Creating slide presentations using computer graphics software.
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Biomedical subjects
Publications and source records attributed to A D Mercando.
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Either of these programs will accomplish the task of storing and organizing a personal bibliography. Reference Manager is more widely used, but more costly. Although it contains more input formats than Papyrus, most of the common formats used in medicine are supported by both programs. Importing is the best way to establish a personal database with many references, since it avoids manually typing the data. The import interface in Reference Manager is simpler to use at first, and faster than Papyrus's, but either program accomplishes the task with relative ease. The authors of Papyrus are receptive to updating import formats and adding new formats to their libraries as requested by users. Why not use MEDLINE alone instead of downloading and maintaining a personal reference list? These programs are more useful than MEDLINE in their output formatting capabilities. The most useful output feature is the generation of bibliographies for manuscripts, and both programs accomplish this task nicely. Papyrus includes fewer specific journal formats than Reference Manager, but both programs permit the user to add detailed output specifications to their personal journal lists.
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Any of these remote control packages will accomplish the task of controlling another PC from a distant machine. Since all of the programs are easy to use, perform the same functions, and provide excellent security, there is no one clear winner. If your aim is to control Windows programs remotely, then Carbon Copy for Windows is the fastest software. It falls short in running DOS based programs and has greater hardware requirements because it is a Windows application. Norton pcAnywhere is a reliable program that rivals Carbon Copy for Windows' speed, even when controlling a Windows program remotely. Its support for DOS is better. Close-Up is the easiest to install, will run DOS programs without problem, and can run Windows programs as well. Under Windows, DOS programs can be executed in a window or as a full screen application. However, its speed ratings when working in Windows have been among the slowest. Carbon Copy for the Mac brings most of the features of the Windows version of this program to the Macintosh environment. The software allows users to control remote Macintosh computers, and to perform file transfers in the background. It does not permit a PC to control a Mac or a Mac to control a PC. List prices for these programs are $179 to $199 for packages with host and remote software, but street prices range from approximately $100 to $120. A 9600 baud modem with data compression (yielding a net speed of about 14,400 bits/sec) and error correction costs approximately $200 to $300.(ABSTRACT TRUNCATED AT 250 WORDS)
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Although electrophysiologic studies are often used to assess antiarrhythmic drug efficacy in patients with ventricular tachycardia (VT), the reproducibility of these studies during therapy has not been definitively established. Confirmation studies were performed during drug therapy in 64 patients (51 men, mean age 63 years) with sustained ventricular arrhythmias induced during initial study to assess the reproducibility of drug effect. All patients had coronary artery disease. The stimulation protocol used included the serial introduction of up to 3 premature ventricular stimuli during sinus rhythm and with ventricular pacing at 2 pacing rates. Rapid ventricular pacing techniques were also used. Antiarrhythmic drug efficacy was confirmed in 77% of patients. Sustained VT was induced at repeat electrophysiologic study in 19% of patients during antiarrhythmic therapy that was previously thought to be effective. In summary, electrophysiologic study results during antiarrhythmic therapy exhibit significant day-to-day variability. Sustained VT can be induced during antiarrhythmic therapy that was previously defined as effective by programmed stimulation in a substantial number of patients.
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A prospective study correlated the effect of quinidine or procainamide versus no antiarrhythmic drug on sudden cardiac death, total cardiac death and total death in 406 elderly patients with heart disease and asymptomatic complex ventricular arrhythmias detected by 24-hour ambulatory electrocardiograms. Of 397 patients treated with quinidine, 184 (46%) developed adverse effects during the first 2 weeks of therapy and were given no further antiarrhythmic therapy. Of 9 patients treated with procainamide, 2 (22%) developed adverse effects during the first 2 weeks of therapy and were given no further antiarrhythmic therapy. Adverse effects developed during long-term therapy in 6 patients (2%) receiving quinidine and in 3 patients (33%) receiving procainamide. Mean follow-up was 24 +/- 15 months in both groups. Sudden cardiac death, total cardiac death and total death occurred in 21, 43 and 65% of patients receiving quinidine or procainamide, respectively, and in 23, 44 and 63% of patients receiving no antiarrhythmic drug, respectively (difference not significant). Survival by Kaplan-Meier analysis showed no significant difference between the 2 groups for sudden cardiac death, total cardiac death or total death through 4 years. Patients with abnormal left ventricular ejection fraction had a 3.4 times higher incidence of sudden cardiac death, a 2.4 times higher incidence of total cardiac death and a 1.4 times higher incidence of total death than patients with normal left ventricular ejection fraction. These data showed no significant difference in sudden cardiac death, total cardiac death or total death between patients treated with quinidine or procainamide or with no antiarrhythmic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac refractory periods are routinely measured during electrophysiologic testing. Informal observations suggested that the effective refractory period lengthened with a prolongation of the time in sinus rhythm (basic cycle length time) between successive runs of drive stimuli (S1S1s). If this were true, failure to control the basic cycle length time could affect the results and interpretation of electrophysiologic testing. To study this phenomenon, the effective refractory period was studied in 20 patients during sinus rhythm and two ventricular paced rates with up to three extrastimuli, while varying the basic cycle length time from 2 to 3, to 10 to 20 s. With each of the stimulation sequences used, the effective refractory period lengthened as the basic cycle length time increased ("basic cycle length time-effective refractory period effect"). The effect was most pronounced when extrastimuli were used during the two ventricular paced rates. As the basic cycle length time increased from 2 to 3 to 20 s, the mean effective refractory period determined during sinus rhythm increased from 296 to 300 ms; with the first ventricular paced rate, the effective refractory period increased from 259 to 272 ms (p less than 0.0003) and with the second ventricular paced rate, the effective refractory period increased from 250 to 263 ms (p less than 0.01). The basic cycle length time-effective refractory period effect became more pronounced as the number of extrastimuli increased. With the second ventricular paced rate, as basic cycle length was increased from 2 to 3 to 20 s, the mean prolongation in the cumulative effective refractory period (S1 to final extrastimulus) as the number of extrastimuli increased from 1 to 2 to 3, was 13 (p less than 0.01), 42 (p less than 0.0003) and 82 ms (p less than 0.001), respectively. Results were confirmed in 17 instances by redetermining the effective refractory period at the 2 to 3 s basic cycle length time after the final 20 s basic cycle length time determination, and demonstrating that it was similar to the effective refractory period after the initial 2 to 3 s basic cycle length time. No further prolongation of the effective refractory period could be demonstrated by increasing basic cycle length time from 20 to 60 s, and no significant effect of medications on the basic cycle length time-effective refractory period effect could be demonstrated.
Implantable device detection of tachydysrhythmias remains unreliable and inexact. False responses may occur because of misinterpretation of sinus tachycardia (ST) as a supraventricular tachydysrhythmia (SVTD). Timing of atrioventricular (AV) activation and ventricular dispersion identified and discriminated between ST and SVTDs in 11 dogs. Three bipolar epicardial electrodes recorded left atrial and left and right ventricular depolarizations simultaneously during normal sinus rhythm (NSR) (mean of 5 beats in 11/11 dogs), ST produced by phlebotomy (50 beats in 10 episodes in 6/11) or isoproterenol infusion (105 beats in 21 episodes in 10/11), sinus bradycardia (SB) produced by vagal stimulation (140 beats in 29 episodes in 10/11), and during atrial flutter (AFL) (15 beats in 3 episodes in 3/11) and atrial fibrillation (AF) (152 beats in 31 episodes in 9/11) induced by programmed electrical stimulation. During lidocaine infusion, NSR (55 beats in 11 episodes in 10/11 dogs), SB (84 beats in 17 episodes in 7/11), AFL (10 beats in 2 episodes in 1/11), and AF (103 beats in 21 episodes in 7/11) were recorded. During isoproterenol infusion, SB (45 beats in 9 episodes in 5/11), AFL (15 beats in 3 episodes in 2/11), and AF (64 beats in 13 episodes in 5/11) were recorded in addition to ST. The interval between the left atrial and left ventricular intrinsic deflections (A-V1) and between the left and right ventricular intrinsic deflections (V1-V2) of each beat was measured. The mean value (msec) of A-V1 and V1-V2 in each episode was compared to NSR in the same dogs. A difference of greater than or equal to 16 ms was used for differentiation. In all cases except SB with first-degree AV block, V1-V2 in each episode was insignificant (0-14 msec), categorizing the rhythms as supraventricular. During NSR, ST and SB without AV block, delta A-V1 was small (0-15 msec). In contrast delta A-V1 was greater than or equal to 16 ms in 6/8 episodes of AFL. The remaining two episodes could be differentiated by the greater number of atrial versus ventricular beats. AF could be detected by the variability of A-V1.(ABSTRACT TRUNCATED AT 250 WORDS)
The efficacy and tolerance of disopyramide and mexiletine used alone and in combination were studied in 21 patients with frequent (greater than or equal to 30/h) ventricular premature complexes. Ambulatory electrocardiographic monitoring was performed at baseline and during therapy with disopyramide alone, mexiletine alone and a combination of disopyramide and mexiletine. During single drug therapy, the dose of disopyramide was 602 +/- 152 mg/day and that of mexiletine was 738 +/- 144 mg/day. During combination therapy with smaller doses of disopyramide (524 +/- 134 mg/day) and mexiletine (652 +/- 146 mg/day), no patient had side effects. At baseline before therapy, the mean number of ventricular premature complexes per hour, was 608 +/- 757, of couplets per hour was 22.4 +/- 45.8 and of episodes of nonsustained ventricular tachycardia/24 h was 219.7 +/- 758.2. The mean number of ventricular premature complexes per hour was reduced to 156 +/- 217 with disopyramide alone, 188 +/- 298 with mexiletine alone and 76 +/- 144 with combination therapy (p less than 0.05 for combination therapy versus disopyramide or mexiletine alone; p = NS for disopyramide versus mexiletine). Individually, an effective regimen (greater than 83% reduction in ventricular premature complexes and abolition of nonsustained ventricular tachycardia) was found in 5 (24%) of 21 patients during therapy with disopyramide alone, in 3 (14%) receiving mexiletine alone and in 13 (62%) receiving combination therapy (p less than 0.05 for combination therapy versus disopyramide or mexiletine; p = NS for disopyramide versus mexiletine). Thus, the antiarrhythmic effects of disopyramide and mexiletine are additive.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac pacing can inhibit or terminate a tachyarrhythmia but may also accelerate it to a more malignant rhythm. The automatic implantable cardioverter defibrillator (AICD) terminates ventricular tachycardia and fibrillation and has thus enhanced patient survival. The combination of the two may yet be the most effective means of controlling ventricular tachyarrhythmias and fibrillation.
Electrical devices can be used for preventing and terminating tachycardia and for achieving hemodynamic improvement during a continuing tachycardia. Conventional approaches to tachycardia prevention include pacing at physiologic rates to prevent brady-cardia-related tachycardia or tachycardias associated with prolonged QT-interval syndromes. More exotic techniques, such as those involving stimulation during the refractory period, are undergoing investigation. Some tachycardias cannot be easily terminated or recur incessantly. Hemodynamics can be improved by pacing methods that result in a narrower QRS complex by coupled pacing and, in supraventricular tachycardias, by pacing rapidly enough to create atrioventricular block. Most clinical tachycardias are caused by reentry. Careful analysis of the timing of individual stimuli that successfully terminate tachycardias indicate that critical relations exist in the conduction velocity, refractoriness and physical properties and dimensions of the reentry circuit and the remaining myocardium. Elucidating these relations has permitted inferences into the mechanisms by which pacing terminates or accelerates tachycardias. A vast number of pacing patterns have evolved for use in tachycardia termination. None of these appear to be foolproof. There is widespread and justified concern about the risk of acceleration of tachycardia when antitachycardia pacing is used in the ventricle. Experience indicates that only a few patients are suitable for termination of ventricular tachycardia by pacing, but these carefully selected patients may do well. Both the results and the potential for widespread use may be better with pacing for termination of supraventricular tachycardia. Life-threatening tachycardias or fibrillation can be terminated by direct-current countershock. Although many technical problems remain, implantable cardioverter-defibrillators, possibly combined with antitachycardia pacemakers, will play an increasing role in the management or serious arrhythmias.
Electrical devices play an increasingly important role in the control of tachyarrhythmias. Antitachycardia pacing and automatic defibrillation have been severely limited by the poor specificity of tachycardia discrimination in commercially available devices. Although absolute heart rate has been the principal means of automatic diagnosis, several new detection algorithms and methods are being investigated. Multiple electrode timing comparison, signal processing and pattern recognition are employed in these newer techniques. Although each offers some improvement over present technology, none is capable of identifying all arrhythmias. The methods employing comparison of atrial and ventricular rates, without additional criteria, are unable to detect ventricular tachycardia in the presence of 1:1 retrograde conduction. Electrographic analysis techniques require very stable electrodes and may not tolerate normal morphologic variations. A combination of two or more approaches may ultimately be required. All techniques will require that certain critical variables be programmable to allow for individualization in each clinical situation. Soft-ware-controllable devices and those capable of sensing from both the atria and the ventricles will provide the sophistication necessary for the implementation of complex tachycardia detection algorithms. This report reviews automatic tachycardia detection techniques in current use and under investigation.