Recapitulation of menstrual migraine with tamoxifen.
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Adult↗
Biomedical subjects
P Mathew
Publications and source records attributed to P Mathew.
Folate receptor type beta is a neutrophilic lineage marker and is differentially expressed in myeloid leukemia.
BACKGROUND: The membrane-associated folate receptor (FR) type beta is elevated in the spleen in patients with chronic myeloid leukemia (CML) and acute myeloid leukemia (AML). In this study, the authors investigated possible cell type and differentiation stage specificity of expression of FR-beta in normal and leukemic hematopoietic cells. METHODS: An affinity-purified rabbit polyclonal antibody specific for FR-beta was employed for immunostaining representative bone marrow smears and peripheral blood smears from normal individuals and from a limited number of patients with various leukemias. Multiple samples of normal bone marrow and peripheral blood were analyzed for the expression of FR-beta and selected CD antigens by two- or three-color flow cytometry. RESULTS: Of the morphologically identifiable cells, only neutrophils were positive for FR-beta. The leukemic blasts in CML patients showed expression of FR-beta with no apparent relation to the occurrence of the Philadelphia chromosome. Among acute nonlymphocytic leukemias, FR-beta was expressed in promyelocytic leukemia, in the myeloblast populations of myelomonocytic and erythroleukemias, and variably in M1/M2 AML. Neither the blasts of acute lymphocytic leukemia nor the more mature cells of chronic lymphocytic and hairy cell leukemias expressed FR-beta. The less differentiated FR-beta positive AML samples also were positive for CD34 and HLA-DR. Flow cytometric analysis of normal bone marrow and peripheral blood revealed low or insignificant coexpression of FR-beta with CD34, CD19, and CD3, whereas significant coexpression was observed with high levels of CD33, CD13, and CD11b; coexpression of FR-beta with CD14 was high in the immature bone marrow cells, comparable to that in myeloid cells, but relatively low in peripheral blood. CONCLUSIONS: The results of this study suggest a narrow expression pattern of FR-beta marking the neutrophilic lineage and the possibility of defining a subtype or subtypes of myeloid leukemia based on FR-beta expression. The identification of FR-beta positive leukemias and the absence of the receptor in normal CD34 positive cells may enable selective receptor-mediated targeting of leukemic cells.
Animals↗
Electrophysiology and endocardial mapping of induced atrial fibrillation in patients with spontaneous atrial fibrillation.
We analyzed the patterns of atrial activation and characterized the electrophysiologic properties of regional atrial sites in the, right atrium and left atrium at the onset of atrial fibrillation (AF) induced with programmed right atrial (RA) stimulation. Intraatrial conduction, atrial electrogram return cycle lengths for the first AF cycle, RA and left atrial (LA) activation maps during AF, and the stability and reproducibility of atrial activation sequences at AF onset and maintenance were analyzed in 23 patients with AF. Correlation of intracardiac electrograms with surface electrocardiographic morphology was attempted. Maximum intraatrial conduction delay for high RA premature beats was observed at the coronary sinus ostium (n = 15), His bundle region (n = 13) or interatrial septum (n = 15). The return cycle lengths for the first AF cycle showed increasing conduction delay with increasing prematurity of the last extrastimulus in most patients. Suprisingly, discrete atrial electrograms with regular or irregular cycle lengths were present at the onset of electrocardiographic documented coarse AF in 13 of 15 patients (87%). Fragmented or chaotic atrial activity were present in 2 of 15 patients (13%) in coarse AF but observed at > or = 1 atrial sites in 7 of 8 patients (88%) with fine AF (p = 0.001). The atrial activation sequence at the onset of the induced AF elicited by high RA extrastimuli usually showed the earliest activation site at the crista terminalis (9 patients) or interatrial septum (9 patients). In contrast, induced AF elicited from other RA sites usually showed earliest atrial activation at the septum (3 patients) or coronary sinus ostium (3 patients). Atrial activation sequences for the first induced AF cycle were usually reproducible in most patients. Atrial activation patterns during the first 10 cycles for AF were stable in RA and LA regions in 6 of 23 patients (260%) but demonstrated significant change(s) at > or = 1 region in 17 of 23 patients (74%) (p <0.05). We conclude that pacing induced AF elicited by RA premature beats commences as a regular or irregular rapid atrial tachycardia consistent with a transitional, but often organized, arrhythmia. The activation sequence and electrophysiologic behavior of the first induced AF cycle is consistent with intraatrial reentry and reproducible in most patients. More than 1 atrial activation sequence can sometimes be observed, emphasizing the dynamic nature of the initial RA reentrant circuits.
Aged↗
Colony-Stimulating Factors in the Therapeutic Approach to Sepsis.
Sepsis and its complications continue to be a leading cause of death in the United States despite availability of potent broad-spectrum antimicrobial agents. Current in vitro, ex vivo, animal, and human data are reviewed. Present data shows that colony-stimulating factors (CSFs), granulocyte CSFs, and granulocyte-macrophage CSFs are very effective in raising the leukocyte count and shortening the number of neutropenic days. CSFs in some studies improved outcome of neutropenic septic patients especially when given very early. However, there are studies that do not show any benefit. CSFs appear to be safe and should be limited to septic, neutropenic patients whose duration of neutropenia is anticipated to be prolonged, or to patients who are seriously ill.
Journal Article↗
Subcutaneous methadone in terminally ill patients: manageable local toxicity.
Methadone has been found to be useful in pain uncontrolled by large doses of conventional opioids such as hydromorphone and morphine. While the subcutaneous route is effective and may afford cost-savings over the intravenous route in patients unable to take oral medication, its utility for the administration of methadone may be hampered by local toxicity, specifically erythema and induration. To examine the issue of limiting toxicity, we analyzed our inpatient hospice experience in six consecutive patients who received subcutaneous methadone for severe cancer pain. We confirm the high incidence of local toxicity, but note that the severity is subject to considerable individual variation. Furthermore, toxicity is uniformly manageable by site rotation and the use of dexamethasone infused concurrently with the methadone. We recommend that the infusion of subcutaneous methadone should be considered in the appropriate patients who can be closely monitored.
Adult↗
Prospective clinical evaluation of a programmed atrial stimulation protocol for induction of sustained atrial fibrillation and flutter.
UNLABELLED: We sought to define a minimum standardized protocol for induction of atrial fibrillation [AF] and/or atrial flutter. In contrast to ventricular stimulation protocols, a stimulation protocol for induction of AF or atrial flutter has not been critically evaluated. Since suppression of inducible AF or atrial flutter is used as one of the endpoints of success of pharmacologic and ablation therapies, there is an obvious need to define a minimally appropriate electrical stimulation protocol for induction of AF or atrial flutter. We prospectively evaluated 70 patients, 44 with spontaneous atrial flutter or AF and 26 controls without documented atrial arrhythmias. A standardized programmed stimulation protocol, which employed up to three atrial extrastimuli delivered at two atrial sites at two atrial drive pacing lengths, was used in attempt to reproduce sustained AF and atrial flutter. The study endpoint was induction of sustained (> 30 s) AF or atrial flutter. Sustained AF or atrial flutter was induced in 39/44 (89%) patients and 2/26 (7%) of controls (p < 0.01). The arrhythmia induced was atrial flutter in 19/21 (91%) of atrial flutter patients, AF in 17/18 (94%) AF patients, both atrial flutter and AF in 5 AF/atrial flutter patients (100%). Two patients with atrial flutter had both AF/atrial flutter and 1 patient with AF had atrial flutter induced. The arrhythmia was induced from first stimulation site in 37 patients (85%) using a single extrastimuli in 9 (20%) patients, double extrastimuli 18 (41%) patients and triple extrastimuli in 10 (23%) patients. Two patients (5%) required stimulation from second site with two and three extrastimuli, respectively. The overall sensitivity and specificity of this stimulation protocol were 89% and 92%, respectively with a positive predictive accuracy of 95%. CONCLUSIONS: 1. Up to three atrial extrastimuli and two atrial sites are needed to increase yield of AF/atrial flutter induction at electrophysiologic study. 2. Induction of either AF or atrial flutter correlates well with the presence of a similar spontaneous arrhythmia. 3. A baseline determination of the induction mode may be desirable prior to evaluation of interventions directed at AF or atrial flutter.
Aged↗
Myelodysplastic syndromes in the adolescent.
Myelodysplastic syndromes (MDS) are a group of acquired blood diseases that are the result of abnormal bone marrow function. The ineffective production of red cells, platelets, and white blood cells can lead to symptomatic anemia, bruising, infections, and the likelihood of evolution into acute myelogenous leukemia. While MDS is uncommon in the adolescent patient, a surprising number of affected individuals are also affected with a predisposing constitutional syndrome. The treatment of MDS in the adolescent patient is in part determined by symptoms and also by the historical outcomes associated with each of five morphologic categories of presentation. Improved supportive care has allowed for increasingly more children with MDS to survive into the second decade of life. The management of MDS in affected adolescents presents a number of interesting and worthwhile challenges to health care professionals.
Adolescent↗
Interventional therapeutic procedures in patients with a preexisting dual site right atrial pacing system for refractory atrial fibrillation.
This report illustrates the complexity of internal atrial defibrillation and implantable cardioverter-defibrillator therapy in patients with dual site atrial pacing systems.
Adult↗
Unexplained bleeding, arterial stenosis, alopecia, and a splenic catastrophe.
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Adult↗
Risk stratification and clinical outcome of minimally symptomatic and asymptomatic patients with nonsustained ventricular tachycardia and coronary disease: a prospective single-center study.
The Multicenter Automatic Defibrillator Implantation Trial (MADIT) showed improved survival with defibrillator therapy but was restricted to coronary artery disease patients with nonsustained ventricular tachycardia (NSVT) and inducible nonsupressible VT. The outcome of patients without inducible VT or inducible but suppressed VT still remains unclear. We performed risk stratification at electrophysiologic (EP) study in 111 consecutive unselected patients with nonsustained VT and coronary artery disease and randomized them to drug or device therapy. Follow-up on selected therapy was 1-71 (mean 27 +/- 20) months. Of 111 patients, 39 patients (35%) had inducible sustained VT at baseline EP study and were stratified to a "higher" risk group (group 1) for sudden death. In 9 of these patients (group 1A), sustained VT was suppressed with class IA antiarrhythmic drugs; in the remaining 30 patients (group 1B) sustained VT was not suppressed with class IA antiarrhythmic drugs. The other 72 of 111 patients (65%) had no inducible sustained VT at EP study and were stratified to a "lower"-risk group (group 2) for sudden death. Mean LVEF in group 1 was 30 +/- 10% versus 37 +/- 9% in group 2 (p = 0.001). Selected therapy in group 1 was an implantable cardioverter defibrillator (16 patients) or guided drug therapy (electrophysiologically guided class I antiarrhythmic drugs = 7 patients; Holter-guided class III antiarrhythmic drugs = 16 patients). In group 2, empiric drug therapy included beta blockers in 29 patients or Holter-guided class III antiarrhythmic drugs in 17 patients, with no antiarrhythmic drug therapy being administered in 26 patients. Mean LVEF tended to be lower in patients receiving class III antiarrhythmic drug therapy (34 +/- 12%) than in patients receiving beta blockers (40 +/- 10%, p = 0.06). Three-year total survival was comparable in group 1 (70%) and in group 2 (81%), but sudden cardiac death mortality tended to be lower in group 1 versus group 2 (0 vs 9%, p = 0.09). Patients receiving class III antiarrhythmic therapy had significantly higher 3-year all cause (40%, p = 0.04) and sudden death (25%, p = 0.06) mortality than patients receiving beta blockers (17% and 8% respectively) or no antiarrhythmic drug therapy (4% and 0%, respectively). The following conclusions can be drawn from this analysis: (1) Electrophysiologically guided drug therapy and implantable defibrillators can minimize the risk of sudden cardiac death in patients with coronary artery disease and inducible sustained VT stratified to higher risk of sudden death. A comparable outcome with respect to sudden death prevention in drug-suppressed or drug-refractory patients suggests limited prognostic benefit of class IA drug testing. (2) Lower-risk patients with severely depressed LVEF and minimal or no symptoms do not have a favorable outcome with respect to sudden and all-cause mortality on Holter-guided class III drug therapy. However, asymptomatic patients with mildly depressed left ventricular function have low sudden death event rates on beta blocker or no antiarrhythmic drug therapy.
Aged↗
ALK, the chromosome 2 gene locus altered by the t(2;5) in non-Hodgkin's lymphoma, encodes a novel neural receptor tyrosine kinase that is highly related to leukocyte tyrosine kinase (LTK)
Anaplastic Lymphoma Kinase (ALK) was originally identified as a member of the insulin receptor subfamily of receptor tyrosine kinases that acquires transforming capability when truncated and fused to nucleophosmin (NPM) in the t(2;5) chromosomal rearrangement associated with non-Hodgkin's lymphoma, but further insights into its normal structure and function are lacking. Here, we characterize a full-length normal human ALK cDNA and its product, and determine the pattern of expression of its murine homologue in embryonic and adult tissues as a first step toward the functional assessment of the receptor. Analysis of the 6226 bp ALK cDNA identified an open reading frame encoding a 1620-amino acid (aa) protein of predicted mass approximately 177 kDa that is most closely related to leukocyte tyrosine kinase (LTK), the two exhibiting 57% aa identity and 71% similarity over their region of overlap. Biochemical analysis demonstrated that the approximately 177 kDa ALK polypeptide core undergoes co-translational N-linked glycosylation, emerging in its mature form as a 200 kDa single chain receptor. Surface labeling studies indicated that the 200 kDa glycoprotein is exposed at the cell membrane, consistent with the prediction that ALK serves as the receptor for an unidentified ligand(s). In situ hybridization studies revealed Alk expression beginning on embryonic day 11 and persisting into the neonatal and adult periods of development. Alk transcripts were confined to the nervous system and included several thalamic and hypothalamic nuclei; the trigeminal, facial, and acoustic cranial ganglia; the anterior horns of the spinal cord in the region of the developing motor neurons; the sympathetic chain; and the ganglion cells of the gut. Thus, ALK is a novel orphan receptor tyrosine kinase that appears to play an important role in the normal development and function of the nervous system.
Amino Acid Sequence↗
Detection of the t(2;5)(p23;q35) and NPM-ALK fusion in non-Hodgkin's lymphoma by two-color fluorescence in situ hybridization.
The non-Hodgkin's lymphoma (NHL) subset commonly referred to as large cell lymphoma (LCL) has historically been characterized by it's marked cytological, immunological, and clinical heterogeneity. One potential defining feature of these lymphomas, the t(2;5)(p23;q35), occurs in 25% to 30% of anaplastic LCLs and is also found in cases with diffuse large cell or immunoblastic morphology. We recently identified nucleophosmin (NPM) and anaplastic lymphoma kinase (ALK) as the genes on chromosomes 5 and 2, respectively, that are juxtaposed by this translocation. To provide a complementary approach to the use of classical cytogenetics or polymerase chain reaction-based methods for the detection of this abnormality, we have developed a two-color fluorescent in situ hybridization (FISH) assay for the t(2;5) that may be used for the analysis of both interphase nuclei and metaphase chromosomes. Three overlapping chromosome 5 cosmid clones located immediately centromeric to the NPM gene locus and an ALK P1 clone located telomeric to the chromosome 2 breakpoint were labeled with digoxigenin or biotin, respectively, and used to visualize the derivative chromosome 5 produced by the t(2;5), evident as juxtaposed or overlapping red and green fluorescent signals. This NPM-ALK FISH assay was initially validated by analysis of a series of cytogenetically characterized cell lines, with the presence of the der(5) chromosome showed specifically only in those lines known to contain the t(2;5). The assay was then applied in a blinded fashion to a series of eight cytogenetically t(2;5)-positive clinical specimens and seven known t(2;5)-negative cases, including three NHL and four Hodgkin's disease biopsy samples. Whereas the t(2;5)-negative cases were negative by FISH, all eight t(2;5)-positive cases were positive. One additional case, initially thought to be positive for the translocation by cytogenetics, was proven to not be a classic t(2;5) by interphase and metaphase FISH. These data indicate that the FISH assay described is a highly specific and rapid test that should prove to be a useful adjunct to the currently available methods for detection of the t(2;5).
Anaplastic Lymphoma Kinase↗
Right and left ventricular hemodynamic performance during sustained ventricular tachycardia.
Several factors may influence hemodynamic tolerance of a ventricular tachycardia (VT) episode but, to date, only VT rate has been used as a major detection criterion in selecting implantable cardioverter-defibrillator therapy algorithms. We examined hemodynamic changes during VT in humans and a possible correlation between left and right ventricular hemodynamic indexes. Right ventricular hemodynamic indexes could reflect systemic hemodynamics but previous studies have been inconclusive. Patients with coronary artery disease and a history of recurrent, sustained VT were studied. Aortic pressure and right and left ventricular pressures were simultaneously recorded with 2 dual micromanometer-tipped high-fidelity pressure catheters during sinus rhythm and during induced sustained monomorphic VT. Beat-to-beat analysis was performed using custom-made software. Nine patients (7 men, mean age 60 +/- 8 years, mean ejection fraction 24 +/- 8%) with 11 VT episodes (mean cycle length 283 +/- 48 ms) were studied. During VT, left and right ventricular systolic pressures showed a mean decrease of 57% and 26%, respectively, with weak correlation (r = 0.67, p = 0.06) between both values. There was also an increase in mean left and right ventricular end-diastolic pressures of 26% and 74%, respectively, and no correlation was seen (r = -0.2, p = 0.6). A significant correlation was found between changes in left and right ventricular maximal positive dP/dt (55% and 28% decrease, respectively (r = 0.69, p = 0.03) and between changes in left and right ventricular maximal negative dP/dt (64% vs 39% decrease, r = 0.71, p = 0.02). Most ventricular time parameters in both ventricles differed significantly during VT compared with sinus rhythm; however, only the decrease in right ventricular time to end-diastolic pressure correlated with the decrease in left ventricular systolic pressure, at the 10th VT beat (r = 0.8, p = 0.01). We conclude that left and right ventricles are hemodynamically unequally affected during rapid VT. Although right ventricular pressures cannot be reliably used to assess changes in the hemodynamic status of the left ventricle, additional parameters, such as dP/dt or changes in ventricular time intervals, should be further evaluated for inclusion in implantable cardioverter-defibrillator algorithms.
Aged↗
Acute effects of dual-site right atrial pacing in patients with spontaneous and inducible atrial flutter and fibrillation.
OBJECTIVES: We tested the ability of dual-site right atrial pacing to prevent atrial fibrillation (AF) or atrial flutter induced by single-site atrial pacing and correlated its efficacy with clinical patient characteristics, atrial activation times and refractory periods. BACKGROUND: Prevention of recurrent AF with long-term dual-site right atrial pacing has been demonstrated in our previous studies. However, the mechanism of antiarrhythmic benefit is unclear. METHODS: Using standard electrophysiologic methods, baseline electrocardiographic and electrophysiologic measurements (mean +/- SD) were obtained. Programmed atrial stimulation was performed for AF or atrial flutter induction. Atrial pacing was performed at two drive cycle lengths (600 and 400 ms) and followed by one to three atrial extrastimuli at one to four pacing sites in the right atrium. In patients with inducible AF or atrial flutter, reinduction was then attempted during a dual-site atrial pacing drive train. This was achieved by simultaneously pacing at the high right atrium and coronary sinus ostium at an identical rate to the baseline stimulation, with the atrial extrastimuli being delivered at the pacing site responsible for the initial AF episode initiation. RESULTS: Twenty patients (10 men, 10 women, mean [+/- SD] age 64 +/- 16 years) with symptomatic AF (n = 10) or atrial flutter (n = 10) were studied. There was a significant abbreviation of the P wave duration to 103 +/- 17 ms with dual-site pacing compared with sinus rhythm (120 +/- 12 ms, p = 0.005) and high right atrial pacing (121 +/- 17 ms, p = 0.005). This was also associated with a characteristic change in P wave configuration with an inferior and leftward axis shift. The effective refractory period at the high right atrium remained unchanged with dual-site atrial pacing compared with single-site high right atrial pacing. Sixteen patients had inducible AF or atrial flutter and could be tested after dual-site atrial pacing. The induced atrial tachyarrhythmia was suppressed in nine patients (56%), who had either induced AF (n = 5) or atrial flutter (n = 4). The difference in the effective refractory period between the high right atrium and the coronary sinus ostium pacing sites was significantly greater (33 +/- 12 ms) in patients with suppression of atrial tachyarrhythmia with dual-site atrial pacing compared with patients without suppression (15 +/- 13 ms, p = 0.001). P wave abbreviation did not correlate with arrhythmia suppression. There was no correlation between suppression of inducible AF or atrial flutter and demographic or clinical patient characteristics. CONCLUSIONS: Dual-site right atrial pacing from the high right atrium and coronary sinus ostium can suppress inducible AF or atrial flutter elicited after single-site high right atrial pacing in selected patients. Acute suppression is more likely in patients with greater dispersion of right atrial refractoriness between these two sites.
Adult↗
Evaluation of a programming algorithm for the third tachycardia zone in a fourth-generation implantable cardioverter-defibrillator.
The clinical efficacy of electrical algorithms for termination of slow ventricular tachycardia (VT) and ventricular fibrillation (VF) in implantable cardioverter-defibrillators (ICDs) is well established. Such algorithms have not been equally well defined for fast VT reversion. We report the testing of a prospectively designed algorithm for ICDs to treat fast VT that is inherently less responsive to antitachycardia pacing than slow VT. Fourth-generation ICD devices were programmed to three prospectively defined tachycardia detection zones as follows: cycle lengths < or = 260 ms for VF, 270-330 ms for fast VT, and > 330 ms for slow VT. The initial selected therapy for the VF zone was a high-energy biphasic shock (> 15 J), while a 3- or 5-J biphasic shock was usually administered for fast VT, and antitachycardia pacing was initially attempted for slow VT. Initial therapy was followed by backup therapy with high-energy shocks. Twenty-eight patients, 24 of whom were males, all with organic heart disease, with a mean age of 65 +/- 9 years, received either a Medtronic 7219D (23 patients), 7219C (2 patients), 7218SP1 (2 patients), or 7218C (1 patient) ICD with a nonthoracotomy lead system. The defibrillation threshold was 10 +/- 5 J. At predischarge electrophysiologic testing, a single 3- or 5-J shock terminated all episodes of fast VT tested. During a follow-up of 18 +/- 9 months, there were four nonarrhythmic deaths. Fourteen patients (50%) had a total of 21 VF, 44 fast VT, and 202 slow VT episodes. Twenty-three of 24 (96%) VF, 33 of 39 (84%) fast VT, and 193 of 202 (95.5%) slow VT episodes were terminated with the first delivered therapy in each therapy algorithm (p = NS). The overall efficacy of the entire electrical therapy algorithm was 100% for VF, 100% for fast VT, and 98% for slow VT episodes (p = NS). No patient experienced syncope or presyncope during fast VT or VF in this study. We conclude that a third detection and therapy zone can be successfully programmed in ICDs to define a range of fast VT episodes that can be effectively terminated with lower energy cardioversion shocks with comparable success and freedom from arrhythmic symptoms to electrical therapies used for slow VT and VF.
Aged↗
Effects of high-frequency atrial pacing in atypical atrial flutter and atrial fibrillation.
Atypical atrial flutter has, hitherto, been relatively refractory to termination by rapid atrial pacing. High-frequency pacing (HFP) in the atrium, for termination of atrial flutter or atrial fibrillation (AF), and the electrophysiologic effects related to it have not been examined. We examined the clinical efficacy, safety, and electrophysiologic mechanisms of HFP using 50-Hz bursts at 10 mA applied at the high right atrium in patients with atypical atrial flutter (group 1) or AF (group 2), using a prospective randomized study protocol. Four burst durations (500, 1000, 2000, and 4000 ms) were applied at the high right atrium repetitively in random sequence in 22 patients with spontaneous atrial flutter or AF. Local and distant right and left atrial electrogram recordings were analyzed during and after HFP. HFP resulted in local and distant right and left atrial electrogram acceleration in 8 of 10 patients (80%) in group 1 but caused less frequent local atrial electrogram acceleration (6 of 12 patients) and no distant atrial electrogram effects in group 2 (p < .05 versus group 1). The HFP protocol was effective in arrhythmia termination in 6 of 10 patients in group 1 but in no patient in group 2 (p < .05 versus group 1). Standard HFP protocol applied at the high right atrium can frequently alter atrial activation in both atria and can terminate atypical atrial flutter. Efficacy in AF is limited, probably due to limited electrophysiologic actions beyond the local pacing site.
Adult↗
Interaction between electronic article surveillance systems and implantable defibrillators: insights from a fourth generation ICD.
We present a case report of an inappropriate discharge from a fourth generation implantable cardioverter defibrillator (ICD) as a result of exposure to electromagnetic interference. A 60-year-old man implanted with a Medtronic 7219D defibrillator experienced shocks without preceding symptoms while walking through an electronic surveillance system in a store. Though this has been reported, the mechanism of the interaction remains unexplained. The electrogram storage capabilities of this particular device enabled us to establish that this resulted from inappropriate sensing of the electromagnetic interference.
Defibrillators, Implantable↗
Internal atrial defibrillation: effect on sinus and atrioventricular nodal function and implanted cardiac pacemakers.
Internal atrial defibrillation (IAD) has been extensively evaluated for clinical efficacy but the need for concomitant demand pacing and the effect of IAD shocks on pacemaker function is not well studied. We prospectively evaluated: (1) the incidence of bradycardia as a result of IAD shocks; and (2) effect of these shocks on functioning of implanted cardiac pacemakers. Consecutive consenting patients with atrial fibrillation (AF) requiring cardioversion or undergoing electrophysiological study were selected for IAD. IAD shocks were delivered using the right ventricle to right atrium (RV-RA), right ventricle to superior vena cava (RV-SVC), right atrium to axillary patch (RA-AX), and right atrium to left pulmonary artery or coronary sinus (RA-LPA/CS) lead configurations. Mean RR interval before and after the shocks and the time interval from shock delivery to first QRS complex were analyzed for unsuccessful and successful shocks. Pacing and sensing function was analyzed in patients with previously implanted pacemakers. Twenty-five patients, 18 men, mean age 67.9 +/- 10 years were included in the study. A total of 305 shocks (264 unsuccessful, 41 successful) were analyzed. For unsuccessful shocks the mean post-IAD shock RR interval (795 +/- 205 ms) and the time to first post-IAD shock QRS complex (970 +/- 438 ms) were both significantly greater than the pre-IAD shock RR interval (685 +/- 131 ms, P < 0.001). The increase in post-IAD shock RR interval and time to first post-IAD shock QRS complex was seen with all four lead configurations used. With successful shocks the mean post-IAD shock sinus cycle length (1,105 +/- 450 ms) and time to first post-IAD shock QRS complex (1,126 +/- 443 ms) were both also significantly greater than the pre-IAD shock RR interval (766 +/- 172 ms). Nine patients (36%) had episodes of significant bradycardia after shock delivery. Shocks of up to 20 J using the RA-LPA/CS lead configuration did not affect pacemaker function. IAD can result in transient bradycardia related to sinus and atrioventricular nodal effects requiring backup ventricular pacing. Shocks can be safely delivered using RA-LPA or RA-CS lead configurations in patients with implanted bipolar cardiac pacemakers.
Aged↗