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Biomedical subjects

L D German

Publications and source records attributed to L D German.

At least 37 records · Page 2Linked to original sources
PubMed1986

Characterization of retrograde conduction by direct endocardial recording from an accessory atrioventricular pathway.

Accessory pathway electrograms are rarely recorded in patients with Wolff-Parkinson-White syndrome. In one patient, during electrophysiologic study, simultaneous local ventricular (V) accessory pathway (AP) and atrial (A) deflections were recorded during bipolar catheter endocardial mapping over the pathway. Analysis of changes in electrographic intervals during performance of the ventricular extrastimulus technique allowed characterization of the retrograde conduction properties of the pathway. As coupling intervals were decreased, an initial increase was seen in the AP2A2 interval with subsequent ventriculoatrial block between the accessory pathway and atrium. When coupling intervals were further decreased, the V2AP2 interval lengthened with ultimate block between the ventricle and accessory pathway. These findings support the concept of impedance mismatch as the cause of conduction block in accessory pathways with the distal junction of the accessory pathway being the most vulnerable.

Adult↗
PubMed1986

Effects of acute tachycardia on left ventricular adenine nucleotide levels and subsequent tolerance to ischemia.

Electrophysiologically guided surgical procedures for the ablation of supraventricular and ventricular dysrhythmias often require prolonged periods of tachycardia to complete intraoperative mapping studies. It is unknown whether tachycardia depletes the myocardium of high-energy compounds or alters subsequent tolerance to ischemia. In the present study, 12 anesthetized dogs were paced from the right ventricle at a cycle length of 250 msec for 60 minutes. In seven animals, drill biopsy specimens were taken from the left ventricular free wall for analysis of adenine nucleotide levels and their breakdown products before and after pacing and after 20 minutes of recovery from pacing. In the remaining five animals, the heart was made totally ischemic immediately after tachycardia and the time to the onset of ischemic contracture was determined and compared to that of five nonpaced control dogs. Acute tachycardia resulted in no significant reduction in adenine nucleotide levels compared to control values. Furthermore, in hearts rendered totally ischemic after tachycardia, the mean time to ischemic contracture was 65.6 +/- 1.3 minutes versus 63.6 +/- 2 minutes in nonpaced control animals (no significant difference). These data show that pacing-induced tachycardia in the normal heart does not decrease adenine nucleotide levels or affect subsequent tolerance to ischemia. These results may be clinically relevant to patients without coronary artery disease who undergo operative procedures necessitating prolonged periods of tachycardia for intraoperative mapping to identify the site of arrhythmogenesis.

Adenine Nucleotides↗
PubMed1985

Comparison of two-dimensional echocardiographic and angiographic findings in arrhythmogenic right ventricular dysplasia.

Comparison of 2-dimensional (2-D) echocardiographic and right ventricular (RV) angiographic findings was performed in 10 patients with arrhythmogenic RV dysplasia. Diagnosis was based on accepted electrocardiographic and angiographic criteria. Nine patients underwent invasive electrophysiologic study, which confirmed RV source of ventricular tachycardia (VT) in 7. Biopsy findings of RV dysplasia were available in 3 patients. Two-dimensional echocardiography and angiography corresponded closely when diffuse RV enlargement and hypokinesia were present. Such diffuse findings were not invariably present. Localized abnormalities consisting of bulging or sacculation of the RV wall were noted by both techniques, even in the absence of diffuse changes. Echocardiographic evidence of localized disease predicted the presence of similar lesions at angiography, but agreement as to specific location was poor. Subjectivity in interpreting subtle RV abnormalities by either technique and the inherent differences in information provided by the 2 methods probably account for the inconsistencies. In the patient with suspected arrhythmogenic RV dysplasia, 2-D echocardiographic evidence of diffuse RV enlargement, otherwise unexplained, strongly supports the diagnosis and angiography may be avoided. Isolated local changes seen by echocardiography should increase suspicion of RV dysplasia, but complementary angiographic study is warranted.

Adolescent↗
PubMed1985

Cardiac function in patients on chronic amiodarone therapy.

Antiarrhythmic agents may depress cardiac contractility and worsen heart failure. Few data are available describing the chronic effects of amiodarone on myocardial function. To assess the effects of amiodarone on cardiac function, we studied 41 consecutive patients with first-pass or equilibrium radionuclide angiography prior to and 3 months after drug therapy was initiated. The mean heart rate, systolic blood pressure (BP), and diastolic BP were not significantly altered by treatment. The mean ejection fraction was 36% +/- 19 (mean +/- 1 SD) at the time of drug initiation and 36% +/- 17 3 months later (p less than 0.05). Nineteen patients had an ejection fraction greater than 30% and 16 had an ejection fraction less than 30%. The mean change in ejection fraction for these two subgroups showed no statistically significant difference, although a decrease in EF greater than 10% was seen in three patients (symptomatic in two), necessitating an increase in diuretic dose. No correlation between amiodarone dose and change in ejection fraction (r = -0.12, p greater than 0.05) was noted. There was no correlation between baseline ejection fraction and change in ejection fraction over this 3-month period (r = -0.36, p greater than 0.05). In summary, amiodarone does not depress left ventricular function and as a result can be used safely in patients with mild to moderate impairment of left ventricular function. In patients with stable left ventricular function, serial tests of left ventricular function may not be necessary.

Adult↗
PubMed1985

Frequency-dependent effects of verapamil on atrioventricular nodal conduction in man.

We sought to determine if verapamil induces frequency-dependent prolongation of atrioventricular nodal conduction in 10 consecutive patients studied in the electrophysiology laboratory. We used a maintenance infusion of verapamil designed to produce plasma concentrations of verapamil in the "therapeutic" range and that did not alter heart rate or blood pressure significantly. Frequency-dependent prolongation of atrioventricular nodal conduction (AH interval) was demonstrated in all 10 patients (p less than .001), and no change in HV conduction time with decreasing cycle length was noted in any patients while receiving verapamil. Two patterns of use-dependent response were seen. In four patients frequency-dependent prolongation of the delta(AH) interval [delta(AH) = AHverapamil - AHcontrol at a given cycle length] was seen with each decrement in pacing cycle length. In six patients frequency-dependent prolongation of the delta(AH) interval was not manifest until the fifth to eighth pacing cycle length tested. There was no association between the pattern observed and the initial heart rate or AH interval. After an abrupt change in pacing cycle length, the kinetics of delta (AH) interval prolongation were rapid; equilibrium was achieved by five to eight pulses in all patients. There was no correlation between the magnitude of prolongation of the AH interval noted at a particular cycle length and the concentration of verapamil during the maintenance infusion. These results indicate that verapamil causes use-dependent prolongation of atrioventricular nodal conduction in man.

Atrioventricular Node↗
PubMed1985

Right ventricular isolation procedures for nonischemic ventricular tachycardia.

Nonischemic ventricular tachycardia most commonly arises in the right ventricular free wall and is frequently refractory to medical therapy. Many different types of surgical procedures have been employed to treat medically refractory nonischemic ventricular tachycardia arising in the right ventricle, but the results of these procedures have been less than optimal. The majority of these surgical procedures have been directed toward ablation of the site (or sites) of origin of the tachyarrhythmia and have failed because of the frequent occurrence of multifocal or polymorphic ventricular tachycardia in these patients. We first employed localized surgical isolation procedures to control nonischemic ventricular tachycardia arising in the right ventricular free wall in 1979. These localized procedures evolved into the development of a technique for isolating the entire right ventricular free wall from the remainder of the heart to control ventricular tachyarrhythmias arising from multiple sites in the right ventricle. Case histories are reported of two patients who underwent localized isolation procedures in 1979 as well as two patients who underwent total disconnection of the right ventricle in 1982. The follow-up period in these four patients ranges from 2 to 5 years and the control of their tachyarrhythmias has been uniformly successful. However, surgical isolation of the entire right ventricular free wall has resulted in progressive dilatation of the right ventricle as documented by serial echocardiography. The pathophysiology of the progressive right ventricular dilatation postoperatively is discussed in terms of etiology and prevention, and the indications for application of localized and total isolation procedures for nonischemic right ventricular tachycardia are outlined.

Adolescent↗
PubMed1984

Functional properties of accessory atrioventricular pathways in Wolff-Parkinson-White syndrome. Clinical implications.

The Wolff-Parkinson-White syndrome is an uncommon cardiac disorder due to the presence of an accessory atrioventricular pathway resulting in ventricular pre-excitation and supraventricular tachycardias. The recognition of the Wolff-Parkinson-White syndrome is important because of the potential for the development of extremely rapid ventricular rates during atrial fibrillation that may lead to ventricular fibrillation and sudden death. The diagnosis of the Wolff-Parkinson-White syndrome is obvious when classic delta waves and short P-R intervals are present, but the electrocardiographic manifestations of the syndrome may be subtle and vary considerably from patient to patient. Certain commonly used antiarrhythmic medications may be useful for the treatment of reciprocating tachycardia in these patients and yet prove to be ineffective--or even deleterious--in preventing excessively rapid conduction to the ventricles during atrial fibrillation. An appreciation of the functional properties of the accessory pathways in the Wolff-Parkinson-White syndrome and how they are affected by pharmacologic agents should result in improved recognition of this entity and more effective medical management of patients with a risk of sudden death.

Anti-Arrhythmia Agents↗
PubMed1984

Ventricular tachycardia. Mechanisms, diagnosis, and management.

This article discusses ventricular tachycardia with reference to the various proposed mechanisms, diagnosis, and management. Criteria for the diagnosis of ventricular tachycardia caused by reentry, automaticity, and triggered activity are presented. The use of various drugs as well as the role of electrophysiologic testing is discussed.

Anti-Arrhythmia Agents↗
PubMed1984

Surface electrocardiographic clues suggesting presence of a nodofascicular Mahaim fiber.

Standard electrocardiograms from 87 consecutive patients with tachycardia of left bundle branch block configuration were analyzed retrospectively for features that might be characteristic of tachycardia utilizing a nodofascicular Mahaim fiber. The study group consisted of 13 patients with nodofascicular tachycardia, 34 with supraventricular tachycardia and aberrant conduction over the His-Purkinje system, 22 with ventricular tachycardia and 18 with antidromic tachycardia utilizing a right-sided accessory atrioventricular pathway. Six variables present during tachycardia of left bundle branch block configuration were predictive of a nodofascicular fiber: cycle length between 220 and 450 ms, QRS axis of 0 to -75 degrees, QRS duration 0.15 second or less, R wave in lead I, rS wave in precordial lead V1 and a precordial transition from a negative to a positive QRS complex after lead V4. All six criteria were present in 16 of the 87 patients. No patient with ventricular tachycardia satisfied these criteria, whereas 3 of 34 with supraventricular tachycardia, 1 of 18 with antidromic tachycardia and 12 of 13 with tachycardia using a nodofascicular fiber did. It is concluded that analysis of the surface electrocardiogram during tachycardia may suggest the presence of a nodofascicular fiber.

Adolescent↗
PubMed1984

Electrical termination of tachyarrhythmias by discrete pulses.

Reentrant tachycardias can often be terminated by discrete pacing stimuli that penetrate the reentrant circuit. The ability of discrete stimuli to terminate an arrhythmia depends on the timing of the stimulus, the distance from the site of reentry where the stimulus is applied, the electrophysiologic properties of the myocardium between the site of stimulation and the site of reentry, and the size of the reentrant circuit. Modes of pacing used to terminate tachycardia have included single or multiple timed extrastimuli, overdrive pacing, burst pacing and competitive asynchronous (underdrive) pacing. Patient-triggered devices that deliver asynchronous pacing stimuli are routinely available. Newer devices have been developed that automatically sense the onset of tachycardia and respond with pacing stimuli. These devices have been highly effective in selected patients with supraventricular tachycardia. The seriousness of occasional pacing-induced acceleration of ventricular tachycardia or conversion to ventricular fibrillation has limited the application of these devices in patients with ventricular arrhythmias. Pre-implantation electrophysiologic studies are necessary to document arrhythmia mechanisms and to determine the feasibility of various pacing modalities in treating the tachycardia. The potential for complicating arrhythmias (atrial fibrillation/flutter or ventricular fibrillation) must also be tested. Future devices designed for terminating tachycardias with discrete pulses should be capable of being programmed to respond with one or more of the various modalities available. These devices should automatically and reliably sense both tachycardia onset and termination, and should adjust their responses appropriately if initial stimulation sequences fail to terminate the arrhythmia.

Atrial Flutter↗
PubMed1984

Utility of electrophysiologic studies in the management of tachycardia, sudden death, and syncope.

The demonstrable value of EP studies for any given diagnostic or therapeutic category, in the last analysis, is largely a function of the subjects studied. Extrapolations from published data (that generally reflect a highly select patient population) to an individual patient can be fraught with error. Considerations of sensitivity and specificity must be balanced against the important need for information in patients at risk from life-threatening arrhythmias. We must never forget, however, that the EP substrate for any arrhythmia is not, as one might wish, a "black box" that should be expected to respond in a reproducible fashion to stimulation. The substrate is dynamic and subject to modification by change in autonomic tone, stretch, blood flow, basal rate, pH, electrolytes, oxygenation, and exposure to perhaps as yet undiscovered humoral mediators. The challenge to the clinical electrophysiologist is therefore not to exaggerate his efforts in one direction (i.e. programmed stimulation) while disregarding the other variables mentioned. Nor should we be disappointed and discard this approach because our expectations of an oversimplified model of arrhythmia testing are not fulfilled. Thus, in addition to careful stratification of patients, baseline studies should perhaps be carried out with more deliberate consideration of autonomic tone (exercise, isoproterenol), stretch (volume, handgrip, afterload), stress (physical and psychological), local anesthetic used, and body position. Only in this way will the scientific basis for acute and chronic EP testing be firmly established.

Death, Sudden↗