Biomedical subjects

A D Mercando

Publications and source records attributed to A D Mercando.

61 records · Page 4Linked to original sources

PubMed1988

Differentiation of arrhythmias in the dog by measurement of activation sequence using an atrial and two ventricular electrodes.

Timing of atrioventricular activation and ventricular dispersion identifies and discriminates between beats of different origin. In eight dogs, three bipolar epicardial electrodes recorded left atrial and left and right ventricular depolarizations simultaneously during arrhythmias induced by programmed electrical stimulation and coronary artery occlusion and release. The interval between the left atrial and left ventricular intrinsic deflections (A-V1) and between the left ventricular and right ventricular intrinsic deflections (V1-V2) of each beat was measured. Recordings were of normal sinus rhythm (NSR) (mean of five beats in 8/8 dogs), atrial flutter (AFL) (five beats of one episode), atrial fibrillation (AF) (144 beats in 29 episodes in 7/8), monomorphic ventricular tachycardia (MVT) (24 beats with six morphologies in 2/8), polymorphic ventricular tachycardia (PVT) (63 beats in 15 episodes in 5/8) and premature ventricular contractions (PVC) (29 beats with 29 morphologies in 5/8). Supraventricular rhythms can be differentiated from ventricular rhythms by V1-V2 timing. The mean difference in V1-V2 during AFL and AF vs NSR was 1 ms (range of 0-3 ms). The change from sinus during MVT ranged from 18 to 43 ms (m 31 ms) and during PVC 10 to 75 ms (m 38 ms). Thirty-five of 35 of these ectopic ventricular morphologies exhibited 10 ms or more timing difference compared to corresponding beats of NSR. PVT was consistently distinguished from supraventricular rhythms and MVT by the variability of V1-V2. A-V1 intervals can be used to distinguish supraventricular arrhythmias from sinus rhythm; a 32 ms difference existed for AFL. AF could be detected by the variability in AV1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Survival of patients with the automatic implantable cardioverter defibrillator.

Between May 1982 and May 1988, 37 patients (28 males and 9 females, mean age 57.6, range 16-76 years) of approximately 600 evaluated for sustained ventricular tachycardia and/or fibrillation (VT/VF) were treated with an automatic implantable cardioverter defibrillator (AICD). Twenty-eight of the patients had coronary artery disease, 7 had nonischemic cardiomyopathy, 1 had amyloid heart disease, and 1 had rheumatic heart disease. The mean ejection fraction was 32.2 +/- 12.9% (range, 9-64%). Eleven patients have died at a mean of 16.7 months after implantation. The cumulative survival rate was 81% at 1 year, 77% at 2 years, 68% at 3 years, and 53% at 4, 5, and 6 years. Considering only sudden deaths, the survival was 97% at 1 and 2 years, 90% at 3 years, and 80% at 4, 5, and 6 years. Twenty-one of the 37 patients received spontaneous shocks. If the first shock marks the time to death in the absence of an AICD, the cumulative survival rate would have been 56% at 1 year, 42% at 2 years, 29% at 3 years, and 14% at 4, 5, and 6 years. The maximum amount of time to a first appropriate shock was 39.7 months. Thirty-nine devices have been explanted: 28 for battery depletion; 5 for infections; 3 for improper sensing; 2 for electronic failure; and 1 at the time of cardiac transplantation. The average time to failure of the 28 units removed for battery depletion was 19.8 +/- 6.9 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗

PubMed1987

Long-term efficacy of antitachycardia pacing for supraventricular and ventricular tachycardias.

Over a 14-year period, 53 patients received implanted pacemakers to assist in the control of recurrent tachycardias. Indications were: prevention of tachycardia in 2 patients with supraventricular tachycardia (SVT), and 4 with ventricular tachycardia (VT); termination of tachycardia (15 SVT, 20 VT); and long-term periodic programmed electrical stimulation with potential for tachycardia termination (12 VT). Pacemakers for prevention of VT were implanted in 3 patients with prolonged QT interval syndromes and 1 in whom Holter monitoring showed a significant reduction in ectopic activity during pacing. Pacers were implanted for tachycardia termination only after patients underwent a rigorous protocol aimed at achieving 100 trials of the proposed modality. Patients with tachycardia also requiring antibradycardia pacemakers received pacemakers capable of noninvasive programmed stimulation for use during follow-up. There were no tachycardia recurrences among those patients in whom pacemakers were implanted for prevention. Pacers capable of outpatient programmed stimulation were useful, and it may be desirable to expand their use. The 15 patients with pacers designed for termination of SVT were followed for a mean of 68 months. Among these, actuarial continuation of pacing efficacy was 93% at 1 year, and 78% at 5 years. The 20 patients with pacers for termination of VT were followed for a mean of 37 months. Actuarial efficacy was 78% at 1 year, and 55% at 5 years. Sudden death occurred in 4 of these patients, none clearly pacer related. Pacemakers can play a major therapeutic role in some patients with recurrent tachycardias. The role of such pacemakers in patients with VT may be expanded with the advent of combined pacer-defibrillators.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1987

Comparison of the characteristics of nonsustained ventricular tachycardia on Holter monitoring and sustained ventricular tachycardia observed spontaneously or induced by programmed stimulation.

The characteristics of nonsustained ventricular tachycardias (VT) on Holter monitor recordings were compared with the characteristics of sustained VT noted spontaneously or induced by programmed stimulation in 50 patients with a history of spontaneous sustained VT. At baseline before antiarrhythmic therapy, all patients had nonsustained VT (triplets or longer) on Holter recordings and sustained VT inducible by programmed stimulation. The mean rate of the fastest nonsustained VT on Holter monitoring (150 +/- 52 beats/min) was significantly slower that that of induced sustained VT (246 +/- 56 beats/min) (p less than 0.001). Compared with nonsustained VT on Holter monitoring, sustained VT by programmed stimulation were faster in 45 of 50 patients, similar in 2 and slower in 3. There was a poor correlation between the rates of nonsustained VT and sustained VT (r = 0.2195). The duration of the longest nonsustained VT was fewer than 6 beats in 24 patients and 6 beats or more in 26. The mean rates of induced sustained VT were not significantly different between patients with shorter (fewer than 6 beats) and longer (6 or more beats) nonsustained VT. In 12 patients, the rate of spontaneous sustained VT was available. The rate of spontaneous sustained VT (217 +/- 59 beats/min) was similar to that of sustained VT by programmed stimulation (277 +/- 60 beats/min). There was a close correlation (r = 0.8036) between the rates of spontaneous and induced sustained VT. However, the rate of nonsustained VT on Holter monitoring (151 +/- 76 beats/min) was significantly slower than the rate of spontaneous sustained VT (p = 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗

PubMed1987

Prognostic value of the changes in the mode of ventricular tachycardia induction during therapy with amiodarone or amiodarone and a class 1A antiarrhythmic agent.

The prognostic value of 3 previously reported programmed stimulation efficacy criteria was studied in 70 patients taking amiodarone for sustained ventricular tachycardia (VT). At baseline all patients had VT inducible by programmed stimulation. After amiodarone loading (935 +/- 271 mg/day for 16 +/- 7 days), efficacy of amiodarone was determined by 3 programmed stimulation criteria (criterion I = VT not inducible or 15 beats or less; criterion II = VT not inducible or harder to induce; criterion III = VT not easier to induce). Amiodarone was effective in 12, 25 and 49 of 70 patients by criteria I, II and III, respectively. There were 16 recurrences or cardiac arrest during the follow-up period (19 +/- 19 months). Actuarial arrhythmia-free survival rates at 1 and 2 years were: 90% and 90% in patients with efficacy by criterion I and 78% and 78% in patients with inefficacy, respectively; 84% and 84% in patients with efficacy by criterion II and 78% and 78% in patients with inefficacy, respectively; and 80% and 80% in patients with efficacy by criterion III and 79% and 79% in patients with inefficacy, respectively (difference not significant for all). From the results of follow-up at 2 years, sensitivities of criteria I, II and III were 92%, 75% and 33%, respectively. Specificities were 17%, 26% and 70%, respectively, and predictive accuracies were 43%, 43% and 67%, respectively. Thus, patients with efficacy by criterion I appear to have a better prognosis when compared with patients with inefficacy. However, many patients with inefficacy by criterion I had a good outcome (nonspecificity).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1987

Combination of tocainide and quinidine for better tolerance and additive effects in patients with coronary artery disease.

The efficacy and tolerance of tocainide used alone and in combination with quinidine were studied in 20 patients with coronary artery disease and frequent (greater than 30/h) ventricular premature complexes. Holter electrocardiographic monitoring was performed at baseline and during therapy with tocainide alone, quinidine alone and a combination of tocainide and quinidine. During single drug therapy, the dose of tocainide was 1,680 +/- 437 mg/day and that of quinidine was 1,340 +/- 235 mg/day. During combination therapy, with smaller doses of tocainide (1,350 +/- 394 mg/day) and quinidine (1,060 +/- 268 mg/day) in many patients, no patient had side effects. At baseline before therapy, the mean ventricular premature complexes/h were 629 +/- 567, couplets/h were 23.9 +/- 29.7 and nonsustained ventricular tachycardias/24 h were 60.5 +/- 152.2. Compared with baseline values (100%), the frequency of ventricular premature complexes was reduced to 33 +/- 44% with quinidine, 39 +/- 30% with tocainide and 10 +/- 16% with combination therapy (p less than 0.01 for combination versus quinidine or tocainide alone; p = NS for quinidine versus tocainide). Individually, an effective regimen (greater than 83% reduction of ventricular premature complexes and abolition of nonsustained ventricular tachycardia) was found in 3 (15%) of 20 patients receiving tocainide alone, in 6 (30%) receiving quinidine alone and in 16 (80%) receiving combination therapy (p less than 0.01 for tocainide versus combination, quinidine versus combination; p = NS for tocainide versus quinidine). Thus, the antiarrhythmic effects of quinidine and tocainide are additive.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1986

Measurement of differences in timing and sequence between two ventricular electrodes as a means of tachycardia differentiation.

The use of two ventricular sensing electrodes to determine electrical activation sequence could provide a method for differentiation of normal from abnormal rhythms by implantable antitachycardia devices. Simultaneous recordings from two ventricular sites were obtained during dual chamber pacemaker implantation (5/8 patients), cardioverter-defibrillator implantation (2/8 patients), or programmed electrical stimulation study (1/8 patients). Recordings were made in normal sinus rhythm (NSR) (5 beats each in 8/8 patients), during ventricular tachycardia (VT) (38 beats with 7 morphologies in 3 patients) and during premature ventricular contractions (PVCs) (20 beats with 8 morphologies in 6 patients). Leads were placed transvenously in the right ventricle in 6 patients, and epicardially on the left ventricle in two. Intervals between the intrinsic deflection of the two ventricular electrograms ranged from 0 to 91 ms (mean of 26 ms) during NSR, from 13 to 141 ms (mean of 66 ms) during VT, and from 10 to 72 ms (mean of 40 ms) during PVCs and were reproducible within each patient for each type of rhythm. In all patients, the difference in sequence and timing between the dual electrograms in NSR beats vs. ectopic beats allowed for the differentiation of normal and abnormal complexes. These differences in each patient ranged from 23 to 210 ms (mean of 81 ms) during VT and from 3 to 89 ms (mean of 44 ms) during PVCs. Fourteen of the 15 ectopic morphologies exhibited greater than 20 ms difference in timing compared to their corresponding NSR beats. Combined with the appropriate software, multiple ventricular leads may be used by antitachycardia devices to discriminate between normal and abnormal ventricular activity.

Aged↗