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ObjectivesThe purpose of this study was to evaluate adult congenital heart disease (CHD) training among U.S. cardiology fellowship programs.BackgroundAlthough training recommendations for caring for adults with CHD exist, the educational patterns and numbers of specialists remain unknown.MethodsWe surveyed U.S. directors of 170 adult cardiology and 45 pediatric cardiology (PC) fellowship programs. Adult program surveys contained 1 single-response and 10 multiple-choice questions; pediatric program surveys contained 1 single-response and 13 multiple-choice questions.ResultsNinety-four adult cardiology fellowship directors (55%) and 34 PC directors (76%) responded. Of adult programs, 70% were in university hospitals and 40% were associated with PC groups. Those with PC-affiliation had more adult CHD clinics (p < 0.02) and more adult CHD inpatient (p < 0.02) and outpatient (p < 0.002) visits than those without PC affiliation. Most PC programs were in children’s hospitals (38%) or children’s hospitals within adult hospitals (50%). Eighty-two percent had associated adult cardiology programs. Pediatric programs followed adult CHD patients in various care settings. Over one-third of adult and pediatric programs had ≤3 lectures annually regarding adult CHD. Nine adult and 2 pediatric programs offered adult CHD fellowships, and only 31 adult and 11 pediatric fellows pursued advanced CHD training in the last 10 years.ConclusionsAdult CHD didactic and clinical experiences for cardiology fellows vary widely. Few programs offer advanced CHD training, and the number of specially trained physicians is unlikely to meet projected workforce requirements. Adult cardiology programs with PC affiliation have increased CHD experience and might provide good educational models.

The single sucrose gap voltage clamp technique has been used to study the relation between membrane electrical activity and tension generation in right ventricular papillary muscles from New Zealand White rabbits at various stages of development. In response to voltage clamp-controlled depolarization, muscles from newborn rabbits develop monotonically increasing tension that reaches a steady state level, whereas more mature myocardium responds to similar depolarization by developing an early peak of tension before relaxing to a steady state level. The ratio of early peak or phasic tension to steady state or tonic tension increases significantly with maturation. Calcium (Ca2+) loading of immature myocytes enhances phasic tension in a subsequent test depolarization. Although the voltage dependence of tonic tension increases monotonically in all age groups, phasic tension, seen only in the more mature myocardium, displays a “bell-shaped” dependence on voltage.Addition of ryanodine, known to interfere with Ca2+release from the sarcoplasmic reticulum, markedly reduces the phasic component of tension in mature myocardium, and the voltage clamp-induced tension in the adult closely resembles that of the normal newborn.These results suggest that tension development in immature myocardium is supported largely by the influx of Ca2+across the sarcolemma. As the myocardium matures, the sarcoplasmic reticulum plays an increasingly important role in tension generation. A developmental schema is presented to account for the observed malurational changes in excitation-contraction coupling. The clinical implications of these changes are discussed as they relate to the practice of pediatric cardiology.

Fractionated ventricular electrograms recorded during catheter mapping may arise from areas of asynchronous depolarization associated with slow conduction, the substrate for reentrant ventricular tachycardia, but can also be a nonspecific abnormality or even artifact. To determine whether fractionated sinus rhythm electrograms are associated with slow conduction in humans, the results of endocardial catheter mapping and pacing at 133 endocardial sites in 13 patients were analyzed. Eleven patients had sustained monomorphic ventricular tachycardia and two patients had old myocardial infarction without ventricular tachycardia. Functional evidence of slow conduction at the recording site was assessed by pacing at that site and measuring the interval between the stimulus artifact (S) and the onset of the QRS complex in the 12 lead electrocardiogram (ECG). During pacing at 89 of 90 sites without fractionated sinus rhythm electrograms, the S-QRS interval was less than 40 ms, a value consistent with rapid propagation of the stimulated wave front away from the pacing site. During pacing at 21 (49%) of 43 sites with fractionated sinus rhythm electrograms, the S-QRS interval was greater than 40 ms (range 40 to 140), consistent with slow conduction at the pacing site (p less than 0.001 versus nonfractionated sites). In 9 of the 11 patients with ventricular tachycardia analysis of the paced QRS configuration, electrograms during induced ventricular tachycardia or programmed stimulation during tachycardia suggested that a site with a long S-QRS interval during pacing was located at or near a ventricular tachycardia circuit. Therefore, fractionated sinus rhythm electrograms are often associated with slow conduction, which may be the substrate for reentrant ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Subthreshold stimuli have been reported to prolong the refractory period of myocardial tissue. This report presents the first case of reproducible acceleration of a reentrant tachycardia by apparently subthreshold stimuli delivered to the os of the coronary sinus during the atrial refractory period in a child with incessant orthodromic tachycardia utilizing a posteroseptal pathway. Mechanisms by which these stimuli could influence the tachycardia circuit are proposed, and the potential usefulness of this finding for mapping tachyarrhythmias is discussed.

Analysis of local endocardial electrograms recorded during reentrant ventricular tachycardia does not provide direct information as to the participation of the recording site in the tachycardia circuit. To determine if programmed electrical stimulation at the recording site can assist in localizing areas of slow conduction that are participating in the tachycardia circuit, seven patients with sustained monomorphic ventricular tachycardia were studied. The cardiac cycle was scanned with single stimuli delivered during ventricular tachycardia at multiple endocardial sites.In four patients, an endocardial site was identified at which stimuli advanced the tachycardia with marked conduction delay and without alteration of the ventricular activation sequence, as indicated by a lack of change in the configuration of the QRS complex and endocardial electrograms distant from the stimulation site. This finding was seen only during stimulation at sites displaying abnormal electrograms and is consistent with premature depolarization of an area of slow conduction within the tachycardia focus by stimuli delivered at or near that area. Attempted endocardial catheter ablation at or adjacent to these sites in three patients was followed by persistent noninducibility of ventricular tachycardia in one patient, marked modification of the configuration and cycle length of inducible tachycardia in one patient and transient noninducibility of tachycardia in one patient.Programmed electrical stimulation during ventricular tachycardia at sites with abnormal electrograms may provide information about the proximity of the stimulation site to the tachycardia circuit.