Prevalence of arrhythmias detected by 24-hour ambulatory electrocardiography and value of antiarrhythmic therapy in elderly patients with unexplained syncope.
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Aged↗
Biomedical subjects
A D Mercando
Publications and source records attributed to A D Mercando.
Reproducibility of electrophysiologic testing during antiarrhythmic therapy for ventricular arrhythmias secondary to coronary artery disease.
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.
Adult↗
Prevalence of silent myocardial ischemia detected by 24-hour ambulatory electrocardiography, and its association with new coronary events at 40-month follow-up in elderly diabetic and nondiabetic patients with coronary artery disease.
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Prognostic significance of silent ischemia in elderly patients with peripheral arterial disease with and without previous myocardial infarction.
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Effect of quinidine or procainamide versus no antiarrhythmic drug on sudden cardiac death, total cardiac death, and total death in elderly patients with heart disease and complex ventricular arrhythmias.
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)
Aged↗
Time dependence of ventricular refractory periods: implications for electrophysiologic protocols.
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.
Adolescent↗
Differentiation of sinus rhythms from supraventricular tachydysrhythmias by activation sequence and timing.
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)
Animals↗
Antitachycardia pacing and implantable cardioverter defibrillators.
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.
Adolescent↗
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↗
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↗
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.
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