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PubMed1978

[Management of patients after pacemaker implanation (author's transl)].

Although pacemaker therapy is characterized by a high degree of reliability, follow-up of pacemaker patients is necessary to provide early detection of pacemaker failure and optimal setting of programable pacemakers as well as to render adequate treatment of underlying disease. The most common cause of pacemaker failure is battery depletion. In spite of the available data on the mean life-expectancy of the various batteries, the individual time of depletion cannot be predicted with accuracy. Furthermore, a defect in the electronic circuitry and/or electrode may still be rarely encountered even though technical standards are high and, occasionally, threshold elevation or lead dislocation may occur in spite of conscientious implantation technique. For patients with programable pacemakers, follow-up monitoring also enables adjustment for optimal pacemaker function. Thus, through lowering of the current or narrowing of the pulse width, the life of the battery can be prolonged or, on incrementation of these 2 parameters, an increasing threshold can be compensated for within certain limits. More important, however, is the possibility of inductive pacemaker rate changes through external programing to yield the most favorable pulse interval with respect to the underlying disease. Since, in addition to impairment of the cardiac conduction system, other disease processes are frequently presented--approximately one in three patients has coronary artery disease and almost half of the patients have congestive heart failure--follow-up visits not only serve the purpose of monitoring pacemaker function but also provide an opportunity to insure an optimal clinical condition of the patient. Accurate interpretation of pacemaker function prerequisites knowledge of the type of stimulation (fixed rate, synchronized, hysteresis, magnet rate, interference frequencies), of the battery (mercury-zinc, lihium, nickel-cadmium, isotope), of the programability (rate, current, pulse width) as well as the location of impulse capture and detection and through ascertainment of secured position of the lead and generator. While the pacemaker rate enables interpretation of the state of charge of the battery, evaluation of capture and tracing threshold permit assessment of the presence of a threshold elevation, lead dislocation, an electrode fracture or a defect in the electronic circuity. Stimulation of extracardiac muscle areas may be indicative of improper positioning and inadequate isolation of the generator, lead dislocation or lead perforation.

Arrhythmias, Cardiac↗
PubMed2002

Cardiac troponin T lysine 210 deletion in a family with dilated cardiomyopathy.

BACKGROUND: The gene for cardiac troponin T (TNNT2) is 1 of 7 autosomal disease genes implicated in familial dilated cardiomyopathy (FDC). Identical deletions in exon 13 of TNNT2 have been reported in 2 families with FDC, but little is known about the frequency of this deletion among patients with FDC and idiopathic dilated cardiomyopathy (IDC) and the associated phenotype. METHODS AND RESULTS: Exon 13 of the cardiac troponin T gene was sequenced in 61 subjects with FDC and 53 subjects with IDC. A 3-base pair deletion (DeltaLys210), identified in 1 family with at least 7 clinically affected family members, is reported. Age of disease onset and disease severity varied widely among affected individuals; phenotypic findings included dilated cardiomyopathy, sudden cardiac death, conduction system disease including atrial fibrillation and atrioventricular block, and heart failure. Sudden-onset, rapidly progressive disease was observed in younger individuals. CONCLUSIONS: Cardiac troponin T exon 13 lysine deletions can cause FDC of varying severity and are an important but uncommon cause of FDC.

Cardiomyopathy, Dilated↗