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Biomedical subjects

M H Lehmann

Publications and source records attributed to M H Lehmann.

At least 19 recordsLinked to original sources

Long-term effects of percutaneous laser balloon ablation from the canine coronary sinus.

BACKGROUND: Radiofrequency catheter ablation of left-sided accessory pathways is becoming the first line of therapy for patients with symptomatic Wolff-Parkinson-White syndrome. Nevertheless, alternative ablation techniques merit development, at least as supplementary modalities for cases in which conventional ablation approaches may prove unsuccessful. We recently reported the short-term results with transcatheter laser balloon ablation from the coronary sinus in a canine model, proving that the procedure is feasible for the potential ablation of left-sided accessory pathways. We now report the effects of percutaneous transcatheter laser balloon ablation in a chronic canine model. METHODS AND RESULTS: Twenty adult mongrel dogs were studied. After baseline coronary arteriography, left ventriculography, and coronary sinus angiography were obtained, 15 dogs received two or three consecutive laser doses from the coronary sinus of 30-40 W for 15-30 seconds, for a total cumulative energy of 1,200-2,400 J. The five remaining animals underwent a procedure consisting of balloon sham inflation without laser exposure and served as controls. After a mean follow-up of 6 weeks, the angiographic procedures were repeated, and the animals were killed. The mean extent of the fibrotic lesion was 15 mm long, 6 mm wide, and 4.5 mm deep and involved the coronary sinus wall, atrium, and, frequently, the summit of the posterior left ventricular wall. Six animals (four in the study group and two in the control group) showed asymptomatic narrowing of the coronary sinus lumen but always with total angiographic reconstitution due to extensive collateral circulation. The circumflex artery and mitral valve were intact angiographically and histologically in all animals. CONCLUSIONS: Percutaneous transcatheter laser balloon ablation via the coronary sinus produces a lesion that may be anatomically well suited for left-sided accessory pathway ablation. Although coronary sinus narrowing may occur, adverse physiological effects are unlikely due to the development of extensive collateral circulation. Systematic clinical studies of this new approach to catheter ablation appear warranted.

Animals

Operative mortality with implantation of the automatic cardioverter-defibrillator.

Operative mortality was studied in 939 consecutive patients undergoing initial implantation of an automatic implantable cardioverter-defibrillator (AICD) at 15 hospitals. Twenty-nine (3.1%) patients died during the first 30 days after surgery. Among patients who survived beyond the first 30 postoperative days, ejection fraction data were available in 219; compared with the mortality group, these survivors had a significantly higher ejection fraction (34 +/- 15 vs 26 +/- 10%, respectively, p less than 0.001), despite similar age, sex, underlying heart disease, type of presenting arrhythmia and prevalence of concomitant surgery. The causes of perioperative death were sudden in 7 (24%), tachyarrhythmic/nonsudden in 5 (17%), cardiac nonarrhythmic in 9 (31%), and noncardiac in 8 (28%). Twenty-four (83%) of the deaths occurred before hospital discharge, and in all 9 instances of in-hospital sudden and tachyarrhythmic/nonsudden death, the initial recorded rhythm was sustained ventricular tachycardia or fibrillation; in 5 (56%) of these 9 patients the AICD had been in a deactivated state since implantation. Other possible contributory factors in the 12 sudden or tachyarrhythmic/nonsudden deaths included acute myocardial ischemia or infarction in 2 (17%), and "device proarrhythmia" in 3 (25%) that were AICD-related in 2 and secondary to an antitachycardia pacemaker in another; defibrillation threshold testing was not performed in 3 patients (1 of whom had terminal ventricular fibrillation). Thus, in this multicenter experience with thoracotomy requiring AICD implantation, operative (30-day) mortality was 3.1% and correlated inversely with left ventricular ejection fraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Cohort Studies

Sudden cardiac death: management of high-risk patients.

Sudden cardiac death remains a leading cause of death in the United States, accounting for more than 350,000 deaths each year, and the survival rate of victims remains low. Most survivors face a significant risk for recurrence. The typical substrate is chronic--abnormal myocardium with fibrosis (often from previous myocardial infarction) and left ventricular dysfunction. Acute triggers for sudden cardiac death are primarily electrical, ischemic, metabolic, neurohormonal, and pharmacologic. In most electrocardiographically documented cases of sudden cardiac death, the trigger-substrate interaction appears to result in ventricular tachycardia and fibrillation. After initial resuscitation, survivors need a thorough cardiovascular evaluation, including definition of coronary anatomy, left ventricular function, and wall-motion abnormalities, as well as an electrophysiologic evaluation. An attempt must be made to determine what each survivor's correctable triggers are. Management should address all reversible triggers, such as acute ischemia and electrolyte abnormalities, and should include modifying or correcting the arrhythmogenic substrate. Empiric antiarrhythmic therapy offers no advantage in such modification. Pharmacologic therapy with antiarrhythmic drugs should be guided by an objective therapeutic endpoint, which is best accomplished through the use of programmed ventricular stimulation and serial electrophysiologic studies. Other therapeutic options include surgical suppression of ventricular tachycardia and implantation of a cardioverter defibrillator.

Arrhythmias, Cardiac

Recovery of retrograde fast pathway excitability in the atrioventricular node reentrant circuit after concealed anterograde impulse penetration.

The recovery of the retrograde fast pathway excitability in atrioventricular (AV) node reentry has been difficult to assess with ventricular extrastimulation because of difficulty in achieving sufficiently short intranodal coupling intervals and the potential interposition of "lower common pathway" nodal tissue. To circumvent these methodologic obstacles in 10 patients with inducible AV node reentrant tachycardia, a fixed atrial extrastimulus (A2) coupled to a basic atrial drive (A1) at a cycle length of 500 ms was utilized to reproducibly initiate AV node reentrant echoes. A ventricular extrastimulus (V3) was then introduced after A2 at progressively shorter coupling intervals (A2V3) in an attempt to pre-excite the retrograde fast pathway after concealed anterograde penetration by A2. In six patients, retrograde fast pathway pre-excitation was achieved at critical A2V3 intervals, as evidenced by the appearance of A3 by up to 28 +/- 6 ms in advance of the expected first AV node reentrant echo. In five of the six cases, the V3A3 interval was virtually unaltered (less than or equal to 5 ms decrease) when A2 was omitted. In seven patients, at a critically short A2V3 coupling interval (195 +/- 27 ms ), V3 abruptly failed to elicit A3 and concomitantly abolished all AV node echoes; yet when A2 was omitted, an A3 response returned, with V3A3 identical to previous values.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Effects of transdermal scopolamine on heart rate variability in normal subjects.

A decrease in cardiac parasympathetic tone is a recognized finding in patients with ischemic heart disease, sudden cardiac death and heart failure, correlating closely with disease severity and overall survival. To study the clinical potential of vagomimetic intervention, the effect of transdermal scopolamine on fluctuations in heart rate was studied in 32 healthy adult subjects using both time-domain (mean RR interval, standard deviation of the mean RR interval, mean of the differences between consecutive RR intervals) and frequency-domain measures (spectrum analysis of 128 consecutive RR intervals) of heart rate variability. After an exposure of 24 hours, transdermal scopolamine resulted in a significant increase in all indexes tested. The increase was most pronounced in the 0.25-Hz respiratory peak of the RR interval power spectrum, compatible with a strong vagomimetic mode of action of transdermal scopolamine. Results indicate that transdermal scopolamine may have potential merit as a selective vagotonic agent in certain patients with myocardial infarction, heart failure or ventricular arrhythmias.

Administration, Cutaneous

Percutaneous transcatheter laser balloon ablation from the canine coronary sinus: implications for the Wolff-Parkinson-White syndrome.

Transcatheter direct current electrical shocks for ablation of left-sided accessory pathways in Wolff-Parkinson-White patients have led to serious complications. We report the feasibility of percutaneous transcatheter laser balloon ablation of left-sided accessory pathways from the coronary sinus using a 1,064-nm, continuous wave Nd:YAG laser triple lumen catheter with an optical fiber terminating in a cylindrical diffusing tip within a 2-cm-long, 3-mm-diameter balloon transparent to Nd:YAG laser radiation. In eight mongrel dogs (18 to 31 kg), the laser balloon catheter was positioned via an 8 French guide catheter in the distal and proximal coronary sinus. During balloon inflation, two to three consecutive laser doses of 30 W x 20 sec were applied to each site (cumulative energy, 1,200 to 1,800 J). Coronary angiography, left ventriculography, and coronary sinus injection were performed before and after laser exposure. After percutaneous transcatheter laser balloon ablation, there was no evidence of mitral regurgitation, left circumflex artery, coronary sinus obstruction, or perforation. Coagulation necrosis and/or polymorphonuclear infiltrates involving the atrioventricular groove and left atrial wall over a mean length of 17 mm were present in all eight dogs sacrificed 6 +/- 1 hr postablation. In conclusion, percutaneous transcatheter laser balloon ablation from the coronary sinus is free of immediate major complications and may be feasible for potential interruption of left-sided accessory pathways.

Animals

Amiodarone-induced changes in lipid metabolism.

Hypothyroidism is a major cause of secondary hypercholesterolemia. Amiodarone treatment alters both the levels of serum lipids and thyroid hormones. We investigated whether the amiodarone-induced changes in lipid metabolism are related to the changes in thyroid hormone levels. Eighteen patients received amiodarone (31 +/- 3 g cumulative dose) for six weeks. Serum triglyceride, total-cholesterol, high density lipoprotein-cholesterol and its subfractions, apolipoproteins B and AI, and plasma post-heparin lipoprotein lipase and hepatic triglyceride lipase activities were determined. Amiodarone treatment caused significant increases in serum total-cholesterol (baseline 4.4 +/- 0.21 (SE), 6 weeks 5.12 +/- 0.26 mmol/l, P less than 0.01), in low density lipoprotein cholesterol (baseline 2.61 +/- 0.26, 6 weeks 3.36 +/- 0.21 mmol/l, P less than 0.05) and in apolipoprotein B (baseline 1.95 +/- 0.15, 6 weeks 2.26 +/- 0.13 mmol/l, P less than 0.01) concentrations. Serum high density lipoprotein and its subfractions, or apolipoprotein AI levels did not change. Plasma post-heparin lipoprotein lipase activity increased (baseline 137 +/- 21, 6 weeks 168 +/- 21 U/ml, P less than 0.01) while hepatic triglyceride lipase did not change. Amiodarone also caused an increase in serum thyroxine (baseline 110 +/- 8, 6 weeks 136 +/- 6 mmol/l, P less than 0.05), although values remained in euthyroid range. In summary, amiodarone therapy increased the concentrations of atherogenic lipoproteins in the serum similar to that seen in hypothyroidism. On the other hand the effect of amiodarone on lipoprotein lipase was opposite to that seen in hypothyroidism. Therefore, amiodarone-induced changes in lipid metabolism cannot be explained solely on the basis of the changes in circulating thyroid hormone levels.

Aged

Clinical management of patients with atrioventricular nodal reentrant tachycardia.

A broad array of therapeutic options is currently available for the management of patients with AV nodal reentrant tachycardia. While acute termination of tachycardias is readily achieved, either by vagal maneuvers or intravenous medication, the decision to embark on a long-term therapeutic plan to prevent recurrences must be clinically individualized. When a chronic pharmacologic approach is desired, electrophysiologic testing is invaluable for confirming the diagnosis and selecting appropriate medication. However, the growing awareness of potential proarrhythmic effects and the inconvenience and expense of lifelong drug therapy, coupled with other advances in the field, have made nonpharmacologic approaches more attractive. This is especially so for symptomatic younger patients. The definitive cure rates achievable with surgery are now being approached by transcatheter AV nodal modification procedures that ablate AV nodal reentrant tachycardia while preserving anterograde AV nodal conduction. Over the next decade, it is likely that the latter technique will become widely used for the long-term management of symptomatic AV nodal reentrant tachycardia.

Anti-Arrhythmia Agents

Reemployment following implantation of the automatic cardioverter defibrillator.

One hundred one patients who received an implantable automatic cardioverter defibrillator (ACD) were evaluated to determine the reemployment rate and factors associated with return to work. Forty-seven were employed before ACD implantation. Their mean (+/- standard deviation) age was 53 +/- 11 years, 83% were men, 75% had coronary artery disease, 76% presented with cardiac arrest and 28% had concomitant cardiac surgery. The mean ejection fraction of these patients was 0.41 +/- 0.15. At follow-up, 29 patients (62%) had resumed work at 11 +/- 9 weeks after implantation. Those who returned to work were better educated (15 vs 11 years, p less than 0.001) and less likely to have a history of prior myocardial infarction (p less than 0.05). There were no significant differences between patients who returned to work and those who did not in terms of age, sex, race, functional class, ejection fraction, extent of coronary artery disease, reason for ACD, or concomitant surgery. Multivariate analysis revealed that level of education was the single best predictor of reemployment status. The only other factors found to add significant predictive power in a stepwise analysis were extent of coronary artery disease and marital status. The model using these 3 variables had a sensitivity of 83% and a specificity of 72%. It was concluded that (1) most patients employed before ACD implantation are able to return to work after the procedure, and (2) nonmedical factors play an important role in the resumption of work-related activities. These findings have important quality-of-life and cost-effectiveness implications for ACD implantees.

Aged

Wide QRS tachycardia in the conscious adult. Ventricular tachycardia is the most frequent cause.

Hemodynamic stability during wide QRS tachycardia is commonly, albeit erroneously, taken as evidence for a supraventricular mechanism. To determine the magnitude for potential misdiagnosis in applying this notion clinically, we analyzed 20 consecutive cases of regular wide QRS tachycardia in conscious adult patients (mean age, 64 years). The most common heart disease was atherosclerotic (75%), with an associated history of remote myocardial infarction in 73% of the cases. Tachycardia was sustained for a mean of 4.8 hours prior to medical evaluation, with a mean rate of 186 beats per minute and mean systolic blood pressure of 111 mm Hg. A diagnosis of ventricular tachycardia (VT) was established in 17 cases (85%). In the patients with VT, atrioventricular dissociation was recognized on the 12-lead electrocardiogram in 38%, with Wellens' morphological features favoring the diagnosis in 73%. Following conversion to sinus rhythm, electrophysiological testing in 17 patients reproduced the clinical arrhythmia in 94% (with a replication rate of 100% in 15 patients with VT), with at least one additional unsuspected VT morphology induced in 53% of patients with VT. Thus, VT should be considered the most likely cause of regular wide QRS tachycardia in the conscious adult patient, especially with a history of remote myocardial infarction. Recognition of this simple principle and careful examination of the 12-lead electrocardiogram may help to prevent the misapplication of pharmacotherapy in the vast majority of these patients.

Aged

The excitable gap in atrioventricular nodal reentrant tachycardia. Characterization with ventricular extrastimuli and pharmacologic intervention.

Our purpose was to characterize the excitable gap during atrioventricular nodal reentrant tachycardia (AVNRT) to elucidate the electrophysiologic substrate of this clinically familiar microreentrant arrhythmia. Accordingly, in 11 patients with classic slow-fast AVNRT (mean cycle length, 342 +/- 41 msec), a single ventricular extrastimulus (V2) was periodically delivered after a spontaneous tachycardia beat (V1) until ventricular refractoriness was reached. With this technique, an excitable gap was considered present when atrial preexcitation of at least 20 msec could be achieved along with tachycardia resetting (noncompensatory pause after V2). The range of V1V2 intervals that resulted in atrial preexcitation constituted the preexcitation zone. Five patients (45%) showed evidence of an excitable gap at baseline, with a maximal atrial preexcitation achievable of 33 +/- 6 msec, representing 9 +/- 1% of the tachycardia cycle length. Verapamil was then administered to all 11 patients with the purpose of slowing the anterograde tachycardia wavefront before arrival of V2. This resulted in widening of the preexcitation zone in three patients by a mean of 50 +/- 37 msec, with a corresponding increase in maximal atrial preexcitation to 70 +/- 32 msec, or 16 +/- 4% of AVNRT cycle length, and the appearance of atrial preexcitation in two patients who lacked it during baseline. In the remaining six patients, AVNRT was not sustained after verapamil or was too unstable for evaluation. During baseline, V2A2 conduction time increased by only 5 +/- 3 msec throughout the preexcitation zone, with values at the outer border unchanged after verapamil, implying a fully excitable gap in the retrograde limb. In all patients with a preexcitation zone, AVNRT was consistently reset by V2, both at baseline and after verapamil, with a "flat" but mainly "increasing" response pattern as V1V2 was shortened. Hence, a significant number of patients with AVNRT have evidence of an excitable gap whose demonstrability can be facilitated by pharmacologic intervention; documentation of an increasing resetting response pattern, most apparent after verapamil, provides new evidence for a reentrant mechanism in AVNRT; and while not definitively proven, the presence of a fully excitable gap during AVNRT is most consistent with a microreentry circuit that incorporates an anatomic obstacle.

Atrioventricular Node

Electrophysiological determinants of antidromic reentry induced during atrial extrastimulation. Insights from a pacing model of Wolff-Parkinson-White syndrome.

The electrophysiology of antidromic reentry, a less common phenomenon than orthodromic reentry, remains a poorly understood aspect of the Wolff-Parkinson-White (WPW) syndrome. We used a pacing model of ventricular preexcitation in patients without WPW, so that electrophysiological events in the normal pathway during atrial extrastimulation (A1-A2 technique) could be precisely delineated without the obscuring effect of an actual accessory pathway. Ventricular preexcitation was simulated by an A1-V1 sequential basic drive with A2-V2 extrastimulation at progressively shorter A1-A2 (equal to V1-V2) coupling intervals. At each coupling interval tested within the zone of atrioventricular (A-V) nodal effective refractory period (since anterograde block of A2 was considered mandatory for manifestation of antidromic reentry), responses were assessed after A2 alone (method I), V2 alone (method II), and A2 plus V2 (method III, the complete preexcitation model). The entire pacing protocol was performed at two A-V intervals, short (50 msec) and long (150-180 msec), thereby simulating different proximities between the A pacing site and "accessory pathway" location. Of 47 consecutive unmedicated patients screened for the study protocol, 38 failed to meet minimal prerequisites for possible initiation of antidromic reentry because of failure in 18 (38% of total) to achieve anterograde A-V nodal block of A2, even though 1:1 ventriculoatrial conduction to cycle lengths less than or equal to 500 msec (less than or equal to 400 msec in 12) was present; and poor or absent ventriculoatrial conduction in the others. The nine remaining candidates underwent the full pacing protocol. Antidromic reentry (retrograde atrial response following V2 in method III) was observed in only two cases (4% of total), and both were associated with retrograde His-Purkinje system delays (documented by method II) occurring in tandem with a long A-V interval, thereby allowing for completion of retrograde A-V nodal recovery after penetration by A2. Indeed, such a prolonged recovery time prevented initiation of antidromic reentry in six of the nine patients (proven by intact ventriculoatrial conduction in method II). Retrograde A-V nodal block of V2, independent of A2, prevented an antidromic echo in one case. Findings in our model help to clarify the various factors, including specific anterograde and retrograde A-V nodal properties; anatomic relation between the accessory and normal pathways; and the retrograde His-Purkinje system delays, that must prevail in a concerted fashion to permit the initiation of antidromic reentry during the A1-A2 technique in patients with the WPW syndrome.

Atrioventricular Node