Roundtable discussion ... cardiovascular disease management programs.
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Cardiovascular Diseases↗
Biomedical subjects
T Klitzner
Publications and source records attributed to T Klitzner.
Roundtable discussion ... are MCOs implementing programs to meet the challenges of baby-boomer women entering menopause?
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Aged↗
Hereditary long QT syndrome in the postoperative cardiac patient.
The purpose of the present article is to evaluate the diagnostic implications of the long QT syndrome presenting in postoperative cardiac patients. Diagnosis of long QT syndromes may be complicated by an inability to measure the QT interval correctly due to postoperative electrocardiographic changes such as right bundle-branch block. For this reason, a study of the effect of right bundle-branch block on the QT interval was undertaken. Electrocardiograms of 17 randomly selected patients undergoing a right ventriculotomy for repair of tetralogy of Fallot were evaluated for QT prolongation pre- and postoperatively. Preoperatively, no patient demonstrated QT interval prolongation. After surgery, however, right bundle-branch block created an apparent prolongation of the QT interval in 9 of the 17 patients (53%). These results suggest that in postoperative cardiac patients QT prolongation and familial long QT syndromes may be difficult to diagnose. It is, therefore, important to exclude the long QT syndrome in patients with ventricular tachycardia even if a more obvious explanation such as previous cardiac surgery is present. Usually a careful family history and preoperative electrocardiogram are all that is required.
Arrhythmias, Cardiac↗
Fractionated endocardial electrograms are associated with slow conduction in humans: evidence from pace-mapping.
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)
Adult↗
Clinical and electrophysiologic effects of amiodarone in patients with atrial fibrillation complicating the Wolff-Parkinson-White syndrome.
The clinical and electrophysiologic effects of oral amiodarone were evaluated in 10 patients with a history of spontaneous atrial fibrillation and a rapid ventricular response, complicating the Wolff-Parkinson-White syndrome. Five patients developed ventricular fibrillation during an episode of atrial fibrillation. Seven patients underwent electrophysiology study and arrhythmia induction, both before and during chronic amiodarone treatment. During a mean 30 months of follow-up (range 8 to 59 months), no recurrences of atrial fibrillation or ventricular fibrillation were noted. One patient had recurrent supraventricular tachycardia and underwent surgery. One had serious and five had minor side effects. Arrhythmia suppression was associated with prolongation of the anterograde accessory pathway (+38%, p less than 0.01) and atrial (+34%, p less than 0.01) effective refractory periods. Amiodarone also slowed the ventricular response to induced atrial fibrillation, prolonging the mean (+90%, p less than 0.01) and minimum (+104%, p = 0.01) R-R intervals. Thus, amiodarone is a safe and effective alternative for arrhythmia prevention if surgery is inadvisable or is not desired by the patient.
Adult↗
Resetting of ventricular tachycardia: implications for localizing the area of slow conduction.
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.
Aged↗
Excitation-contraction coupling in developing mammalian myocardium: evidence from voltage clamp studies.
The single sucrose gap voltage clamp technique was used to study excitation-contraction coupling processes in right ventricular papillary muscles from New Zealand White rabbits at various stages of development. In response to voltage clamp controlled depolarizations, muscles from newborn rabbits were found to exhibit a monotonically increasing tension response reaching a steady state level that was maintained for the duration of depolarization. In contrast, more mature myocardium responded to similar depolarizations by developing an early peak of tension before relaxing to a steady state level. Measurement of the ratio of early peak or phasic tension to steady state or tonic tension revealed a statistically significant increase in the phasic tension component with maturation. In addition, Ca2+ loading of immature myocytes via a conditioning voltage clamp step resulted in enhancement of phasic tension in subsequent test depolarizations. Finally, the voltage dependence of tonic tension was found to be the same in all age groups. In contrast, the voltage dependence of phasic tension, seen only in the more mature myocardium, differed from that of tonic tension. The results of this investigation suggest that tension development in the immature myocardium is supported largely by the influx of Ca2+ across the sarcolemma. As the myocardium matures, intracellular Ca2+ uptake and rerelease by the sarcoplasmic reticulum plays an increasingly important role in tension development. A developmental schema is presented to account for the observed maturational changes in excitation-contraction coupling.
Age Factors↗
Limitations of bipolar and unipolar conditioning stimuli for inhibition in the human heart.
Noncapturing, conditioning electrical stimuli (Sc) delivered within the ventricular refractory period can prolong refractoriness and prevent later stimuli from eliciting a propagated response (inhibition). The purpose of this study was to further define the spatial effects of Sc, to determine if the effects of Sc can be enhanced by the use of unipolar as opposed to bipolar stimulation, and to evaluate the effect of Sc on the physiologic spread of excitation during atrioventricular reentry tachycardia. In 23 patients the right ventricular refractory period was determined before and after the introduction of bipolar, unipolar cathodal, and unipolar anodal noncapturing Sc with pulse widths of 2 or 9 msec and strengths of twice diastolic threshold and 10 MA. Pacing and conditioning stimuli were delivered at the same site and at sites separated by 3 mm. During ventricular pacing both bipolar and unipolar Sc prolonged the ventricular refractory period by greater than or equal to 10 msec in 22 of 23 patients when both Sc and pacing stimuli were delivered to the same site. However, when Sc was delivered 3 mm away from the pacing stimuli, the ventricular refractory period increased by greater than or equal to 10 msec in only 1 of 17 patients who received bipolar Sc and in none of 13 patients who received unipolar Sc. In seven patients bipolar conditioning stimuli were delivered as close as possible to the atrial insertion of an accessory atrioventricular connection during circus movement tachycardia with a well-localized accessory pathway. Sc did not terminate or slow tachycardia in any patient.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Enhancement of conduction in an accessory pathway by local noncaptured stimuli.
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.
Cardiac Pacing, Artificial↗
The effects of Ni2+ on ionic currents and tension generation in frog ventricular muscle.
The effect of Ni2+ on E-C coupling events of the frog ventricular muscle were studied using a single sucrose gap voltage clamp technique. The results showed that Ni2+ increased the overshoot potential and depressed and prolonged the plateau of the action potential. Ni2+ also increased the dependence of the overshoot potential on [Na]0 from 18 to 58 mV per decade. In the presence of Ni2+, TTX blocked both the upstroke and the plateau of the action potential. The combination of TTX and Ni2+ suppressed the tension-voltage relation, the time-dependent outward currents and K+ efflux. While suppression of the tension-voltage relation by Ni2+ alone was reversed by increasing [Ca]0, the effects of Ni2+ plus TTX are not reversed by addition of Ca2+. The results suggest that Ni2+ may alter the action potential by slowing the inactivation of the Na+ current and blocking the inward Ca2+ current. Although the tension-suppressant effects of Ni2+ could be attributed to the inhibition of a slowly inactivating Ca2+ current, the effects of Ni2+ in the presence of TTX were less readily explained. Several possible mechanisms are considered which are all consistent with the hypothesis that development of tension in ventricular strips is mediated by both a Ca2+ current and a Ca2+ counter-transport system.
Action Potentials↗
Excitation-contraction coupling in frog ventricle. Possible Ca2+ transport mechanisms.
In frog ventricular muscle generation of tension was found to be under direct and continuous control of membrane potential. No phasic component of tension was found at any membrane potential. Developed tension depended only on the duration and amplitude of depolarization and was independent of previous contractile history. Developed tension, in part, depended on Ca2+ influx through a slowly inactivating component of Isi. Using long voltage clamp steps to achieve steady-state tension, no decline or reversal of developed tension was found at ECa. Increasing the [Ca]o shifted the tension-voltage relation to more negative potentials and increased the net outward current at potentials positive to -10 mV. The increase in tension seemed to be related to the increase in outward membrane current and K+ efflux, as estimated from post clamp K+ accumulations. Increasing [K]o, either by clamp-induced K+-accumulation or by increasing the [K] of the bathing solution, decreased the developed tension. These results suggest that in frog ventricular muscle Ca2+ for activation of tension is transported primarily from the extracellular space. There was no trigger-release of internal stores or recirculation of sequestered Ca2+. Activator Ca2+ was transported in part by a slowly inactivating Isi channel and a coupled transport mechanism. The exact mechanism by which Ca2+ transport and K+ efflux were related could not be identified.
Animals↗