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Biomedical subjects

F E Marchlinski

Publications and source records attributed to F E Marchlinski.

At least 199 records · Page 11Linked to original sources
PubMed1984

The value of catheter mapping during sinus rhythm to localize site of origin of ventricular tachycardia.

We assessed the value of endocardial catheter mapping in 52 patients in sinus rhythm and with 102 morphologically distinct ventricular tachycardias. The local bipolar electrograms from various regions of the left ventricle were assessed and quantitatively classified with respect to the characteristics of amplitude and duration. With the use of this assessment we found that electrograms from the site of origin were of significantly lower amplitude and longer duration; however, because such an overlap occurred with electrograms that were not from sites of origin, this does not serve as a useful clinical marker. Various types of electrograms, including normal, abnormal, fractionated, abnormal late, fractionated late, and longest, were evaluated with respect to sensitivity, specificity, and positive predictive value. None of these types possessed the ability to reliably localize the site of origin of ventricular tachycardia. We therefore conclude that endocardial catheter mapping during sinus rhythm is not useful as a guide in localized surgical therapy of ventricular tachycardia. Surgery guided only by the results of mapping during sinus rhythm would result in a more extensive excision than that directed by maps obtained during ventricular tachycardia and in some cases would result in the exclusion of the area considered to be the site of origin of the tachycardia.

Cardiac Catheterization↗
PubMed1984

Endocardial mapping in humans in sinus rhythm with normal left ventricles: activation patterns and characteristics of electrograms.

Endocardial catheter mapping was performed in 15 patients in sinus rhythm who had no evidence of structural heart disease and normal left ventricles. Mapping was performed with the use of 10 mm interelectrode distance from various left ventricular endocardial sites. In 10 patients a quantitative analysis of electrographic amplitude, duration, and amplitude/duration ratio was performed. The normal left ventricular bipolar electrograms had an amplitude of greater than 3 mV, a duration of less than 70 msec, and an amplitude/duration ratio of greater than 0.045. Local activation times were also assessed in the 15 patients. This analysis revealed two endocardial breakthrough sites, one on the midinferior septum and a second on the anterior wall near the insertion of the anterior papillary muscle. We therefore have defined normal quantitative characteristics of left ventricular bipolar electrograms and the normal left ventricular activation sequence in the intact normal human left ventricle.

Adolescent↗
PubMed1984

Sustained ventricular tachycardia in patients with idiopathic dilated cardiomyopathy: electrophysiologic testing and lack of response to antiarrhythmic drug therapy.

Eleven consecutive patients with idiopathic dilated cardiomyopathy and spontaneous, sustained ventricular tachycardia (VT) of uniform morphology underwent programmed ventricular stimulation and serial antiarrhythmic drug testing. The mean ejection fraction was 30 +/- 6.4%. Sustained VT was induced by programmed electrical stimulation in all 11 patients. A mean of 3.7 +/- 2.4 antiarrhythmic drugs were evaluated by programmed stimulation, including at least one experimental agent in eight patients. In nine of 11 patients VT remained inducible on all drug therapy. During a mean follow-up period of 21 +/- 14 months there were four sudden deaths and two patients with recurrences of VT. In all six patients with sudden death or recurrence of VT, the arrhythmia remained inducible on drug therapy. Three patients who died suddenly had a hemodynamically stable, induced tachycardia on antiarrhythmic therapy. Of eight patients treated with amiodarone, only two were successfully treated. We conclude that in patients with sustained VT and idiopathic dilated cardiomyopathy, VT can be induced by programmed electrical stimulation. VT will usually remain inducible on antiarrhythmic therapy, and sudden death can occur despite slowing and improved tolerance of the induced arrhythmia. Amiodarone may have limited efficacy, and more aggressive therapy, such as surgery or implantation of an automatic internal defibrillator, should be considered in this patient population.

Adult↗
PubMed1983

Programmed ventricular stimulation at a second right ventricular site: an analysis of 100 patients, with special reference to sensitivity, specificity and characteristics of patients with induced ventricular tachycardia.

One hundred patients without ventricular tachycardia (VT) initiated from the right ventricular (RV) apex were subjected to stimulation at the RV outflow tract. Sixty-two patients had no clinical arrhythmias, and 38 had sustained VT, ventricular fibrillation (VF) or cardiac arrest. Of the 38 patients with clinical arrhythmias, 22 (58%) had VT or VF induced from the RV outflow tract. Among the 62 patients without arrhythmias, 5 (13%) had polymorphic nonsustained VT or VF induced, which occurred with triple extrastimuli in all 5 patients. The 22 patients with VT initiated at the RV outflow tract were a heterogeneous group; 10 (45%) patients had cardiac diagnoses other than coronary artery disease (CAD). In contrast were patients whose VT was initiated at the RV apex (n = 84); in this group, 20 patients (22%) had diagnoses other than CAD (p less than 0.05). These 22 patients also were younger (mean age 46 years) than patients whose VT was initiated at the RV apex (mean age 58; p less than 0.01). Of the 16 patients with clinical VT and no induced arrhythmia from either RV site, 7 had CAD (4 with cardiac arrest), 5 had the long QT syndrome, 3 had dilated cardiomyopathy and 1 had valvular heart disease. In conclusion, stimulation at a second RV site increases the sensitivity of RV stimulation in patients with known VT and seldom initiates VT in patients without clinical VT.

Adult↗
PubMed1983

Identifying patients at risk of sudden death after myocardial infarction: value of the response to programmed stimulation, degree of ventricular ectopic activity and severity of left ventricular dysfunction.

The ability of programmed ventricular stimulation to identify risk of sudden death after acute myocardial infarction (MI) was compared with 24-hour electrocardiographic assessment of ventricular ectopic activity and determination of left ventricular (LV) dysfunction. Forty-six patients underwent programmed stimulation 8 to 60 days (mean 22) after documented MI. Programmed stimulation consisted of single and double extrastimuli from the right ventricular apex at 2 times diastolic threshold during ventricular pacing and normal sinus rhythm. Of the 46 patients, 44 underwent electrocardiographic monitoring at least 6 days after MI. In 43 of the 46 patients, LV ejection fraction (EF) and the presence of LV aneurysm were determined. In response to programmed ventricular stimulation, 5 patients had sustained ventricular tachycardia (VT), 5 had nonsustained VT (greater than or equal to 4 beats), 13 had intraventricular reentrant repetitive responses, and 23 had either bundle branch reentrant repetitive responses or no extra responses to programmed ventricular stimulation (negative study). During a mean follow-up of 18 months, 10 patients died, 6 suddenly. One of the 10 patients with sustained or nonsustained VT died suddenly, compared with 3 of 13 patients with intraventricular reentrant responses and 2 of 23 patients with a negative study (difference not significant). Of 25 patients with Grade 0 to 2 ventricular ectopic activity, 3 died suddenly after MI, compared with 3 of 19 patients with Grade 3 or 4 activity (difference not significant). By comparison, the frequency of sudden death was greater in patients with an LVEF of less than 40% (5 of 16 versus 1 of 27 patients) or an LV aneurysm (5 of 13 versus 1 of 30 patients).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Clinical characteristics and long-term follow-up in 119 survivors of cardiac arrest: relation to inducibility at electrophysiologic testing.

Electrophysiologic studies were performed in 119 survivors of cardiac arrest. Sustained ventricular arrhythmias were initiated by programmed ventricular stimulation in 72 patients (61%). Coronary artery disease patients with induced sustained ventricular arrhythmias had a higher incidence of prior myocardial infarction (95 versus 72%) and ventricular aneurysm (59 versus 28%) and a lower ejection fraction (37 versus 50%) than those with no inducible sustained ventricular arrhythmias. Of the 72 patients with inducible ventricular arrhythmias, 11 (15%) died suddenly during a mean follow-up of 18 months (range 15 days to 58 months). In this group, 6 of 41 patients (15%) discharged on a successful antiarrhythmic regimen and 5 of 27 patients (19%) discharged on an unsuccessful regimen or without a predischarge study have died suddenly. Of these 27 patients, 1 of 12 patients treated with amiodarone and 4 of 15 (27%) with conventional antiarrhythmic therapy died suddenly. The remaining 4 patients died of nonarrhythmic causes in the postoperative period. Of 47 patients without inducible sustained ventricular arrhythmias, 15 (32%) died suddenly at a mean follow-up of 20 months, 10 (34%) with and 15 (28%) without empiric therapy. It is concluded that sustained ventricular arrhythmias can be initiated in most patients resuscitated from cardiac arrest. Patients with inducible arrhythmias have greater left ventricular dysfunction than those without inducible arrhythmias. Medical or surgical therapy that prevented the induction of sustained ventricular arrhythmias was predictive of a successful outcome in 85% of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1983

Electrophysiologic studies in nonsustained ventricular tachycardia: relation to underlying heart disease.

Electrophysiologic studies were performed in 83 patients with spontaneous episodes of nonsustained ventricular tachycardia (VT). The clinical arrhythmia was reproduced in 63% (in 42 patients by programmed stimulation and in 10 by isoproterenol infusion). In 15 patients sustained VT could be reproducibly induced by programmed stimulation. Inducibility was related to the associated heart diseases: programmed stimulation induced VT in 25 of 33 patients (75%) with coronary disease, 6 of 18 patients (33%) with cardiomyopathy (dilated in 16, hypertrophic nonobstructive in 2), in 4 of 8 patients (50%) with mitral valve prolapse and in 7 of 24 patients (29%) without structural heart disease. Isoproterenol infusion induced VT in no other patient with coronary artery disease, 1 other patient with mitral valve prolapse, 3 patients with cardiomyopathy, and in 6 of 24 patients without structural heart disease. Sustained VT was induced only in patients with structural heart disease, and correlated with the presence of left ventricular aneurysms: Sustained VT was induced in 9 of 13 patients with left ventricular aneurysms. The study demonstrates that electrophysiologic techniques can reproduce episodes of nonsustained VT in most patients with spontaneous arrhythmias. Some patients who demonstrate only nonsustained VT spontaneously have inducible, sustained VT, most often in the setting of coronary artery disease and left ventricular aneurysms.

Adolescent↗
PubMed1983

Changes in ventricular refractoriness after an extrastimulus: effects of prematurity, cycle length and procainamide.

This study was performed to determine the ability of extrastimuli to change ventricular refractoriness. We prospectively evaluated the effects of stimulus prematurity and paced cycle length (PCL) in 30 patients and the effect of procainamide in 8 patients on changes in the ventricular effective refractory period (ERP) after a right ventricular extrastimulus (S2). An S2 was introduced at preselected coupling intervals at a PCL (S1-S1) of 600 and 400 ms. At each S1-S2 interval, a second extrastimulus (S3) was introduced in 5-ms decrements and the ERP of S2 measured. The decrease in the ERP after an S2 was directly related to prematurity and most of the shortening occurred over a narrow range of S1-S2 intervals. At a PCL of 600 ms, the ERP of S2 at S1-S2 intervals less than or equal to 400 ms was significantly shorter than the ERP of S1 (maximal shortening 23%). At a PCL of 400 ms, the ERP of S2 at S1-S2 intervals less than or equal to 350 ms was significantly shorter than the ERP of S1 (maximal shortening 25%). The ERP of S2 at the shortest S1-S2 interval was greater with a PCL of 600 ms than with 400 ms (200 +/- 31 versus 180 +/- 26 ms, p less than 0.001). However, the total shortening in ERP (ERPS1 - ERPS2 at shortest S1-S2 interval) was similar at both PCLs (55 +/- 14 versus 59 +/- 13 ms). Procainamide significantly prolonged the ERP of S2 at each S1-S2 interval.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1983

Electrophysiologic evaluation of syncope in patients with bifascicular block.

Thirteen patients with syncope and bifascicular block were evaluated by electrophysiologic study (EPS) including programmed stimulation. The mean age was 62 years. Six patients had coronary artery disease, three had cardiomyopathy, and four showed no evidence of organic heart disease. Holter monitoring and neurologic evaluation were nondiagnostic in all patients prior to EPS. EPS demonstrated inducible ventricular tachycardia (VT) in four patients, an HV interval greater than or equal to 70 msec in four, intra- and infra-His block with atrial pacing in one, and was nondiagnostic in four patients. Four of six patients with an HV interval greater than or equal to 70 msec or pacing-induced infranodal block were treated with permanent pacemakers, four of four patients with VT received antiarrhythmic therapy, and three of four patients with nondiagnostic studies received no therapy (one patient received a permanent pacemaker). During a mean follow-up period of 19 months (range 3 to 60 months) all but three patients have been free of syncope. One patient with VT did not take prescribed antiarrhythmic therapy, another patient with VT died suddenly; the remaining patient had a normal study and basilar migraines were subsequently diagnosed. We conclude that: (1) ventricular tachycardia may be a significant cause of syncope in patients with bifascicular block and was induced by programmed stimulation in approximately one third of patients studied; (2) EPS including programmed stimulation is helpful in delineating both the etiology of syncope and appropriate treatment in patients with bifascicular block. A negative study may also be of prognostic value.

Adolescent↗
PubMed1983

Relation of mode of induction and cycle length of ventricular tachycardia: analysis of 104 patients.

One hundred four consecutive patients with ventricular tachycardia (VT) were examined to correlate the cycle length with the mode of initiation of VT (single, double, and triple extrastimuli and rapid pacing). Tachycardias induced with a single extrastimulus were slower (342 +/- 72 ms, mean cycle length) than those induced with double (295 +/- 60 ms) or triple (282 +/- 56 ms) extrastimuli or rapid pacing (293 +/- 40 ms). There were no differences among the last 3 groups. In 38 patients who had endocardial catheter mapping to determine the site of origin of VT, distance from stimulation site to the site of origin was estimated and correlated with mode of initiation. There was no difference in mode of initiation when the stimulation site was close (less than 3 cm), intermediate (3 to 5 cm), or distant (greater than 8 cm) from the site of origin. To address the issue of distance from stimulation site to the site of origin somewhat differently, mode of initiation was correlated with site of previous myocardial infarction in 69 patients with VT initiated from the right ventricular apex. Again, mode of initiation did not differ among patients with septal, inferior, lateral, or multiple myocardial infarctions. Thus, cycle length of VT initiated with a single extrastimulus was slower than that initiated with double or triple extrastimuli or rapid pacing and the mode of initiation of VT was unrelated to site of myocardial infarction or distance between stimulation site and site of origin of VT.

Adult↗
PubMed1983

Electrophysiologic effects of intravenous timolol.

We evaluated the electrophysiologic effects and dose response of the long-acting beta-blocking drug timolol given intravenously to 12 patients during intracardiac electrophysiologic study. Electrophysiologic parameters were measured during control and immediately, 30 minutes, and 48 hours following infusion. Significant changes in electrophysiologic parameters were only observed in the five patients (Group B) who received 0.05 mg/kg and not in the seven patients who received 0.02 mg/kg (Group A). In Group B patients immediately after timolol infusion sinus cycle length increased from 840 +/- 254 msec to 1048 +/- 63 msec (P less than 0.01), A-H interval during normal sinus rhythm increased from 94 +/- 42 msec to 101 +/- 45 msec (P less than 0.05), paced cycle length to A-V nodal Wenckebach increased from 370 +/- 45 msec to 430 +/- 76 msec (P less than 0.05), and A-V nodal effective refractory period increased from 284 +/- 63 msec to 360 +/- 83 msec (P less than 0.01). Significant increases in these electrophysiologic parameters were also noted at 30 minutes following timolol infusion. Other conduction times, atrial and ventricular refractory periods, and corrected sinus node recovery. time were unaltered by timolol. All electrophysiologic parameters returned to control in 48 hours. No adverse effects were observed. We conclude that intravenous timolol in doses of 0.05 mg/kg significantly increases sinus cycle length and prolongs A-V nodal conduction and refractoriness, demonstrates peak effects immediately after intravenous administration, and is well tolerated.

Adolescent↗
PubMed1983

Sustained ventricular tachyarrhythmias during the early postinfarction period: electrophysiologic findings and prognosis for survival.

Forty patients with sustained tachycardia occurring 3 to 65 days after myocardial infarction underwent programmed ventricular stimulation within 3 months of the infarction. Patients were characterized clinically by a complicated initial 48 hours of hospitalization for their acute infarction (85% of study group). The development of bundle branch block in association with infarction occurred with an unusually high frequency (32%). Ventricular tachycardia similar in configuration to spontaneous arrhythmia was induced with programmed ventricular stimulation in 33 (83%) of the 40 patients. In 15 (45%) of these 33 patients, additional morphologically distinct ventricular tachycardia not seen clinically was initiated. The induction of ventricular tachycardia was not significantly related to the time after myocardial infarction at which spontaneous ventricular tachycardia was initially observed. Only 20 of the 40 patients are alive after a mean follow-up period of 20 +/- 15 months. Twelve of the 20 deaths were sudden cardiac deaths. Sixteen of the 33 patients with inducible ventricular tachycardia died; 8 of the 16 deaths were sudden. By comparison, four of the seven patients with no inducible ventricular tachycardia died (probability [p] = not significant), all suddenly. The mode of therapy did not influence subsequent survival. It appears that in patients with sustained ventricular tachycardia occurring more than 48 hours after a recent myocardial infarction, ventricular tachycardia similar to that clinically observed can usually be induced by programmed stimulation. In addition, multiple morphologically distinct ventricular tachycardias, some of which have not been previously observed, are frequently induced. Finally, the prognosis for survival is poor, regardless of inducibility or mode of therapy, and may in part be related to a changing arrhythmia substrate.

Adult↗
PubMed1983

Right ventricular tachycardia: clinical and electrophysiologic characteristics.

This report describes the clinical and electrophysiologic characteristics of 30 patients without myocardial disease who had ventricular tachycardia with the morphologic characteristics of left bundle branch block and inferior axis. The tachycardias were nonsustained in 24 patients, sustained (greater than 30 sec) in six patients, and provocable by exercise in 14 of 23 patients undergoing a standard Bruce protocol. Ventricular tachycardia was induced during electrophysiologic study in 22 of 30 patients. Programmed stimulation induced tachycardia in 10 of 30 patients, most frequently by rapid atrial or ventricular pacing. Isoproterenol infusion facilitated tachycardia induction in 13 of 23 patients. Endocardial activation mapping, performed in 10 patients, confirmed that earliest ventricular activation during tachycardia occurred at the right ventricular outflow tract on the interventricular septum. These tachycardias were unique in their responsiveness to a wide variety of antiarrhythmic drugs, including type I drugs and propranolol. During a mean follow-up of 30 months, no patient has died or experienced cardiac arrest. Two patients appear to be in spontaneous remission, and no patient has developed additional signs of cardiac disease.

Adolescent↗
PubMed1982

Electrophysiologic study for ventricular arrhythmia: effect on total and myocardial-specific creatine kinase activity.

To determine the potential for myocardial injury during electrophysiologic study for ventricular arrhythmia, total creatine kinase and creatine kinase B-subunit enzyme activity were serially measured after the procedure in 24 patients. During electrophysiologic study 14 of the 24 patients had sustained ventricular tachycardia or fibrillation, 4 patients had nonsustained ventricular tachycardia, and 6 patients had no ventricular arrhythmia induced. Cardioversion was necessary because of hemodynamic collapse in 9 of the 14 patients with sustained ventricular tachycardia or ventricular fibrillation. Coronary heart disease was present in 14 of the 24 patients, in 9 of the 14 with sustained ventricular tachycardia or ventricular fibrillation, and in 7 of the 9 patients requiring cardioversion. Total creatine kinase was modestly elevated (greater than twice baseline or greater than normal, or both) 24 hours after electrophysiologic study in 10 (42%) of the patients. Electrophysiologic study with or without the induction of ventricular tachycardia or ventricular fibrillation was not associated with increased creatine kinase B-subunit activity even in patients with coronary heart disease.

Adolescent↗
PubMed1982

Amiodarone for control of sustained ventricular tachyarrhythmia: clinical and electrophysiologic effects in 51 patients.

We evaluated the electrophysiologic effects of amiodarone and its ability to control ventricular arrhythmia in a selected group of 51 patients with refractory sustained ventricular arrhythmia. Amiodarone in doses of 400 to 800 mg/day prolonged refractoriness in the atria, atrioventricular (AV) node, and ventricle as well as conduction through the AV node and His-Purkinje system. Although it had no effect on measurements of sinus nodal function (sinus nodal recovery time and sinoatrial conduction time), it prolonged the sinus cycle length and 2 patients required a permanent pacemaker for symptomatic sinus bradycardia. Amiodarone did not alter the ease of inducibility in any consistent manner, and only 5 of 43 patients (12%) who had inducible ventricular tachycardia before amiodarone therapy had none induced during amiodarone treatment. The clinical effectiveness of amiodarone could be evaluated in 46 patients followed up for 8.6 +/- 6 months (range 0.5 to 22). It provided effective therapy in 23 patients (50%), partly effective therapy in 13 (28%), and was ineffective in 10 (22%). Adverse effects were noted in 28 of 51 patients (55%), and in 11 of these (22%) the drug had to be discontinued because of adverse effects. We conclude that amiodarone is a useful agent for the treatment of refractory sustained ventricular arrhythmia. Its use should be reserved for patients with life-threatening sustained arrhythmia because of the significant incidence of adverse effects. Furthermore, good clinical response can be observed in patients receiving amiodarone in spite of continued inducibility.

Adolescent↗
PubMed1982

Termination of ventricular tachycardia: role of tachycardia cycle length.

The mode of termination of ventricular tachycardia (VT) and its relation to tachycardia cycle length was evaluated in 139 patients. Tachycardia was terminated by programmed stimulation in 110 patients (79%) and cardioversion was required in 29 patients (21%). Single, double, and triple ventricular extrastimuli terminated the tachycardia in 23 of 85 (27%), 39 of 62 (63%), and 7 of 16 patients (44%), respectively. In all patients requiring 1 extrastimulus, in 35 patients (90%) requiring 2 extrastimuli, and in 6 patients (86%) requiring 3 extrastimuli, the tachycardia cycle length exceeded 300 ms. Rapid ventricular pacing terminated tachycardia in 41 of 54 patients (76%). In 21 (51%) of these patients the tachycardia cycle length exceeded 300 ms. However, rapid ventricular pacing caused acceleration of the arrhythmia in 19 patients (35%). The ability of procainamide to modify the termination of VT was studied in 23 patients. In 7 of these patients (30%) procainamide increased the tachycardia cycle length by 49 +/- 42 ms (p less than 0.01) and did not modify the mode of termination. In 6 patients (26%) procainamide increased cycle length by 142 +/- 108 ms (p less than 0.01), but termination was more difficult. In 10 patients (44%) procainamide increased the cycle length by 138 +/- 110 ms (p less than 0.001) and termination was easier. We conclude that termination of VT by timed extrastimuli requires a tachycardia cycle length longer than 300 ms. Rapid pacing or cardioversion is usually required when the cycle length is less than 300 ms. Although procainamide slows tachycardia, it can unpredictably make termination more difficult in 1 of 4 patients.

Adolescent↗
PubMed1982

Amiodarone pulmonary toxicity.

Pulmonary toxicity may occur in association with amiodarone hydrochloride therapy. The clinical features of the pulmonary involvement are mild dyspnea, leukocytosis, hypoxemia, elevation in the erythrocyte sedimentation rate, and restrictive changes on pulmonary function testing. Diffuse interstitial and patchy peripheral alveolar infiltrates, which may frequently involve the upper lobes, characterize the radiologic findings. Accumulation of foamy macrophages in alveolar spaces, hyperplasia of type II pneumocytes, and widening of alveolar septae are noted histologically. Ultrastructural examination shows granular and lamellar membranous structures within distended lysosomes. With cessation of amiodarone therapy and treatment with corticosteroids, clinical symptoms and radiographic abnormalities resolve. The time interval for resolution of radiographic changes appears to be greater than 2 months. The precise role of corticosteroid therapy remains unknown in light of pathologic findings suggesting a metabolic rather than immunologic basis for the toxicity.

Adult↗