Francis E. Marchlinski
Hospital of the University of Pennsylvania
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Featured researches published by Francis E. Marchlinski.
The New England Journal of Medicine | 2008
Jeanne E. Poole; George Johnson; Anne S. Hellkamp; Jill Anderson; David J. Callans; Merritt H. Raitt; Ramakota K. Reddy; Francis E. Marchlinski; Raymond Yee; Thomas Guarnieri; Mario Talajic; David J. Wilber; Daniel P. Fishbein; Douglas L. Packer; Daniel B. Mark; Kerry L. Lee; Gust H. Bardy
BACKGROUND Patients with heart failure who receive an implantable cardioverter-defibrillator (ICD) for primary prevention (i.e., prevention of a first life-threatening arrhythmic event) may later receive therapeutic shocks from the ICD. Information about long-term prognosis after ICD therapy in such patients is limited. METHODS Of 829 patients with heart failure who were randomly assigned to ICD therapy, we implanted the ICD in 811. ICD shocks that followed the onset of ventricular tachycardia or ventricular fibrillation were considered to be appropriate. All other ICD shocks were considered to be inappropriate. RESULTS Over a median follow-up period of 45.5 months, 269 patients (33.2%) received at least one ICD shock, with 128 patients receiving only appropriate shocks, 87 receiving only inappropriate shocks, and 54 receiving both types of shock. In a Cox proportional-hazards model adjusted for baseline prognostic factors, an appropriate ICD shock, as compared with no appropriate shock, was associated with a significant increase in the subsequent risk of death from all causes (hazard ratio, 5.68; 95% confidence interval [CI], 3.97 to 8.12; P<0.001). An inappropriate ICD shock, as compared with no inappropriate shock, was also associated with a significant increase in the risk of death (hazard ratio, 1.98; 95% CI, 1.29 to 3.05; P=0.002). For patients who survived longer than 24 hours after an appropriate ICD shock, the risk of death remained elevated (hazard ratio, 2.99; 95% CI, 2.04 to 4.37; P<0.001). The most common cause of death among patients who received any ICD shock was progressive heart failure. CONCLUSIONS Among patients with heart failure in whom an ICD is implanted for primary prevention, those who receive shocks for any arrhythmia have a substantially higher risk of death than similar patients who do not receive such shocks.
Circulation | 2008
William G. Stevenson; David J. Wilber; Andrea Natale; Warren M. Jackman; Francis E. Marchlinski; Timothy Talbert; Mario D. Gonzalez; Seth J. Worley; Emile G. Daoud; Chun Hwang; Claudio Schuger; Thomas E. Bump; Mohammad Jazayeri; Gery Tomassoni; Harry A. Kopelman; Kyoko Soejima; Hiroshi Nakagawa
Background— Recurrent ventricular tachycardia (VT) is an important cause of mortality and morbidity late after myocardial infarction. With frequent use of implantable cardioverter-defibrillators, these VTs are often poorly defined and not tolerated for mapping, factors previously viewed as relative contraindications to ablation. This observational multicenter study assessed the outcome of VT ablation with a saline-irrigated catheter combined with an electroanatomic mapping system. Methods and Results— Two hundred thirty-one patients (median LV ejection fraction, 0.25; heart failure in 62%) with recurrent episodes of monomorphic VT (median, 11 in the preceding 6 months) caused by prior myocardial infarction were enrolled. All inducible monomorphic VTs with a rate approximating or slower than any spontaneous VTs were targeted for ablation guided by electroanatomic mapping during sinus rhythm and/or VT. Patients were not excluded for multiple VTs (median, 3 per patient) or unmappable VT (present in 69% of patients). Ablation abolished all inducible VTs in 49% of patients. The primary end point of freedom from recurrent incessant VT or intermittent VT after 6 months of follow-up was achieved for 123 patients (53%). In 142 patients with implantable cardioverter-defibrillators before and after ablation for intermittent VT who survived 6 months, VT episodes were reduced from a median of 11.5 to 0 (P<0.0001). The 1-year mortality rate was 18%, with 72.5% of deaths attributed to ventricular arrhythmias or heart failure. The procedure mortality rate was 3%, with no strokes. Conclusions— Catheter ablation is a reasonable option to reduce episodes of recurrent VT in patients with prior myocardial infarction, even when multiple and/or unmappable VTs are present. This population remains at high risk for death, warranting surveillance and further study.
JAMA | 2014
Nassir F. Marrouche; David J. Wilber; Gerhard Hindricks; Pierre Jaïs; Nazem Akoum; Francis E. Marchlinski; Eugene Kholmovski; Nathan Burgon; Nan Hu; Lluis Mont; Thomas Deneke; Mattias Duytschaever; Thomas Neumann; Moussa Mansour; Christian Mahnkopf; Bengt Herweg; Emile G. Daoud; Erik Wissner; Paul M. Bansmann; Johannes Brachmann
IMPORTANCE Left atrial fibrosis is prominent in patients with atrial fibrillation (AF). Extensive atrial tissue fibrosis identified by delayed enhancement magnetic resonance imaging (MRI) has been associated with poor outcomes of AF catheter ablation. OBJECTIVE To characterize the feasibility of atrial tissue fibrosis estimation by delayed enhancement MRI and its association with subsequent AF ablation outcome. DESIGN, SETTING, AND PARTICIPANTS Multicenter, prospective, observational cohort study of patients diagnosed with paroxysmal and persistent AF (undergoing their first catheter ablation) conducted between August 2010 and August 2011 at 15 centers in the United States, Europe, and Australia. Delayed enhancement MRI images were obtained up to 30 days before ablation. MAIN OUTCOMES AND MEASURES Fibrosis quantification was performed at a core laboratory blinded to the participating center, ablation approach, and procedure outcome. Fibrosis blinded to the treating physicians was categorized as stage 1 (<10% of the atrial wall), 2 (≥10%-<20%), 3 (≥20%-<30%), and 4 (≥30%). Patients were followed up for recurrent arrhythmia per current guidelines using electrocardiography or ambulatory monitor recording and results were analyzed at a core laboratory. Cumulative incidence of recurrence was estimated by stage at days 325 and 475 after a 90-day blanking period (standard time allowed for arrhythmias related to ablation-induced inflammation to subside) and the risk of recurrence was estimated (adjusting for 10 demographic and clinical covariates). RESULTS Atrial tissue fibrosis estimation by delayed enhancement MRI was successfully quantified in 272 of 329 enrolled patients (57 patients [17%] were excluded due to poor MRI quality). There were 260 patients who were followed up after the blanking period (mean [SD] age of 59.1 [10.7] years, 31.5% female, 64.6% with paroxysmal AF). For recurrent arrhythmia, the unadjusted overall hazard ratio per 1% increase in left atrial fibrosis was 1.06 (95% CI, 1.03-1.08; P < .001). Estimated unadjusted cumulative incidence of recurrent arrhythmia by day 325 for stage 1 fibrosis was 15.3% (95% CI, 7.6%-29.6%); stage 2, 32.6% (95% CI, 24.3%-42.9%); stage 3, 45.9% (95% CI, 35.5%-57.5%); and stage 4, 51.1% (95% CI, 32.8%-72.2%) and by day 475 was 15.3% (95% CI, 7.6%-29.6%), 35.8% (95% CI, 26.2%-47.6%), 45.9% (95% CI, 35.6%-57.5%), and 69.4% (95% CI, 48.6%-87.7%), respectively. Similar results were obtained after covariate adjustment. The addition of fibrosis to a recurrence prediction model that includes traditional clinical covariates resulted in an improved predictive accuracy with the C statistic increasing from 0.65 to 0.69 (risk difference of 0.05; 95% CI, 0.01-0.09). CONCLUSIONS AND RELEVANCE Among patients with AF undergoing catheter ablation, atrial tissue fibrosis estimated by delayed enhancement MRI was independently associated with likelihood of recurrent arrhythmia. The clinical implications of this association warrant further investigation.
Circulation | 1983
Alfred E. Buxton; Harvey L. Waxman; Francis E. Marchlinski; Michael B. Simson; Dennis M. Cassidy; Mark E. Josephson
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.
Annals of Internal Medicine | 1982
Francis E. Marchlinski; Ted S. Gansler; Harvey L. Waxman; Mark E. Josephson
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.
Circulation | 2004
Sorin Lazar; Sanjay Dixit; Francis E. Marchlinski; David J. Callans; Edward P. Gerstenfeld
Background—Recent studies have demonstrated spatiotemporal organization in atrial fibrillation (AF), with a left-to-right atrial frequency gradient during AF in isolated sheep hearts. We hypothesized that human AF would also manifest a left-to-right atrial frequency gradient. Methods and Results—Thirty-one patients aged 56.7±10.5 years with a history of paroxysmal or persistent (>1 month) AF were included. Recordings were made at each pulmonary vein (PV) ostium and simultaneously from the coronary sinus (CS) and posterior right atrium (RA) during AF. Sequential fast Fourier transforms (FFTs) were performed. FFT profiles were analyzed to determine the dominant frequency (DF). There were 18 patients with paroxysmal AF and 13 with persistent AF. In the paroxysmal group, there was a significant left-to-right atrial DF gradient, with DF highest at the PV/left atrial (LA) junction, intermediate at the CS, and lowest in the RA (6.2±0.8, 5.5±0.7, and 5.1±0.6 Hz, respectively; P<0.001). There were no patients in whom DF was greater at the RA than the PV/LA junction. In the persistent group, there was no significant difference between DF recorded from the LA/PV junction, CS, and RA (6.1±0.7, 5.8±0.6, and 5.8±0.6 Hz, respectively; P=NS). Conclusions—In humans with paroxysmal AF, DFs are highest at the PV/LA junction, intermediate in the CS, and slowest in the posterior RA. These findings agree with animal models that suggest that the posterior LA may play an important role in maintaining paroxysmal AF. The role of the posterior LA in persistent AF requires further study.
Circulation | 2003
Henry H. Hsia; David J. Callans; Francis E. Marchlinski
Background—Although catheter mapping has been used to define the endocardial electrogram characteristics in patients with ventricular tachycardia (VT) and coronary disease, characterization of the electrophysiological substrate in patients with VT and nonischemic cardiomyopathy is limited. Methods and Results—Left ventricular endocardial electroanatomical mapping was performed in 19 patients with nonischemic cardiomyopathy and monomorphic VT with an average of 178±83 sites per chamber mapped. Abnormal bipolar electrogram was defined as endocardial voltage signal amplitude of <1.8 mV. The extent and location of abnormal endocardium was estimated by measuring areas of abnormal electrogram recordings from 3D voltage maps. The origin of VT was approximated by identifying sites of entrainment with concealed fusion or early presystolic activity and/or by pace mapping. Abnormal electrograms were recorded over a 41±28 cm2 area that represented 20±12% of total endocardial surface. The majority of patients (14/19 patients) had only a modest area (<25%) of endocardial abnormality. All patients had abnormal low-voltage endocardial areas located near the ventricular base in the perivalvular region. There were 3±1 VT morphologies per patient. The majority (88%) of the 57 mapped VTs originated from the ventricular base, corresponding to regions with abnormal endocardial electrograms. Conclusions—Electroanatomical mapping in patients with monomorphic VT and nonischemic cardiomyopathy typically demonstrates a modest-sized basal area of endocardial electrogram abnormalities. The VT site of origin corresponds to these basal electrogram abnormalities. These findings have important implications regarding strategies for VT ablation in this setting.
Journal of the American College of Cardiology | 2009
Oscar Cano; Mathew D. Hutchinson; David Lin; Fermin C. Garcia; Erica S. Zado; Rupa Bala; Michael P. Riley; Joshua M. Cooper; Sanjay Dixit; Edward P. Gerstenfeld; David J. Callans; Francis E. Marchlinski
OBJECTIVES The aim of the study was to define the epicardial substrate and ablation outcome in patients with left ventricular nonischemic cardiomyopathy (NICM) and suspected epicardial ventricular tachycardia (VT). BACKGROUND Ventricular tachycardia in NICM often originates from the epicardium. METHODS Twenty-two patients with NICM underwent detailed endocardial and epicardial bipolar voltage maps and VT ablation for suspected epicardial VT. Eight patients with normal hearts and idiopathic VT served to define normal epicardial electrograms. Low-voltage regions were also assessed for wide (>80 ms), split, or late electrograms. RESULTS Normal epicardial bipolar voltage was identified as >1.0 mV on the basis of the reference population. Confluent low-voltage areas were present in 18 epicardial (82%) and 12 endocardial (54%) maps and were typically over basal lateral LV. In the 18 patients with epicardial VT on the basis of activation/pacemapping, the mean epicardial area was greater than the endocardial low-voltage area (55.3 +/- 33.5 cm(2) vs. 22.9 +/- 32.4 cm(2), p < 0.01). Epicardial low-voltage areas showed 49.7% wide (>80 ms), split, and/or late electrograms rarely seen in the reference patients (2.3%). During follow-up of 18 +/- 7 months, ablation resulted in VT elimination in 15 of 21 patients (71%) including 14 of 18 patients (78%) with epicardial VT. CONCLUSIONS In patients with NICM and VT of epicardial origin, the substrate is characterized by areas of basal LV epicardial > endocardial bipolar low voltage. The electrograms in these areas are not only small (<1.0 mV) but wide (>80 ms), split, and/or late, and help identify the substrate targeted for successful ablation.
Journal of the American College of Cardiology | 1997
David J. Callans; Volker Menz; David Schwartzman; Charles D. Gottlieb; Francis E. Marchlinski
OBJECTIVES This study sought to characterize the electrocardiographic patterns predictive of left ventricular sites of origin of repetitive monomorphic ventricular tachycardia (RMVT). BACKGROUND RMVT typically arises from the right ventricular outflow tract (RVOT) in patients without structural heart disease. The incidence of left ventricular sites of origin in this syndrome is unknown. METHODS Detailed endocardial mapping of the RVOT was performed in 33 consecutive patients with RMVT during attempted radiofrequency ablation. Left ventricular mapping was also performed if pace maps obtained from the RVOT did not reproduce the configuration of the induced tachycardia. RESULTS Pace maps identical in configuration to the induced tachycardia were obtained from the RVOT in 29 of 33 patients. Application of radiofrequency energy at sites guided by pace mapping resulted in elimination of RMVT in 24 (83%) of 29 patients. In four patients (12%), pace maps obtained from the RVOT did not match the induced tachycardia. All four patients had a QRS configuration during RMVT with precordial R wave transitions at or before lead V2. In two patients, RMVT was mapped to the mediosuperior aspect of the mitral valve annulus, near the left fibrous trigone; catheter ablation at that site was successful in both. In two patients, RMVT was mapped to the basal aspect of the superior left ventricular septum. Catheter ablation was not attempted because His bundle deflections were recorded from this site during sinus rhythm. CONCLUSIONS RMVT can arise from the outflow tract of both the right and left ventricles. RMVTs with a precordial R wave transition at or before lead V2 are consistent with a left ventricular origin.
Pacing and Clinical Electrophysiology | 1992
Wolfram Grimm; Belinda F. Flores; Francis E. Marchlinski
The incidence and cause of electrocardiographically documented spontaneous implantuble Cardioverter defibrillator (ICD) discharges for a rhythm other than ventricular tachycardia (VT) or fibrillation (VF) (unnecessary shocks) were determined in 241 patients who underwent ICD implantation between March 1983 and November 1991. During follow‐up of 24 ± 20 months, 54 of 241 patients (22%) received a total of 132 unnecessary ICD shocks confirmed by Holler or telemetry monitoring or stored electrograms (Egs) from the ICD. The rhythm preceding these unnecessary ICD shocks was atrial fibrillation in 30 patients, sinus or supraventricular tachycardia (SVT) in 11 patients, antitachycardia pacing triggered by atrial fibrillation or SVT resulting in VT in 5 patients, nonsustained VT in 3 patients, and normal sinus or pacemaker rhythm in 10 patients. Unnecessary ICD discharges occurred most frequently during the first week after implantation or generator replacement (18 of 54 patients [33%]). Unnecessary ICD discharges could be documented more often by stored Egs in patients with devices with Eg storage capability (Ventritex Cadence(tm), 19 of 54 patients [35%]) than by Holter or telemetry monitoring in patients with devices without Eg storage capabilities (34 of 193 patients [18%], P < 0.01), despite a shorter mean follow‐up duration of 14 ± 9 months versus 26 ± 21 months, respectively. Only six of 54 patients (11%) in whom unnecessary ICD discharges occurred had recurrent unnecessary shocks during 22 ± 20 months of follow‐up after treatment directed at the cause of the first episode or device reprogramming to preclude non‐VT rhythm detection. In conclusion, unnecessary ICD shocks are a frequent complication of ICD therapy occurring in at least 22% of patients. The cause of these shocks is most frequently atrial fibrillation with a rapid ventricular response. The availability of Eg storage capabilities facilitates the diagnosis of the electrical event precipitating inappropriate ICD shocks. Diagnosis of the cause of unnecessary shocks allows for the institution of therapy that may reduce the risk for subsequent events.