates that drug therapy that prolongs the QT interval beyond 500 ms be discontinued The management of torsades de pointes differs from that of other forms of ventricular tachycardia Class I, Ic, or III antiarrhythmics, which prolong the QT interval, should be avoided or withdrawn immediately if being used Intravenous -blockers may be effective, especially in the congenital form; intravenous magnesium should be given acutely An effective approach is temporary ventricular or atrial pacing, which can both break and prevent the rhythm.

Chiang CE Congenital and acquired long QT syndrome Current concepts and management Cardiol Rev 2004 Jul Aug;12(4): 222 34 [PMID: 15191637] Goldenberg I et al Sudden cardiac death without structural heart disease: update on the long QT and Brugada syndromes Curr Cardiol Rep 2005 Sep;7(5):349 56 [PMID: 16105490]

Accelerated idioventricular rhythm is a regular wide complex rhythm with a rate of 60 120 beats/min, usually with a gradual onset Because the rate is often similar to the sinus rate, fusion beats and alternating rhythms are common Two mechanisms have been invoked: (1) an escape rhythm due to suppression of higher pacemakers resulting from sinoatrial and AV block or from depressed sinus node function; and (2) slow ventricular tachycardia due to increased automaticity or, less frequently, reentry It occurs commonly in acute infarction and following reperfusion after thrombolytic drugs The incidence of associated ventricular fibrillation is much

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Monnig G et al Implantable cardioverter-defibrillator therapy in patients with congenital long-QT syndrome: a long-term followup Heart Rhythm 2005 May;2(5):497 504 [PMID: 15840474] Passman R et al Polymorphic ventricular tachycardia, long Q-T syndrome, and torsades de pointes Med Clin North Am 2001 Mar;85(2):321 41 [PMID: 11233951] Priori SG et al Association of long QT syndrome loci and cardiac events among patients treated with beta-blockers JAMA 2004 Sep 15;292(11):1341 4 [PMID: 15367556] Wehrens XH et al Novel insights in the congenital long QT syndrome Ann Intern Med 2002 Dec 17;137(12):981 92 [PMID: 12484714] Welde AA Is there a role for implantable cardioverter defibrillators in long QT syndrome J Cardiovasc Electrophysiol 2002 Jan;13(1 Suppl):S110 3 [PMID: 11852886]

Most patients with ECG evidence of sick sinus syndrome are asymptomatic, but rare individuals may experience syncope, dizziness, confusion, palpitations, heart failure, or angina Because these symptoms are either nonspecific or are due to other causes, it is essential that they be demonstrated to coincide temporally with arrhythmias This may require prolonged ambulatory monitoring or the use of an event recorder

Abnormalities of conduction can occur between the sinus node and atrium, within the AV node, and in the intraventricular conduction pathways Most symptomatic patients will require permanent pacing (see AV block, below) Dual-chamber pacing is preferred because ventricular pacing is associated with a higher incidence of subsequent atrial fibrillation, and subsequent AV block occurs at a rate of 2% per year In addition, resultant pacemaker syndrome can result from loss of AV synchrony Treatment of associated tachyarrhythmias is often difficult without first instituting pacing, since digoxin and other antiarrhythmic agents may exacerbate the bradycardia Unfortunately, symptomatic relief following pacing has not been consistent, largely because of inadequate documentation of the etiologic role of bradyarrhythmias in producing the symptom Furthermore, many of these patients may have associated ventricular arrhythmias that may require treatment; however, carefully selected patients may become asymptomatic with permanent pacing alone

Adan V et al Diagnosis and treatment of sick sinus syndrome Am Fam Physician 2003 Apr 15;67(8):1725 32 [PMID: 12725451] Brignole M Sick sinus syndrome Clin Geriatr Med 2002 May; 18(2):211 27 [PMID: 12180244] Dretzke J et al Dual chamber versus single chamber ventricular pacemakers for sick sinus syndrome and atrioventricular block Cochrane Database Syst Rev 2004;(2):CD003710 [PMID: 15106214] Lamas GA et al Quality of life and clinical outcomes in elderly patients treated with ventricular pacing as compared with dual-chamber pacing Pacemaker Selection in the Elderly Investigators N Engl J Med 1998 Apr 16;338(16):1097 104 [PMID: 9545357]

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