ISSN:0268-4705    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The success of radiofrequency catheter ablation in the treatment of atrioventricular junctional, or atrioventricular nodal, reentrant tachycardia has rekindled interest in the electrophysiological and anatomical characteristics of the reentrant circuit. We conclude that there is no evidence that within the atrioventricular nodal area, which contains both the compact node and transitional cells, there are anatomically delineated dual or multiple pathways. Rather, the two main atrial inputs into the atrioventricular nodal area (posterior and anterior) seem to be the anatomically relevant structures for “slow” and “fast” pathways. Two other inputs (sinus septum and left atrial) may be the cause for multiple pathways in some individuals. Nonuniform anisotropic properties of the zone of transitional cells may account for slow or fast conduction in the same area, depending on directional differences of wavefronts. We prefer the term atrioventricular junctional reentrant tachycardia rather than atrioventricular nodal reentrant tachycardia because of mounting evidence that perinodal tissue is involved in the reentrant circuit. Finally, the role and origin of double extracellular electrograms is discussed. Further research is required to establish whether an anatomical or an electrogram-guided approach for catheter ablation is preferred.

ISSN:0268-4705    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Patients with hypertrophic cardiomyopathy are at increased risk for sudden death. Recent studies have improved our ability to risk-stratify such patients and have elucidated several potential mechanisms of sudden death and syncope. Certain noninvasive tests, such as signal-averaged electrocardiography and measurements of cardiac autonomic function and QT/QT dispersion, are often abnormal in hypertrophic cardiomyopathy, but are not useful for risk stratification. Myocardial ischemia determined by exercise thallium scintigraphy, however, identifies young patients with hypertrophic cardiomyopathy who are at high risk for cardiac arrest and syncope. Nonsustained ventricular tachycardia on ambulatory Holter monitoring in the absence of symptoms of impaired consciousness is associated with a benign prognosis and is not predictive of sudden death. Conversely, ventricular tachycardia induced at electrophysiologic study identifies adult patients with hypertrophic cardiomyopathy who subsequently experience sudden death. Finally, characterization of the natural history of the genetic defects will increasingly become an integral part of risk evaluation in hypertrophic cardiomyopathy.

ISSN:0268-4705    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Arrhythmogenic right ventricular dysplasia is a relatively newly described clinical entity that is more and more frequently recognized. It may explain an increasing number of unexpected, sudden deaths in young adults that are or are not preceded by cardiac symptoms. A genetic transmission of the disease has been suggested by the study of familial cases. A location on chromosome 14 appears to be responsible for this disease. In some patients, a superimposed inflammatory process mixed with the pattern of arrhythmogenic right ventricular dysplasia may explain the progressive deterioration of left ventricular function. The systematic study of electrocardiograms demonstrates prolongation of the QRS complex and repolarization abnormalities in the right precordial leads due to a parietal block. Multiple therapeutic approaches are now available. The first line of therapy remains antiarrhythmic drugs,which are effective in most cases.Ablative techniques,implantable difibrillators,and heart transplantation have been used in the most severe examples of the disease.

ISSN:0268-4705    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:0268-4705    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:0268-4705    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:0268-4705    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The following consideration of this past year's published studies uses the cited reports as important examples of the ongoing characterization of the molecular basis of cardiac disease and the process of cardiac development. Mutations in cardiac troponin T and α- tropomyosin have been identified in familial hypertrophic cardiomyopathy, as have new β - myosin heavy chain gene mutations. The general relation between β- myosin heavy chain gene mutations that produce a charge change versus conservative amino acid replacements and sudden death remains unresolved. New fibrillin 1 gene mutations have been identified in patients with Marfan syndrome, the neonatal form of Marfan syndrome, and ectopia lentis. The same mutation is rarely found in more than one family. The association of supravalvar aortic stenosis and elastin gene mutations was further strengthened. The complexity of the relation between dystrophin mutations and the cell-specific loss of dystrophin expression can result in patients having cardiomyopathy and no myopathy. X-chromosome inactivation was shown to be the basis of cardiomyopathy in women with a single mutated dystrophin allele. New candidate genes that control cardiac morphogenesis and myocyte differentiation were proposed. New evidence to support 22q11 microdeletions as a common basis of nonsyndromic conotruncal malformations was published. These studies represent an important beginning. Although mutant genes have been recognized in affected individuals with various syndromes and congenital cardiac abnormalities, our understanding of how a genotype yields a given phenotype remains to be established.

ISSN:0268-4705    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Systolic and diastolic cardiac function improve during the transition from fetus to newborn to adult. This perinatal maturation is temporally correlated with and at least partially dependent on subcellular changes in the expression of several gene products that regulate cytosolic Ca2+concentration. Expression of the Na+-Ca2+exchanger of the sarcolemma is highest in the fetus, whereas expression of the sarcoplasmic reticulum Ca2+pump and the voltage-dependent Ca2+channel of the sarcolemma increase in conjunction with the perinatal maturation of cardiac function. Whereas cardiac relaxation in the normal mature heart depends primarily on the sarcoplasmic reticulum Ca2+pump, relaxation in the fetal heart appears to be more dependent on transsarcolemmal Ca2+flux. Like the fetal heart during prolonged relaxation, the failing human heart exhibits impaired relaxation and abnormal Ca2+flux regulation. Although altered expression of several gene products has been demonstrated in the failing heart, the responsible factor(s) remains unknown.

ISSN:0268-4705    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The practice of pediatric electrophysiology has been altered drastically and irrevocably over the past 5 years. With the advent of widespread application of transcatheter radiofrequency ablative techniques in young patients, decisionmaking in the management of childhood arrhythmias has focused less on palliative medical therapies and more on the potential for curative, nonsurgical interventions. This review examines the published contributions in the area of pediatric catheter ablation, antiarrhythmic drug therapy, postoperative arrhythmias, fetal arrhythmias, and electrocardiographic phenomena after cardiac transplantation.

ISSN:0268-4705    

出版商:OVID    

年代:1995

数据来源: OVID