PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Cardiac Conduction System Disease”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1989

Hereditary long QT syndrome associated with cardiac conduction system disease.

This report describes the cardiac conduction abnormalities, detected by invasive electrophysiological study, in two identical siblings with symptomatic congenital long QT syndrome. Both patients had evidence of intra-Hisian conduction delay in response to programmed atrial stimulation and pacing induced infranodal block was seen in one of the two patients. The response of the observed conduction delay to autonomic interventions is described. The observed electrophysiologic abnormalities are consistent with previously reported pathological findings and document the association of functional conduction system disease with congenital QT prolongation.

Adolescent↗
PubMed1997

Symptomatic conduction system disease in cardiac amyloidosis.

Symptomatic conduction system disease in cardiac amyloidosis and its management has been reported infrequently. We report our experience of patients with amyloidosis having symptomatic conduction system disease requiring permanent pacemaker implantation.

Aged↗
PubMed1999

[Cardiovascular complications of collagen diseases].

Recent progress in the field of clinical epidemiology and diagnosis of major cardiovascular complications of collagen diseases were reviewed including systemic lupus erythematosus, systemic sclerosis, polymyositis.dermatomyositis, polyarteritis and mixed connective tissue disease. Major cardiac complications comprise pericarditis, myocardial disease, cardiac conduction system disease, coronary artery disease and valvular disease. Vascular complications comprise necrotizing vasculitis as a major organic involvement and Raynaud's phenomenon as a major functional involvement. Due to the recent development of sensitive methods of evaluating cardiovascular abnormalities, clinical diagnosing rate of cardiovascular complications in the early stage has been considerably increasing in patients with collagen diseases. On the other hand, number of patients with atherosclerotic cardiovascular complications due to long-term corticosteroid therapy has been also gradually increasing.

Anti-Inflammatory Agents↗
PubMed2002

PRKAG2 cardiac syndrome: familial ventricular preexcitation, conduction system disease, and cardiac hypertrophy.

Genetic studies of families with inherited cardiac rhythm disturbances have established a molecular basis for ventricular arrhythmogenic disorders. Genes responsible for the long QT syndrome, Brugada syndrome, and polymorphic ventricular tachycardia have been identified. The elucidation of genetic defects responsible for more commonly occurring supraventricular rhythm disturbances have not been as forthcoming, with the exception of SCN5A mutations known to cause conduction system disease. Recently, we identified the genetic cause of a familial arrhythmogenic syndrome characterized by ventricular preexcitation and tachyarrhythmias (Wolff-Parkinson-White syndrome), progressive conduction system disease, and cardiac hypertrophy. The causative gene was shown to be the gamma-2 regulatory subunit (PRKAG2) of AMP-activated protein kinase. The role of AMP-activated protein kinase in the regulation of the glucose metabolic pathway in muscle suggests that genetic defects in PRKAG2 may induce a previously undescribed cardiac glycogenosis syndrome.

AMP-Activated Protein Kinases↗
PubMed2001

Cardiomyopathy in animal models of muscular dystrophy.

Arrhythmia and cardiomyopathy frequently accompany muscular dystrophy. In the last year, the cardiovascular consequences of muscular dystrophy gene mutations have been established through studies of murine models. These models have highlighted the potential role of primary defects in cardiac muscle as well as those secondary cardiovascular outcomes that arise from severe muscle disease. This review focuses on three areas. Recent studies using mouse models have shown that the dystrophin-associated proteins, the sarcoglycans and alpha-dystrobrevin, are critical for both cardiac and skeletal muscle membrane function, yet may exert their roles by different molecular mechanisms. New findings have shown that cytoskeletal proteins at the nuclear membrane, such as emerin and lamin AC, cause muscular dystrophy and cardiomyopathy with cardiac conduction system disease. Finally, the mechanism of cardiac and muscle degeneration in myotonic dystrophy has been re-evaluated through a series of studies using murine models. Implications for human therapy are considered in light of these new findings.

Animals↗