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Biomedical subjects

S Saksena

Publications and source records attributed to S Saksena.

At least 37 records · Page 2Linked to original sources
PubMed2000

Catheter mapping of spontaneous and induced atrial fibrillation in man.

The clinical electrophysiologic study of atrial fibrillation [AF] has recently progressed from static characterization of the substrate to the dynamic investigation of both induced and spontaneous AF in man. Prior studies have demonstrated inhomogeneity and greater dispersion of atrial refractoriness in patients with AF, but recently atrial electrical remodeling with consequent abbreviation of atrial refractory periods has also been reported. Yet further experimental observations have suggested the existence of additional arrhythmogenic mechanisms for certain AF subsets. These include studies that have demonstrated a stable atrial flutter circuit in one atrium with fibrillatory conduction or a focal atrial tachyarrhythmia arising commonly in the left atrium. Efforts at catheter mapping of AF are now in progress. New mapping techniques and novel devices are currently being employed. We have performed catheter mapping simultaneously in right and left atrial sites at onset and during sustained pacing-induced and spontaneous AF in patients with ischemic and/or hypertensive heart disease. Atrial premature complexes that initiated spontaneous AF typically had coupling intervals ranging from 260 to 400 ms and most frequently arose in the crista terminalis, right atrioventricular junction or superior left atrium. AF at onset showed discrete electrograms at virtually all right and left atrial regions mapped and the region of earliest atrial activation during AF was in close proximity to the premature complexes in over 90% of patients. The regional atrial activation sequence for the first 10 AF beats demonstrated stable or unstable patterns in individual patients. In contrast to spontaneous AF, the initial arrhythmia of induced AF was seen to have a significantly different site of earliest atrial activation but similar discrete electrograms in different atrial regions. However, as with spontaneous AF, the site of extrastimulus delivery was in close proximity to the first induced beat. We conclude that regional catheter mapping of AF is feasible and safe in man and organized electrical activity is frequently observed at AF onset in patients with heart disease. Both right and left atrial regions can be the source of atrial premature complexes and at the onset of spontaneous AF. Induced AF may have differing activation patterns than spontaneous AF but both demonstrate earliest activation in proximity to the initiating atrial premature complex. These findings may help explain therapeutic benefits of right and left atrial interventions and pacing therapies in AF.

Atrial Fibrillation↗
PubMed2000

Electrophysiologic assessment in selecting patients for multisite atrial pacing.

Electrophysiologic mechanisms of atrial fibrillation (AF) initiation are being actively studied. Multisite atrial pacing has shown, in acute studies, significant potential for prevention of AF. Dual site pacing reduces of intra and inter-atrial conduction time, atrial refractoriness dispersion, and to a limited extent atrial premature beats which modify the atrial remodelling induced by AF. Recently, two clinical trials have shown long term efficacy of multisite atrial pacing. At 3 years of follow-up, 56% of patients are free of AF recurrence with dual site right atrial pacing. Rhythm control was achieved in 86 of patients. Similar results are observed with biatrial resynchronization. In both studies, primary indication for multisite atrial pacing was AF prevention in more than 50% of patients. Selection of patients based solely on long P wave duration and prolonged interatrial conduction is not necessary as clinical outcome and comparable. These patients are comparable to patients who did not have these characteristics. Ongoing multicenter trials will likely definitively answer this question. However, preexcitation of diseased atrial regions or site of ectopic activity previously selected by high density atrial mapping or suppression of inducible AF may offer an interesting future development of multisite atrial pacing.

Atrial Fibrillation↗
PubMed2000

Plasma elimination of cholyl-lysyl-fluorescein (CLF): a pilot study in patients with liver cirrhosis.

BACKGROUND: Cholyl-lysyl-fluorescein (CLF) is a fluorescein-labelled bile acid whose biological behaviour closely resembles that of naturally occurring cholyl glycine. AIM: The aim of this study was to analyze the CLF plasma elimination in patients with liver cirrhosis. METHODS: A dose of CLF at 0.02 mg/kg b.w. was administered i.v. in 26 patients with liver cirrhosis and 9 healthy volunteers. Blood samples were collected before injection and then at 10 min intervals over 60 min. Plasma fluorescence was measured by a luminescence spectrometer and residual fluorescence over the time of the study was compared in each group. Routine liver function tests (rLFTs) were performed before each injection. RESULTS: Plasma elimination of CLF was significantly impaired in patients with cirrhosis compared to healthy subjects with p values <0.0001 at each analyzed time point. CLF test showed 100% sensitivity for liver cirrhosis when residual fluorescence was measured 30, 40, 50 and 60 min after injection. Routine LFTs showed 85% sensitivity for bilirubin, 84% for total bile acids, 69% for aspartate aminotransferase 62% for albumin and 50% for alkaline phosphatase. CLF elimination measured 60 min after injection correlated with Child-Pugh score (r=0.3945; p<0.05) and albumin (rs=0.6451; p<0.001). No adverse reaction or side effects of CLF were observed. CONCLUSIONS: CLF test clearly distinguished between the two analyzed groups and was more sensitive than routine liver function tests. The test appears safe, simple to perform and analyze and after validation in larger cohorts of patients may have the potential to become a useful dynamic test of liver function.

Adult↗
PubMed2000

Wilson's disease with superimposed autoimmune features: report of two cases and review.

We describe two females, 15 and 23 years old, respectively, who presented with classical features of Wilson's disease (WD) and several features of autoimmune hepatitis (AIH). The first patient was initially diagnosed as AIH and treated with prednisolone which caused clinical improvement, with an increase of serum albumin from 22 to 30 g/L, and a decrease of aspartate aminotransferase from 103 to 47 U/L. Subsequent diagnosis of WD and introduction of penicillamine gave excellent improvement and complete normalization of liver function tests. The second patient, at first also diagnosed as having AIH, was treated with steroids and azathioprine with initial improvement, but subsequent deterioration. The diagnosis of WD was made 2 years after initial diagnosis of AIH, as the patient reached end-stage liver disease and required a transplant. Therefore, d-penicillamine treatment was not attempted. We conclude that, in patients with AIH, a thorough screening for WD is necessary, particularly when the response to steroid therapy is poor. Conversely, in patients suffering from WD with superimposed features of AIH, a combination of steroids and penicillamine may be of benefit.

Adolescent↗
PubMed1999

Regional endocardial mapping of spontaneous and induced atrial fibrillation in patients with heart disease and refractory atrial fibrillation.

We performed simultaneous catheter mapping of right and left atrial regions at onset and during sustenance of spontaneous atrial fibrillation (AF) in patients with ischemic and/or hypertensive heart disease. Seventeen patients with structural heart disease had spontaneous and electrically induced AF episodes mapped from their onset simultaneously in multiple right and left atrial regions. Atrial premature complexes (APCs) that initiated spontaneous AF had coupling intervals ranging from 260 to 400 ms (mean 332 +/- 61), most commonly arising from the lateral right atrium (31%), right atrioventricular junction (13%), atrial septum (6%), superior left atrium (25%), or inferior left atrium (25%). APC morphology on surface electrocardiograms did not correlate with origin in specific atrial regions. The earliest regions of atrial activation for the first AF cycle were the lateral right atrium (n = 5), superior left atrium (n = 4), distal or mid coronary sinus (n = 4), atrial septum (n = 2), and right atrioventricular junction at the His bundle location (n = 2). Spontaneous AF at onset usually showed discrete but irregular electrograms at virtually all right and left atrial sites mapped, with a reproducible region of AF initiation in all 8 patients with multiple events. The region of earliest atrial activation at spontaneous AF onset was in close proximity to the APC origin in 15 of 16 patients (94%), and 39 of 40 episodes (97%) mapped. Stable patterns of right and left atrial activation were observed at AF onset in 14 patients. Induced AF elicited with right atrial stimulation demonstrated different sites of earliest regional atrial activation at onset compared with spontaneous AF events in 4 of 8 patients. However, discrete intracardiac electrograms were also present in induced AF in all of the mapped atrial regions. Furthermore, the site of extrastimulus delivery in induced AF was also found to be in close proximity to the earliest region of atrial activation for the first AF beat. We conclude that spontaneous AF is initiated by APCs arising in different right or left atrial regions in patients with structural heart disease and the initial region of atrial activation in AF is in proximity to the region of APC origin. Organized and repetitive electrical activation is frequently observed in both right and left atria at AF onset. Although electrically induced AF may have different activation patterns than spontaneous AF at onset in many patients, both types of AF demonstrate organization and earliest atrial activation in proximity to the initiating APC.

Aged↗
PubMed1999

Living anatomy of the atrioventricular junctions. A guide to electrophysiologic mapping. A Consensus Statement from the Cardiac Nomenclature Study Group, Working Group of Arrhythmias, European Society of Cardiology, and the Task Force on Cardiac Nomenclature from NASPE.

Current nomenclature for the atrioventricular (AV) junctions derives from a surgically distorted view, placing the valvar rings and the triangle of Koch in a single plane with antero-posterior and right-left lateral coordinates. Within this convention, the aorta is considered to occupy an anterior position, although the mouth of the coronary sinus is shown as being posterior. Although this nomenclature has served its purpose for the description and treatment of arrhythmias dependent on accessory pathways and atrioventricular nodal reentry, it is less than satisfactory for the description of atrial and ventricular mapping. To correct these deficiencies, a consensus document has been prepared by experts from the Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. It proposes a new anatomically sound nomenclature that will be applicable to all chambers of the heart. In this report, we discuss its value for description of the AV junctions, establishing the principles of this new nomenclature.

Atrioventricular Node↗
PubMed1999

Prevention of implantable-defibrillator shocks by treatment with sotalol. d,l-Sotalol Implantable Cardioverter-Defibrillator Study Group.

BACKGROUND: Patients with implantable cardioverter-defibrillators often receive adjunctive antiarrhythmic therapy to prevent frequent shocks. We tested the efficacy and safety of sotalol, a beta-blocker with class III antiarrhythmic effects, for this purpose. METHODS: In a multicenter trial, patients were stratified according to left ventricular ejection fraction (< or =0.30 or >0.30), randomly assigned to double-blind treatment with 160 to 320 mg of sotalol per day (151 patients) or matching placebo (151 patients), and followed for 12 months. Kaplan-Meier analyses of the time to an event were performed. Three end points were used: the delivery of a first shock for any reason or death from any cause, the first appropriate shock for a ventricular arrhythmia or death from any cause, and the first inappropriate shock for a supraventricular arrhythmia or death from any cause. RESULTS: Compliance with double-blind treatment was similar in the two groups. There were seven deaths in the placebo group and four in the sotalol group. As compared with placebo, treatment with sotalol was associated with a lower risk of death from any cause or the delivery of a first shock for any reason (reduction in risk, 48 percent; P<0.001 by the log-rank test), death from any cause or the delivery of a first appropriate shock (reduction in risk, 44 percent; P=0.007), or death from any cause or the delivery of a first inappropriate shock (reduction in risk, 64 percent; P=0.004). Sotalol also reduced the mean (+/-SD) frequency of shocks due to any cause (1.43+/-3.53 shocks per year, as compared with 3.89+/-10.65 in the placebo group; P=0.008). In the sotalol group, the reduction in the risk of death from any cause or the delivery of a first shock for any reason did not differ significantly between patients with ejection fractions of more than 0.30 and those with ejection fractions of 0.30 or less. CONCLUSIONS: Oral sotalol was safe and efficacious in reducing the risk of death or the delivery of a first defibrillator shock whether or not ventricular function was depressed.

Adrenergic beta-Antagonists↗
PubMed1999

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↗
PubMed1999

Interactions of antiarrhythmic drugs with implantable defibrillator therapy for atrial and ventricular tachyarrhythmias.

Implantable cardioverter defibrillators (ICDs) have proven highly successful in the treatment of recurrent ventricular and atrial arrhythmias. Despite their high efficacy in terminating arrhythmias, concomitant therapy with antiarrhythmic drugs in ICD recipients remains common. Antiarrhythmic drugs are employed in an attempt to to limit patient exposure to high-energy shocks, primarily by reducing the number of arrhythmia reccurrences, suppressing coexisting arrhythmias, affecting rate and organization of tachycardias, and increasing efficacy of painless pacing therapies. Data regarding interaction of antiarrhythmic drugs with ICDs are incomplete and mostly based on animal models; however, it is clear that antiarrhythmic drugs affect all aspects of function of devices such as defibrillation threshold, pacing threshold, and sensing of both atrial and and ventricular arrhythmias. Because significant change in any of these functions may result in a nonfunctional device, and magnitude of drug effect in an individual patient is unpredictable, careful assessment of ICD function after an institution of therapy with antiarrhythmic drugs is mandatory.

Anti-Arrhythmia Agents↗