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Biomedical subjects

F E Marchlinski

Publications and source records attributed to F E Marchlinski.

At least 127 records · Page 7Linked to original sources
PubMed1989

Surgical decisions in the management of sudden cardiac death and malignant ventricular arrhythmias. Subendocardial resection, the automatic internal defibrillator, or both.

Subendocardial resection and implantation of an automatic implantable cardioverter/defibrillator are the current preferred treatments for the management of drug-resistant malignant ventricular arrhythmias and sudden cardiac death. We reviewed retrospectively the case histories of 269 patients who had subendocardial resection and 77 patients who had defibrillator implantation to define clinical characteristics of each group and compare operative and long-term results. All patients treated by subendocardial resection had recurrent sustained ventricular tachycardia as a result of a myocardial infarction. From the standpoint of arrhythmia substrate and cardiac disease, patients receiving the defibrillator were a more heterogeneous group. Forty-eight (62%) had coronary artery disease, 28 (36%) cardiomyopathy, and one patient had a primary electrical abnormality. Among patients receiving the defibrillator, 55% had sustained ventricular tachycardia and 45% polymorphic ventricular tachycardia or ventricular fibrillation. Overall ventricular function was similar in the two groups. Operative mortality rate was better in the group having defibrillator implantation (3% versus 15%). Complications related to the defibrillator device or implantation occurred in 46 (60%) patients, with asymptomatic shocks occurring in 35 patients (45%). Since the defibrillator was not designed to prevent arrhythmias, the arrhythmia-free survival rate was much better in the group having subendocardial resection (95% versus 44% at 3 years). Fewer patients treated by subendocardial resection required antiarrhythmic medications (33% versus 66%). The actuarial survival rate was similar in the two groups (approximately 60% at 4 years), with heart failure the most common cause of death. Thus both subendocardial resection and defibrillator implantation are highly effective in preventing sudden cardiac death. The choice of procedure depends on (1) arrhythmia diagnosis, (2) cardiac disease, and (3) intangible factors.

Aged↗
PubMed1988

Prognosis following sustained ventricular tachycardia occurring early after myocardial infarction.

Eighty-seven patients with sustained ventricular tachycardia (VT) between 3 and 90 days after acute myocardial infarction (AMI) were evaluated to define factors associated with a high risk of arrhythmia recurrence or death. Most patients had poor left ventricular function (mean ejection fraction 29 +/- 12%), multivessel coronary artery disease (71%) and inducible sustained VT with programmed stimulation (87%). During a mean follow-up of 26 months, 36 patients (41%) died and 21 patients had arrhythmia recurrence (with 19 sudden deaths). Factors independently associated with mortality included: (1) treatment before 1981 (p less than 0.01); (2) anterior AMI (p less than 0.05); (3) short time from AMI to first episode of VT (p less than 0.06); and (4) multivessel coronary artery disease (p less than 0.07). Factors independently associated with arrhythmia recurrence were: (1) medical treatment (as opposed to surgical) (p less than 0.01); (2) greater than or equal to 3 episodes of spontaneous VT (p = 0.01); (3) multivessel coronary disease (p less than 0.05); and (4) anterior AMI (p less than 0.07). Medically and surgically treated patients did not differ significantly in overall survival (49 vs 61%, respectively), although short-term (6 month) surgical survival improved from 31% during the first half of the study to 96% in the latter half (p less than 0.01). For patients with sustained VT early after AMI the risk of death and arrhythmia recurrence can be assessed based on clinical and angiographic characteristics; in addition, surgical treatment is associated with a lower incidence of arrhythmia recurrence than medical treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Relation of the intraoperative defibrillation threshold to successful postoperative defibrillation with an automatic implantable cardioverter defibrillator.

To determine the relation between the intraoperative defibrillation threshold and successful postoperative termination of induced ventricular fibrillation (VF) with the automatic implantable cardioverter defibrillator (AICD), 33 patients who underwent AICD implantation were studied. The defibrillation threshold, determined after at least 10 seconds of VF, was 5 J in 2, 10 J in 6, 15 J in 10, 20 J in 10 and 25 J in 5 patients. The AICD energy rating on the first discharge was 28 +/- 1.8 J. Defibrillation of induced VF was demonstrated postoperatively in 29 of 33 (88%) patients. The AICD terminated VF postoperatively in all 18 patients with a defibrillation threshold less than or equal to 15 J. Only 11 of the 15 (73%) patients with a defibrillation threshold greater than or equal to 20 J (p less than 0.04) had VF terminated postoperatively. In all 4 patients in whom the AICD failed to terminate induced VF, the energy difference between the AICD rating and the defibrillation threshold was less than or equal to 10 J. Among the 14 patients with a difference of less than or equal to 10 J between the AICD energy rating and the defibrillation threshold, there were no significant differences between the 4 patients with and the 10 without successful VF termination with respect to the duration of VF induced postoperatively or the AICD lead system. In summary, failure to terminate VF with the AICD is not uncommon (27%) when the defibrillation threshold approaches the energy delivering capacity of the AICD.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Cycle length-dependent effects on normal and abnormal intraventricular electrograms: effect of procainamide.

The effect of procainamide (mean concentration 9.1 +/- 2.0 micrograms/ml) on cycle length-dependent changes in electrographic characteristics was determined in 10 patients with prior myocardial infarction. Intracardiac bipolar electrograms were recorded from an abnormal left ventricular site in the distribution of prior (greater than 6 month) myocardial infarction and from a normal right ventricular site. Pacing was performed for 15 beats from the right ventricular apex at cycle lengths of 600 (or 500), 400 and 300 ms. In the control state, the QRS width, the normal electrogram and in 9 of the 10 patients the abnormal electrogram did not change with decreasing cycle lengths. After procainamide the mean QRS width increased from 203 +/- 32 to 240 +/- 50 ms (+18%, p less than 0.01) at a paced cycle length of 600 (or 500) ms, from 198 +/- 34 to 245 +/- 59 ms (+24%, p less than 0.01) at a paced cycle length of 400 ms and from 197 +/- 36 to 258 +/- 67 ms (+31%, p less than 0.01) at a paced cycle length of 300 ms.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1988

Automatic implantable defibrillator discharge resulting from routine pacemaker programming.

A middle-aged gentleman with an idiopathic dilated cardiomyopathy, drug-refractory sustained ventricular arrhythmia, and high-degree AV block was managed with an automatic implantable cardioverter-defibrillator (AICD) and a Cordis Multicor II VVI pacemaker. During a routine follow-up visit, the pacemaker threshold was determined. Seven seconds after reprogramming the Cordis pacemaker to the "stat" VVI mode, the AICD discharged. The time to discharge after reprogramming the pacemaker equalled the previously determined AICD charge time. No other rhythm disturbance was documented and the rate with double counting of pacemaker stimulus and QRS complex was less than the triggering rate for the AICD. In conclusion, the AICD can be triggered by pacemaker programming signals unrelated to subsequent pacemaker function.

Electric Countershock↗
PubMed1988

Entrainment of ventricular tachycardia: explanation for surface electrocardiographic phenomena by analysis of electrograms recorded within the tachycardia circuit.

Transient entrainment was demonstrated during 59 pacing events in 18 episodes of sustained uniform ventricular tachycardia (VT) while recording electrograms from the site of origin of tachycardia (LE-SOO). During entrainment, the morphology of the initial component of the LE-SOO was identical to the morphology observed during the tachycardia in 13 VTs (group I), but in five VTs (group II), the initial component changed at a "critical" paced cycle length. The presence of the proposed surface electrocardiographic criteria for entrainment--fixed fusion and a first postpacing complex without fusion but occurring at the paced cycle length--were integrally dependent on the morphologic changes in the local presystolic electrogram. Fixed fusion of the surface electrocardiogram at one or more paced cycle lengths was detected during entrainment at 35 of 59 paced cycle lengths in 12 of 18 tachycardias, 10 of which were group I and two of which were group II VTs. Fixed fusion demonstrated by analysis of the LE-SOO was observed at one or more pacing cycle lengths in 17 of 18 VTs. In five tachycardias in which surface electrocardiographic fusion was not observed, fixed fusion was evident on analysis of the left ventricular LE-SOO during right ventricular pacing. The first postpacing interval, as measured at the surface electrocardiogram, was consistently equal to the paced cycle length in only one of 18 tachycardias and was greater than the VT cycle length in eight of 17 tachycardias. A pathway with a long conduction time was demonstrated during entrainment. However, in those 12 VTs in patients in whom pacing was performed at more than one cycle length and there was preservation of the LE-SOO morphology, the conduction time between the stimulus and presystolic electrogram remained constant. Thus, no evidence for "atrioventricular nodal-like" decremental conduction was observed over a wide range of pacing cycle lengths. We conclude that: (1) two of the previously proposed criteria for diagnosis of entrainment (fixed fusion on the surface electrocardiogram and a first postpacing interval equal to the paced cycle length) are overly restrictive criteria for definition of "entrainment" of VT, (2) analysis of endocardial recordings from the site of origin of tachycardia during attempted entrainment of VT is useful for documenting the presence of entrainment, and (3) such analysis provides a basis for the understanding of surface electrocardiographic phenomenon associated with entrainment.

Cardiac Pacing, Artificial↗
PubMed1988

Relationship between the 12-lead electrocardiogram during ventricular tachycardia and endocardial site of origin in patients with coronary artery disease.

Previous studies in patients with sustained ventricular tachycardia (VT) have demonstrated the efficacy of surgical and catheter-mediated ablative procedures based on activation mapping during VT. Since extensive preoperative or intraoperative mapping may be impractical due to time constraints or patient intolerance, we sought to define characteristics of the 12-lead electrocardiogram (ECG) during VT that could suggest a particular endocardial region of origin and thus facilitate mapping studies. Endocardial mapping was performed during 182 VTs in 108 patients with prior myocardial infarction of either the anterior or inferior wall. Endocardial sites of origin (sites from which greater than or equal to 40 msec of presystolic electrical activity was consistently recorded) were identified with use of catheter (154 VTs) or intraoperative (85 VTs) activation mapping (both methods used in 57 Vts). Twelve-lead ECGs obtained during these VTs were characterized by four features: location of infarction, bundle branch block type configuration, quadrant of QRS axis, and precordial R wave progression pattern. A specific combination of these four features was associated with a particular endocardial region containing the mapped site of origin in 87 VTs (48% of total). An association (greater than or equal to 70% positive predictive accuracy) was more likely to be found in the presence of left, as opposed to right, bundle branch block type patterns (53/73 [73%] vs 34/109 [31%]; p less than .001) and in the presence of VT related to inferior, as opposed to anterior, infarction (40/54 [74%] vs 47/128 [37%]; p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Effects of lidocaine and procainamide on normal and abnormal intraventricular electrograms during sinus rhythm.

The effect of lidocaine (n = 6) and procainamide (n = 12) on electrogram characteristics from electrically normal right ventricular and electrically abnormal left ventricular endocardial sites was determined in 18 patients with prior myocardial infarction. Bipolar electrograms were recorded during sinus rhythm with No. 6F catheters positioned at a left ventricular abnormal site (electrograms fulfilling two of the following criteria: amplitude less than 3 mV, duration greater than 70 msec, or an amplitude to duration ratio less than .046) and normal sites at the right ventricular apex (RVA) and right ventricular outflow tract (RVOT). All electrograms were recorded from the same location before and after intravenous lidocaine or procainamide administered to obtain mean serum concentrations of 4.2 +/- 0.6 and 9.42 +/- 2 micrograms/ml respectively. Lidocaine and procainamide had no significant effect on sinus cycle length or electrogram amplitude. After lidocaine, no significant change in QRS width (112 +/- 23 vs 114 +/- 24 msec), left ventricular electrogram duration (76 +/- 21 vs 78 +/- 15 msec), or right ventricular electrogram duration (RVA 33 +/- 9 vs 33 +/- 10 msec, RVOT 31 +/- 9 vs 33 +/- 11 msec) was noted during sinus rhythm. At a paced cycle length of 600 msec, there was also no change in the paced QRS duration (197 vs 198 msec), the RVA electrogram duration (30 vs 32 msec), the RVOT electrogram duration (49 vs 52 msec), or the left ventricular electrogram duration (102 vs 108 msec).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗
PubMed1988

Comparison of individual and combined effects of procainamide and amiodarone in patients with sustained ventricular tachyarrhythmias.

To compare the individual and combined electrophysiological effects of amiodarone and procainamide, 35 patients with sustained ventricular arrhythmias underwent programmed stimulation in the control state, after procainamide (mean concentration, 8.7 +/- 2.8 micrograms/ml), after 13 +/- 2 days of amiodarone (1,400 mg/day x 7 days, then 400 mg/day), and after amiodarone with procainamide (mean procainamide concentration, 7.8 +/- 2.2 micrograms/ml). Sustained ventricular tachycardia (VT) was inducible in all 35 patients during treatment with procainamide alone and with amiodarone alone. Procainamide and amiodarone similarly increased the VT cycle length (+68 vs. +61 msec), the corrected QT interval (+63 vs. +49 msec), and the ventricular effective refractory period measured at paced cycle lengths of 600-550 msec (+23 vs. +21 msec) and 400 msec (+25 vs. +23 msec). Procainamide had a more pronounced effect on QRS duration than amiodarone during sinus rhythm (+18 vs. +8 msec, p less than 0.01) and during paced cycle lengths of 600-550 msec (+32 vs. +23 msec, p less than 0.01) and 400 msec (+37 vs. +28 msec, p less than 0.1) but a similar effect on the QRS duration during VT (+32 vs. +29 msec). During combination therapy, VT initiation was prevented in only two (6%) patients. The combination therapy produced a greater increase (p less than 0.001) than individual therapy in all the electrophysiological intervals assessed, with the exception of the sinus cycle length. On each drug regimen, a cycle length-dependent increase (p less than 0.05) in paced QRS duration was noted (400 more than 600-550 msec).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Spontaneous compared with induced onset of sustained ventricular tachycardia.

Electrophysiological characteristics of the modes of initiation of 16 episodes of spontaneously occurring sustained ventricular tachycardia recorded in 16 patients by two-channel ambulatory electrocardiographic monitoring were compared with the characteristics of ventricular tachycardia induced by programmed electrical stimulation. Eleven episodes of spontaneous ventricular tachycardia began after a single ventricular premature depolarization (VPD), three episodes after two VPDs, and two episodes after five VPDs. By comparison, only four episodes of sustained ventricular tachycardia were induced with a single VPD. Each episode of spontaneous ventricular tachycardia was initiated by a late coupled VPD (RR':QT ratio greater than 1.0). The VPD was often morphologically similar to the ensuing ventricular tachycardia (eight of 11 episodes that began after a single VPD). No correlation was found between the modes of initiation of spontaneous and induced ventricular tachycardia. We hypothesize that concealed decremental slow conduction, reflected in the long coupling intervals of VPDs initiating ventricular tachycardia, is of critical importance in initiating ventricular tachycardia. We conclude that major differences exist in the timing and number of VPDs associated with the onsets of spontaneous and induced sustained ventricular tachycardia.

Adult↗
PubMed1988

Nonuniform recovery of excitability in the left ventricle.

The purpose of this study was to determine left ventricular activation, dispersion of refractoriness, and total recovery time in patients with coronary artery disease and ventricular tachycardia and in patients with the long QT syndrome and to compare these patients with a group of normal patients. Left ventricular endocardial catheter mapping and left ventricular refractory period determination were performed in 18 patients. Group 1 consisted of seven patients with no heart disease and no arrhythmia; group 2 consisted of six patients with previous infarction and sustained ventricular tachycardia; and group 3 consisted of five patients with prolonged QT interval and previous cardiac arrest. Total left ventricular endocardial activation was significantly longer in group 2 (75 +/- 23 msec, mean +/- SD) compared with group 1 (34 +/- 9 msec, p less than 0.01) and group 3 (42 +/- 5 msec, p less than 0.05). Dispersion of refractoriness was significantly greater in group 3 (87 +/- 27 msec) than in group 1 (40 +/- 14 msec, p less than 0.01) and group 2 (53 +/- 14 msec, p less than 0.05). Dispersion of total recovery time was significantly greater in group 2 (90 +/- 30 msec) than in group 1 (52 +/- 14 msec, p less than 0.05) as well as group 3 (114 +/- 43 msec) compared with group 1 (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Nonpharmacologic therapy of ventricular tachycardia.

Nonpharmacologic therapies for patients with sustained ventricular tachycardia have been necessitated by the low frequency of drug-responsive patients. These nonpharmacologic therapies include antitachycardia pacemakers, low-energy cardioverters, defibrillators, surgery and, for the present, catheter ablation. Antitachycardia pacing alone should never be used because of the known incidence of acceleration of ventricular tachycardia to ventricular fibrillation. Thus, all electrical devices must include a back-up defibrillator at the very least. The current automatic implantable cardioverter-defibrillator, which has been implanted in over 1000 patients, has been shown to prevent sudden death. Surgery has offered the only method to cure the arrhythmia by removing the arrhythmogenic substrate. Improved surgical techniques with electrophysiologic guidance have an acceptable mortality and a clinical success rate in 80-90% range. Catheter ablation, which is an experimental procedure at this time, offers the promise of a nonsurgical technique to extirpate the ventricular tachycardia substrate.

Electric Countershock↗
PubMed1987

Results of signal-averaged electrocardiography and electrophysiologic study in patients with nonsustained ventricular tachycardia after healing of acute myocardial infarction.

Programmed stimulation and signal-averaged electrocardiography were performed in 43 consecutive patients with nonsustained ventricular tachycardia (VT) after healing of inferior (29 patients) or anterior wall (14 patients) acute myocardial infarction. Twenty-two patients had inducible sustained VT. Patients with inferior infarction and inducible sustained VT had significantly longer filtered QRS durations (125 +/- 19 vs 112 +/- 15 ms, p less than 0.01) and significantly lower voltage in the last 40 ms of the filtered QRS complex (19 +/- 5 vs 30 +/- 14 microV, p less than 0.05) than those without inducible sustained VT. In contrast, the signal-averaged electrocardiographic measurements in patients with anterior infarction and inducible sustained VT did not differ significantly from those without inducible sustained VT. The results of these studies were compared with those of 2 control groups: 45 patients without ventricular arrhythmias after myocardial infarction and 95 patients with spontaneous and inducible sustained VT after myocardial infarction. The signal-averaged electrocardiographic measurements in patients with spontaneous nonsustained VT after inferior infarction were intermediate between the control group without arrhythmias and the control group with sustained VT. The signal-averaged electrocardiograms in patients with nonsustained VT after anterior infarction were not significantly different from those in patients without ventricular arrhythmias. The study shows that the site of infarction influences the signal-averaged electrocardiogram in patients with VT after myocardial infarction. The signal-averaged electrocardiogram may be useful in identifying patients with nonsustained VT after a remote inferior myocardial infarction who have inducible sustained VT.

Cardiac Pacing, Artificial↗
PubMed1987

Hazards of intravenous verapamil for sustained ventricular tachycardia.

In 11 of 25 patients (44%) with sustained ventricular tachycardia (VT) who received intravenous verapamil (5 to 10 mg), acute severe hypotension or loss of consciousness developed, necessitating immediate cardioversion. Comparison of these 11 patients with the 14 who did not have adverse effects after verapamil revealed no significant difference in age, heart disease, ejection fraction, blood pressure before verapamil administration, other oral or intravenous drugs use, verapamil dose or VT characteristics (rate and morphologic pattern). Although most patients with severe adverse effects after verapamil had prior myocardial infarction, deterioration also occurred in patients without coronary disease and in patients with a normal left ventricular ejection fraction. VT terminated after verapamil infusion in 6 patients. No single electrocardiographic morphologic pattern characterized these patients. A control group of 25 patients presenting with hemodynamically stable VT who received other antiarrhythmic agents was examined. Hypotension developed in only 1 patient during acute therapy and did not require emergency cardioversion. Thus, although verapamil may terminate VT, severe adverse effects occur much more often. Use of verapamil to differentiate supraventricular tachycardia with aberrant conduction from ventricular tachycardia is hazardous.

Adult↗