Biomedical subjects

S J Eisenberg

Publications and source records attributed to S J Eisenberg.

5 recordsLinked to original sources

PubMed1997

Risk of thromboembolism in chronic atrial flutter.

Anticoagulant therapy is not conventionally used in the treatment of patients with atrial flutter. This recommendation has been based on sparse clinical experience, and recent preliminary reports suggest a significant risk of thromboembolism for these patients. A retrospective study was undertaken to assess the frequency of thromboembolic events as well as potential risk factors for these events in a cohort of patients with atrial flutter referred for radiofrequency ablation treatment. Eighty-six consecutive patients with a primary diagnosis of atrial flutter were evaluated. A history of embolic events was noted in 12 of 86 patients (14%) with atrial flutter, with an annual risk of approximately 3%. There were no differences in the prevalence of coronary artery disease, cardiomyopathy, valvular disease, or atrial fibrillation between the 2 groups of patients having an embolic event and those of patients without embolic events. Left ventricular function and left atrial size were also similar between the 2 groups. The only significant risk factor was hypertension (p < 0.05). However, in a regression model with other clinical variables (i.e., age, gender, left atrial size, presence or absence of any cardiac disease, length of time in flutter, left ventricular function, type of flutter, flutter cycle length, type of secondary arrhythmias) no significant predictors were found. Patients with transient ischemic attacks or pulmonary emboli were then excluded from the analysis in order to compare the thromboembolic risk in the present study to that reported in major atrial fibrillation trials. The overall risk becomes 7% (6 of 86), which over a mean follow-up period of 4.5 years yields an annual risk of approximately 1.6%. Although this risk is only 1/3 of that for patients with atrial fibrillation, this risk is higher than previously recognized for patients with chronic atrial flutter. Anticoagulant therapy should be seriously considered for these patients.

Adult↗

PubMed1997

Slow AV nodal pathway ablation utilizing a unique temperature controlled radiofrequency energy system.

Thirty-nine consecutive patients with symptomatic AV nodal reentrant tachycardia (AVNRT) underwent temperature guided slow AV nodal pathway ablation (group 1). Forty-three consecutive patients undergoing nontemperature guided slow AV nodal pathway ablation late in our experience compose the control population (group 2). Slow pathway ablation was achieved in all patients of both groups. The mean fluoroscopy and ablation times for group 1 were significantly shorter than for group 2 (26.1 +/- 14.9 vs 33.9 +/- 18.9 min, P < 0.05; 19.9 +/- 12.1 vs 30.9 +/- 23.3 min, P < or = 0.02). There were no episodes of coagulum formation in group 1, while there were 15 episodes (7.1% of energy applications) in group 2 (P = 0.0006) despite a significantly higher applied power in group 1 (53.4 +/- 25.1 vs 35.6 +/- 9.5W, P = 0.0001). Successful energy applications were associated with significantly higher temperatures than unsuccessful applications in group 1 (55.6 degrees +/- 5.8 degrees C vs. 52.9 degrees +/- 6.8 degrees C, P < or = 0.03). The minimum temperature required for successful ablation was 48 degrees C for two patients (5%) and was > or = 50 degrees C for the remainder of patients (37/39 [95%]). The catheter ablation system used in this study was safe, effective, and prevented coagulum formation while delivering relatively high power. In addition, shorter ablation times and radiation exposure were seen with this system. Although successful energy applications and the production of junctional rhythm were associated with higher achieved temperatures, temperature alone did not predict either endpoint. Future prospective, randomized trials are needed to confirm these findings and further evaluate the value of temperature monitoring.

Atrioventricular Node↗

PubMed1996

Deconvolution: a novel signal processing approach for determining activation time from fractionated electrograms and detecting infarcted tissue.

BACKGROUND: Two important signal processing applications in electrophysiology are activation mapping and characterization of the tissue substrate from which electrograms are recorded. We hypothesize that a novel signal-processing method that uses deconvolution is more accurate than amplitude, derivative, and manual activation time estimates. We further hypothesize that deconvolution quantifies changes in morphology that detect electrograms recorded from regions of myocardial infarction. METHODS AND RESULTS: To determine the accuracy of activation time estimation, 600 unipolar electrograms were calculated with a detailed computer model using various degrees of coupling heterogeneity to model infarction. Local activation time was defined as the time of peak inward sodium current in the modeled myocyte closest to the electrode. Deconvolution, minimum derivative, and maximum amplitude were calculated. Two experienced electrophysiologists blinded to the computer-determined activation times marked their estimates of activation time. F tests compared the variance of activation time estimation for each method. To evaluate the performance of deconvolution to detect infarction, 380 unipolar electrograms were recorded from 10 dogs with infarcts resulting from ligation of the left anterior descending coronary artery. The amplitude, duration, number of inflections, peak frequency, bandwidth, minimum derivative, and deconvolution were calculated. Metrics were compared by Mann-Whitney rank-sum tests, and receiver operating curves were plotted. CONCLUSIONS: Deconvolution estimated local activation time more accurately than the other metrics (P < .0001). Furthermore, the algorithm quantified changes in morphology (P < .0001) with superior performance, detecting electrograms recorded from regions of myocardial infarction. Thus, deconvolution, which incorporates a priori knowledge of electrogram morphology, shows promise to improve present clinical metrics.

Algorithms↗

PubMed1995

Sudden cardiac death and polymorphous ventricular tachycardia in patients with normal QT intervals and normal systolic cardiac function.

This study delineates the clinical spectrum of 15 patients with polymorphic ventricular tachycardia and normal QT intervals in the absence of apparent structural heart disease, adverse drug effects, or electrolyte disturbances. Patients presented with either palpitations (n = 2), presyncope (n = 5), syncope (n = 4), no symptoms (n = 1), or aborted sudden death (n = 3). Mean age was 41 years (range 20 to 64), and mean follow-up 38 months (range 4 to 109). Left ventricular function was normal as determined by either echocardiogram (n = 9) or left ventriculography (n = 9). Episodes of polymorphic ventricular tachycardia (VT) were analyzed in terms of the preceding interval, and the relation of the initiating coupling interval to the QT interval (coupling interval/QT interval = polymorphic VT index). The mean QT for the group as a whole was 0.41 +/- 0.02 second. Patients could be separated into 3 distinct groups. Four patients had polymorphic VT reproducibly induced by exercise and initiated by late-coupled beats (mean polymorphic VT index 1.27 +/- 0.21). Isoproterenol induced polymorphic VT in 3 of 4 patients, and all 4 responded to chronic beta blockade. Two patients had polymorphic VT during episodes of coronary artery spasm, and both responded to calcium channel blockade. Polymorphic VT unrelated to exertion or coronary vasospasm occurred in 9 patients. Tachycardia onset was initiated by closely coupled beats (mean polymorphic VT index 0.95 +/- 0.16), and was preceded by a pause in 4 patients, and no pause in 5 patients. Sudden death occurred in 5 of 9 patients with the shortest polymorphic VT indexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Fibroblast growth factor stimulates angiotensin converting enzyme expression in vascular smooth muscle cells. Possible mediator of the response to vascular injury.

Angiotensin converting enzyme (ACE) activity contributes to the vascular response to injury because ACE inhibition limits neointima formation in rat carotid arteries after balloon injury. To investigate the mechanisms by which ACE may contribute to vascular smooth muscle cell (VSMC) proliferation, we studied expression of ACE in vivo after injury and in vitro after growth factor stimulation. ACE activity 14 d after injury was increased 3.6-fold in the injured vessel. ACE expression, measured by immunohistochemistry, became apparent at 7 d in the neointima and at 14 d was primarily in the most luminal neointimal cells. To characterize hormones that induce ACE in vivo, cultured VSMC were exposed to steroids and growth factors. Among steroids, only glucocorticoids stimulated ACE expression with an 8.0 +/- 2.1-fold increase in activity and a 6.5-fold increase in mRNA (30 nM dexamethasone for 72 h). Among growth factors tested, only fibroblast growth factor (FGF) stimulated ACE expression (4.2 +/- 0.7-fold increase in activity and 1.6-fold increase in mRNA in response to 10 ng/ml FGF for 24 h). Dexamethasone and FGF were synergistic at the indicated concentrations inducing 50.6 +/- 12.4-fold and 32.5-fold increases in activity and mRNA expression, respectively. In addition, when porcine iliac arteries were transfected with recombinant FGF-1 (in the absence of injury), ACE expression increased in neointimal VSMC, to the same extent as injured, nontransfected arteries. The data suggest a temporal sequence for the response to injury in which FGF induces ACE, ACE generates angiotensin II, and angiotensin II stimulates VSMC growth in concert with FGF.

Animals↗