Search PubMed⌕ Search

Biomedical subjects

I Wiener

Publications and source records attributed to I Wiener.

At least 37 records · Page 2Linked to original sources
PubMed1990

Coronary artery spasm and myocardial infarction in a patient with normal coronary arteries: temporal relationship to pseudoephedrine ingestion.

A 28 yr-old male presented with chest pain and acute ST elevation following ingestion of pseudoephedrine. The pain and electrocardiographic changes disappeared after the administration of sublingual Nitroglycerin. Myocardial enzymes did show some evidence for myocardial necrosis. A subsequent coronary arteriogram showed no occlusive lesions. Pseudoephedrine, a sympathomimetic agent, may be implicated in the initiation of coronary spasm and myocardial infarction in some patients.

Adult↗
PubMed1990

Treatment of catecholamine-sensitive right ventricular tachycardia by endocardial catheter ablation.

Endocardial catheter ablation with direct current high voltage shocks was performed in a patient with recurrent syncope due to a catecholamine-sensitive ventricular tachycardia that was drug refractory and occurred in the absence of identifiable heart disease. Pace mapping and catheter activation mapping of the spontaneous and isoproterenol-induced ventricular tachycardia located the tachycardia origin in the right ventricular outflow tract. Ablation dramatically reduced spontaneous ventricular tachycardia and ectopic activity (from 50,000 to less than 100 ectopic beats/24 h). The patient has remained symptom free and without ventricular tachycardia recurrence for 3 years. These observations and review of previous studies suggest that catheter mapping can easily locate the arrhythmia focus in the right ventricular outflow tract and that catheter ablation can be performed at low risk. Catheter ablation is a viable option for the treatment of right ventricular catecholamine-sensitive tachycardias that are unresponsive to antiarrhythmic drugs.

Adult↗
PubMed1989

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↗
PubMed1989

Programmed electrical stimulation at potential ventricular reentry circuit sites. Comparison of observations in humans with predictions from computer simulations.

The purpose of this study was to define specific types of resetting responses to programmed electrical stimulation during human ventricular tachycardia and to use computer simulations of reentry circuits to assess the possible mechanisms and pacing site location relative to the reentry circuit for each type of response. The effects of scanning single stimuli at 35 left ventricular endocardial sites during sustained monomorphic ventricular tachycardia in 12 patients were studied. In considering alterations in QRS configuration and the delay between the stimulus and the advanced QRS, we identified three types of resetting responses to scanning stimuli consistent with stimulation at sites in or near the reentry circuit at 12 abnormal endocardial sites in eight patients. Type 1: all capturing stimuli were followed after a delay by early QRS complexes that had the same configuration as the tachycardia complexes. Type 2: late stimuli reset tachycardia as in type 1 but early stimuli reset the tachycardia after altering the QRS configuration. Type 3: late stimuli reset tachycardia as in type 1, but early stimuli advanced tachycardia with a short stimulus to QRS delay without altering the QRS configuration. In the simulations, premature depolarization of sites in the circuit produced orthodromic and antidromic wavefronts. The orthodromic wavefront propagated through the circuit and exited the circuit at the same site as did the previous tachycardia wavefronts and advanced the tachycardia without altering the configuration of the advanced QRS. The antidromic wavefront of relatively late stimuli was confined within or near the circuit by collision with the orthodromic wavefront of the preceding tachycardia beat and failed to alter ventricular activation distant from the circuit. Therefore, the QRS configuration after the stimulus was unchanged. A type 1 response occurred when all capturing stimuli produced this effect. However, with increasing stimulus prematurity, the antidromic wavefront propagated farther before colliding with an orthodromic wavefront, and under some conditions, it exited the circuit from a site other than the original circuit "exit," and altered the ventricular activation sequence distant from the circuit and, therefore, the QRS configuration, producing a type 2 pattern. The type 3 pattern occurred when the antidromic wavefront of early premature beats captured the original circuit exit. The effect of a stimulus was dependent on the stimulus prematurity, the relative conduction times from the stimulation site to the potential sites of "exit" from the circuit, and the timing of the excitable gap at the stimulation site.(ABSTRACT TRUNCATED AT 400 WORDS)

Cardiac Pacing, Artificial↗
PubMed1988

Complicated atherosclerotic lesions: a potential cause of ischemic ventricular arrhythmias in cardiac arrest survivors who do not have inducible ventricular tachycardia?

Sudden cardiac death that is not due to acute myocardial infarction may be due to primary ventricular tachycardia or to an arrhythmia secondary to a transient episode of ischemia. The purpose of this study was to determine if the incidence of complicated coronary lesions, which may be a cause of unstable ischemic syndromes, is increased in survivors of an aborted sudden death, especially those without ventricular tachycardia inducible by programmed ventricular stimulation. Nineteen consecutive survivors of an aborted sudden death not due to an acute infarction who underwent coronary angiography and programmed ventricular stimulation within 3 weeks of the event were matched for age, sex, previous infarction, and severity of coronary artery disease with 38 control patients with stable coronary artery disease. There was no difference in the incidence of complicated coronary lesions between the total group of sudden death victims and controls (47% vs 42%). However, 6 of the 11 (64%) sudden death patients who did not have inducible ventricular tachycardia had a complicated lesion as compared to only two of the eight (25%) patients with inducible ventricular tachycardia (p = 0.10). Angiograms identified a complicated lesion or functioning myocardium supplied only by collateral vessels as possible sources of transient ischemia in 73% of noninducible sudden death patients and in 25% of inducible sudden death patients (p = 0.04). Thus coronary angiography in cardiac arrest survivors who do not have inducible ventricular tachycardia often suggests a possible mechanism of transient ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1988

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↗
PubMed1987

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↗
PubMed1987

Effect of spatial separation of stimulation sites on ventricular refractoriness during programmed electrical stimulation.

To determine if electrical stimulation during the basic ventricular drive train introduces local effects that influence ventricular refractoriness during endocardial stimulation in humans, 10 patients were studied. With a hexapolar catheter with 3 mm interelectrode distances positioned at the right ventricular apex, the ventricular functional and effective refractory periods were determined for unipolar cathodal stimuli of 2 and 5 times diastolic threshold. Stimulation was performed with both the scanning extrastimulus (S2) and basic ventricular drive stimuli (S1) delivered to the same site and to sites separated by 6 mm. The functional refractory period was not changed by delivering the basic drive and extrastimuli to the same as opposed to separate sites (273.5 +/- 16 vs 273.5 +/- 19 msec during stimulation at 2 times threshold and 270 +/- 16 vs 270 +/- 18 msec at 5 times threshold; p = NS). The longest S1-S2 interval at which S2 failed to capture (effective refractory period) was longer by 5.5 +/- 8.2 msec at twice threshold (0.05 less than p less than 0.10) and 5.5 +/- 3.5 msec at 5 times threshold stimulation (p less than 0.01) when the basic drive and extrastimuli were delivered to separate sites. This is consistent with later activation of the extrastimulus sites during the basic drive when the stimulation sites were separate. Thus, with this method of endocardial programmed electrical stimulation, separation of the stimulation sites for the basic drive and extrastimuli does not affect ventricular refractoriness determined by the extrastimulus technique.

Adult↗
PubMed1986

Contribution of the anode to ventricular excitation during bipolar programmed electrical stimulation.

Anodal excitation may contribute to the initiation of ventricular arrhythmias during bipolar pacing in the canine ventricle. To determine if anodal excitation occurs during bipolar programmed ventricular stimulation in humans, ventricular electrograms adjacent to the anode and cathode were recorded using a specially designed hexapolar electrode catheter in 10 patients. Single extrastimuli were delivered during ventricular pacing at stimulus strengths slightly above the late diastolic threshold and at 2 to 5 times late diastolic threshold. Evidence of anodal excitation was observed in 18 of the 52 combinations (35%) of stimulus strengths and electrode configurations tested, and occurred in 9 of the 10 patients; it consisted of earliest ventricular activation adjacent to the anode (8 patients) or simultaneous activation at the anode and cathode (3 patients). This occurred either with premature stimuli (3 patients) or during the basic drive and extrastimuli (6 patients). Comparison of local activation times during unipolar pacing supported an anodal contribution to excitation during bipolar pacing and suggested that inhomogenous conduction delays were not responsible for these findings. Thus, anodal excitation occurs frequently during bipolar programmed stimulation and produces marked changes in local myocardial activation, which may potentially influence the initiation of ventricular arrhythmias.

Adult↗
PubMed1986

Intramural activation of the human ventricle: findings in normal and abnormal myocardial segments in patients with coronary artery disease.

To define the intramural electrical activation of normal and abnormal myocardial segments in patients with coronary artery disease, mapping was performed using a plunge electrode with 10 electrodes 1 mm apart. Five transmural bipolar electrograms (40 to 500 Hz) were recorded from 79 sites in 13 patients at the time of open-heart surgery. The results were correlated with ventriculography. In 64 sites with normal contraction, activation spread from endocardium to epicardium in 20.5 +/- 2 msec, and no electrograms were abnormal. Activation time did not differ between the different anatomic segments. In the eight hypokinetic sites, activation spread from endocardium to epicardium in 22.2 +/- 2 msec, and no electrograms were abnormal. In the seven sites with akinesis or dyskinesis, abnormal electrograms were noted and were concentrated towards the endocardium. In four patients, the 40% to 80% of electrograms closest to the endocardium were abnormal, while in three patients all transmural electrograms were abnormal. The variable depth of electrically abnormal tissue should be considered in operations and ablative procedures for ventricular arrhythmias.

Adult↗
PubMed1986

Colitis cystica profunda: diagnosis and management.

We have reported a case of colitis cystica profunda, an uncommon, benign disease of the colon presumably due to chronic inflammation, characterized by submucosal mucus-filled cysts. It may be premalignant, having been associated with ulcerative colitis and rectal adenocarcinoma. Diagnosis requires a high degree of suspicion and adequate biopsies, and treatment is by simple excision.

Adult↗
PubMed1986

Comparison of bipolar and unipolar programmed electrical stimulation for the initiation of ventricular arrhythmias: significance of anodal excitation during bipolar stimulation.

To determine if anodal excitation during bipolar stimulation facilitates the initiation of sustained monomorphic ventricular tachycardia, nonsustained polymorphic ventricular tachycardia, or repetitive ventricular responses, both bipolar and cathodal unipolar programmed ventricular stimulation with one to three extrastimuli delivered during ventricular pacing at two rates from the right ventricular apex were performed in 28 patients evaluated for spontaneous sustained ventricular tachycardia or ventricular fibrillation (11 patients), nonsustained tachycardia (eight patients), or syncope (nine patients). In 25 patients a hexapolar pacing catheter was used to record local endocardial activation times adjacent to the cathode and anode and ventricular excitation during bipolar stimulation was defined as predominantly anodal, cathodal, or simultaneous at both anode and cathode. When bipolar and unipolar stimulation were compared there was no difference in the incidence of initiating sustained monomorphic ventricular tachycardia (57% vs 57%), nonsustained polymorphic ventricular tachycardia (14% vs 14%), or repetitive ventricular responses (21% vs 21%), although the response to bipolar vs unipolar stimulation was not concordant in every patient. Evidence of anodal excitation was observed in 11 (44%) patients but did not indicate increased risk of initiation of any ventricular arrhythmia, despite the fact that it was associated with shortening of the ventricular effective refractory period by 5.2 +/- 8.7 msec (p less than .05) during bipolar as opposed to unipolar stimulation. We conclude that unipolar and bipolar stimulation produce a similar incidence of initiation of arrhythmia, despite the frequent occurrence of anodal excitation during bipolar stimulation. Thus, the risk of initiation of nonspecific ventricular arrhythmias during programmed stimulation is unlikely to be reduced by the use of unipolar stimulation.

Adolescent↗
PubMed1985

The role of neurotensin in human gallbladder motility.

Gallbladder contraction in response to a fatty meal is thought to be caused by release of cholecystokinin (CCK). We have previously demonstrated a close correlation between circulating concentrations of CCK and contraction of the gallbladder in normal humans and in gallstone patients. Recent studies in animals, however, have shown that other potentially cholecystokinetic hormonal agents are released by a fatty meal, which suggests that other hormones may be involved in postprandial gallbladder contraction. Neurotensin, a 13-amino acid peptide, is released by fat; we have shown it to cause gallbladder contraction in dogs. In the present study, we measured release of neurotensin in seven normal adult volunteers. We determined the effects of infused neurotensin (4 pmol/kg-min) on gallbladder contractility, measured by ultrasonography in 10 adult volunteers, and we evaluated release of neurotensin in eight patients with gallstones. After ingestion of fat, we found significant release of neurotensin in normal volunteers from a mean basal concentration of 15.9 +/- 3.5 pg/ml to a maximum of 34.7 +/- 0.2 pg/ml. In the gallstone patients after fat ingestion, neurotensin rose from a basal of 16.8 +/- 3.1 pg/ml to a maximum of 53.4 +/- 28.1 pg/ml, which was a significantly greater release than in controls. Intravenous infusion of neurotensin produced dilatation of the gallbladder (from a mean basal volume of 13.7 +/- 2.3 cc to 20.0 +/- 1.8 cc). Neurotensin causes relaxation of the gallbladder in humans and, by contributing to stasis, may be involved in the formation of gallstones.

Adult↗