Fredrick J. Jaeger
Cleveland Clinic
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Featured researches published by Fredrick J. Jaeger.
American Journal of Cardiology | 2003
Vidyasagar Kalahasti; Vijay Nambi; David O. Martin; Cathy Tse-Fun Lam; David Yamada; Bruce L. Wilkoff; Fredrick J. Jaeger; Patrick Tchou; Mina K. Chung
This study tested the hypothesis that prolonged QRS duration independently predicts long-term mortality in patients who underwent risk stratification and treatment for ventricular arrhythmias. Patients who underwent risk stratification by electrophysiologic study were identified. Electrophysiologic study results were defined as positive if sustained monomorphic ventricular tachycardia was induced. Mortality was the primary end point. Of 915 patients studied, mean left ventricular (LV) ejection fraction (EF) was 35.3 +/- 15.7%, 608 (66.4%) had coronary artery disease, 233 (25.5%) had positive electrophysiologic study findings, 298 (32.6%) received implantable cardioverter-defibrillators, and 174 (19%) died (mean follow-up 35.0 +/- 15.0 months). Cox regression analysis identified older age, coronary artery disease, digoxin use, absence of beta blockers, lower LVEF, and prolonged QRS duration to be independent predictors of mortality. QRS duration > or =130 ms, present in 33.6% of patients, was associated with a twofold increase in mortality (hazard ratio 2.1, 95% confidence interval 1.5 to 2.8; p <0.0001). For every 10 ms increase in QRS duration, mortality rate increased 10%. In a subgroup of patients with coronary artery disease and LVEF < or =30%, prolonged QRS duration remained an independent predictor of mortality (hazard ratio 2.6, 95% confidence interval 1.6 to 4.2; p <0.0001). Thus, prolonged QRS duration is a strong independent marker of long-term mortality in patients who undergo risk stratification for ventricular arrhythmias. Whether QRS duration represents only a marker for mortality or if modification of this factor using resynchronization therapies will impact mortality merits further study.
Journal of the American College of Cardiology | 1998
Mina K. Chung; Robert A. Schweikert; Bruce L. Wilkoff; Mark Niebauer; Sergio L. Pinski; Richard G. Trohman; Gregory A. Kidwell; Fredrick J. Jaeger; Victor A. Morant; Dave P. Miller; Patrick Tchou
OBJECTIVES We sought to determine the yield of in-hospital monitoring for detection of significant arrhythmia complications in patients starting sotalol therapy for atrial arrhythmias and to identify factors that might predict safe outpatient initiation. BACKGROUND The need for hospital admission during initiation of antiarrhythmic therapy has been questioned, particularly for sotalol, with which proarrhythmia may be dose related. METHODS The records of 120 patients admitted to the hospital for initiation of sotalol therapy were retrospectively reviewed to determine the incidence of significant arrhythmia complications, defined as new or increased ventricular arrhythmias, significant bradycardia or excessive corrected QT (QTc) interval prolongation. RESULTS Twenty-five patients (20.8%) experienced 35 complications, triggering therapy changes during the hospital period in 21 (17.5%). New or increased ventricular arrhythmias developed in 7 patients (5.8%) (torsade de pointes in 2), significant bradycardia in 20 (16.7%) (rate <40 beats/min in 13, pause >3.0 s in 4, third-degree atrioventricular block in 1, permanent pacemaker implantation in 3) and excessively prolonged QTc intervals in 8 (6.7%) (dosage reduced or discontinued in 6). Time to the earliest detection of complications was 2.1 +/- 2.5 (mean +/- SD) days after initiation of sotalol, with 22 of 25 patients meeting criteria for complications within 3 days of monitoring. Baseline electrocardiographic intervals or absence of heart disease failed to distinguish a low risk group. Multivariate analysis identified absence of a pacemaker as the only significant predictor of arrhythmia complications (p = 0.022). CONCLUSIONS Because clinically significant complications can be detected with in-hospital monitoring in one of five patients starting sotalol therapy, hospital admission is warranted for initiation of sotalol. Patients without pacemakers are at higher risk for these complications.
Pacing and Clinical Electrophysiology | 1992
Elena B. Sgarbossa; Sergio L. Pinski; Fredrick J. Jaeger; Richard G. Trohman; James D. Maloney
In spite of a normal pacemaker/unction, syncope still occurs in some patients with sick sinus syndrome (SSSJ. Causes often remain unknown. To identify predictors and etiologies of this bothersome symptom, we studied 507 patients who received atrial, ventricular, and dual‐chamber pacemakers for SSS. During a mean follow‐up of 62 ± 38 months, actuarial incidence of syncope was 3% at 1 year, 8% at 5 years, and 13% at 10 years. Causes were vasovagal (18%), orthostatic hypotension (25.5%), rapid atrial tachyarrhythmias (11.5%), ventricular tachycardia (5%), acute myocardial ischemia (2.5%), and pacemaker/lead malfunction (6.5%), In 13 patients (29.5%), syncope remained unexplained. The only preimplant predictor for syncope was syncope as primary indication for pacemaker implant. Electrocardiographic correlation with bradycardia was not a predictor of relief of syncope during the follow‐up. In conclusion: (1) syncope in paced patients with SSS has multiple etiologies and may be multifactorial; (2) the only predictor of syncope after pacemaker implant is the occurrence of preimplant syncope as the main indication for pacing; (3) extensive Holier monitoring is not useful to document bradycardic origin of syncope nor to predict its recurrence; (4) SSS probably overlaps with other entities such as autonomic dysfunction, vasovagal syncope, carotid sinus hypersensitivity, and venous pooling, which would provide an explanation for recurrent syncope in patients with normal pacemaker function.
American Heart Journal | 1996
Yoshio Yamanouchi; Safwan Jaalouk; Abbas A. Shehadeh; Fredrick J. Jaeger; Hershel Goren; Fetnat M. Fouad-Tarazi
We tested the hypothesis that patients who have vasovagal syncope during head-up tilt have a greater decrease in their left ventricular volume in response to tilt than do normal subjects. Measurements were done in the supine position and during graded tilt by using two-dimensional echocardiography. We compared seven patients with vasovagal syncope with nine normal volunteers. The rate of reduction of end-diastolic volume index during tilt was faster in the vasovagal group than in normal subjects. A more significant reduction of stroke index and ejection fraction during tilt was found in the vasovagal group than in normal subjects, possibly because of more peripheral translocation of blood volume in the venous system during tilt and an early vagal effect on ventricular contraction.
Journal of the American College of Cardiology | 1994
John J. Schutzman; Fredrick J. Jaeger; James D. Maloney; Fetnat M. Fouad-Tarazi
OBJECTIVES This study assessed the mechanism(s) of the decrease in upright blood pressure in patients with supine hypertension by using the tilt test and a hemodynamic approach. BACKGROUND Orthostatic hypotension in patients with supine hypertension creates a pathophysiologic and therapeutic dilemma. METHODS We studied 28 consecutive patients with history of orthostatic intolerance amounting to recurrent syncope in 13 of them (15 men, 13 women; mean [SD] age 65 +/- 11 years). They all had supine hypertension (systolic blood pressure > 160 mm Hg) and orthostatic hypotension (found to be a decrease in systolic blood pressure > 30 mm Hg during tilt test). Cardiac output, cardiopulmonary volume and systemic resistance were assessed by radionuclide first-pass technique (technetium-99m red blood cell tagging). Total blood volume was determined by radioiodinated serum albumin, and the ratio of cardiopulmonary to total blood volume was used as an index of venous capacitance. RESULTS Twenty-one patients had accentuated venous pooling defined as a tilt-induced decrease in cardiopulmonary volume/total blood volume ratio > 15% from baseline or a supine ratio < 14% (normal 16% to 18%), or both. Seven of the 28 patients had autonomic insufficiency; 6 of the 7 also had venous pooling; 1 patient had autonomic insufficiency only. Neither clinical history nor changes during tilt differentiated the subgroups. Plasma catecholamine levels increased during head-up tilt in all subgroups, and differences in their increase were not significant between patients with venous pooling and those with autonomic insufficiency. However, radionuclide hemodynamic variables revealed that patients with venous pooling compensated for the decrease in stroke volume by increasing peripheral resistance, whereas patients with autonomic dysfunction did not. CONCLUSIONS Orthostatic hypotension in patients with supine hypertension may have multiple etiologies. Hemodynamic assessment with determination of cardiopulmonary volume and systemic vascular resistance differentiated between venous pooling and autonomic insufficiency in these patients; head-up tilt and plasma catecholamine levels did not. These findings may have important therapeutic implications.
American Heart Journal | 1994
James D. Maloney; Fredrick J. Jaeger; Carlos Rizo-Patron; Dennis W.X. Zhu
The role of permanent cardiac pacing for the management of neurocardiogenic syncope is controversial; however, it does have a secondary role in appropriately selected individuals. Neurocardiogenic syncope includes vaso-vagal and enhanced antagonism of sympathetic-parasympathetic mechanisms. Differentiation of the so-called cardiac inhibitory, vasodepressor, and mixed forms of these disorders is frequently misleading when establishment of effective treatment strategies is attempted. Cardiac pacing can artificially restore near-normal heart rate and atrioventricular synchrony during a neurocardiogenic syncopal episode; however, cardiac pacing does not alter the peripheral vasodilatation, nor does it prevent the occurrence of the reflux response. Syncopal patients with carotid sinus hypersensitivity or vasovagal responses that include marked bradycardia and loss of atrioventricular synchrony can be supported by dual-chamber cardiac pacing in combination with other therapeutic interventions that diminish the severity of the reflex response. The conditions of patients with carotid sinus syndrome and carotid sinus hypersensitivity are frequently improved with cardiac pacing, and the conditions of elderly patients with vasovagal syncope are commonly improved with artificial pacing. The classic younger patient with malignant vasovagal syncope derives less benefit from artificial pacing; however, in carefully selected persons dual-chamber pacing combined with drug therapy and education decreases syncopal episodes and permits a return to normal activities.
Pacing and Clinical Electrophysiology | 1990
Fredrick J. Jaeger; Lori Schneider; James D. Maloney; Robert P. Cruse; Fetnat M. Fouad-Tarazi
We investigated the relative merits of the ocular compression test and the head‐up tilt test to aid differentiation of syncope and seizures in young patients. Sixteen patients (10 males and 6 females) with a mean age of 14 ± 4.7 (SD) years (range 7–22 years) underwent graded head‐up till (15°, 30°, and 45° for 2 minutes each, then 60° for 20 minutes) following positive ocular compression testing defined as precipitation of asystole for at least 3 seconds (mean 5 seconds ± 2 seconds, range 3–12 seconds). Each patient presented with recurrent unexplained loss of consciousness (mean number of episodes 30 ± 45, mean duration of illness 52 ± 40 months), and seven patients were receiving anticonvulsant medications, three of these had normal EEGs. Eleven patients (69%) developed vasovagal syncope during head‐up tilt, reproducing their clinical episodes (systolic blood pressure decreased from 105 ± 10 mmHg to 84 ± 13 mmHg, diastolic blood pressure from 75 ± 9 to 22 ± 25 mmHg, and heart rate from 89 ± 13 beats/mm to 37 ± 20 beats/min). Asystole occurred in two patients during vasovagal syncope lasting 11 seconds in one and 16 seconds in the other, and, it was associated with myoclonic movements in both (convulsive syncope). Based on these findings, and given the perceived potential hazards of the ocular compression test, the head‐up tilt test may be a safer procedure that adds useful information to the diagnostic evaluation of these patients.
American Journal of Cardiology | 1997
Fredrick J. Jaeger; Sergio L. Pinski; Richard G. Trohman; Fetnat M. Fouad-Tarazi
QT modulation was explored in 31 patients with cardioinhibitory neurocardiogenic syncope. Despite a marked in increase in RR intervals, the QT interval remained stable.
Pacing and Clinical Electrophysiology | 1993
Fredrick J. Jaeger; James D. Maloney; Lon W. Castle; Fetnat M. Fouad-Tarazi
To test the hypothesis that hypovolemia is associated with an increased incidence of vasovagal syncope during head‐up tilt (HUT) 45 patients with history of syncope or presyncope were studied. Blood volume (radio‐iodinated serum albumin) was determined, then subjects underwent a graded HUT (from 15°–60° HUT) with cuff blood pressure and ECG monitoring. All patients were kept on their own medications during evaluation. Thirty patients (12 male, 18 female, mean age 50 ± 19 [SD] years) had hypovolemia, defined as blood volume < 90% of lab normal for corresponding sex, while 15 patients (7 male, 8 female, mean age 52 ± 21 years) were normovolemic with blood volume ranging from 91%‐110% of sex‐matched normal subjects. The normovolemic patients served as controls. During HUT, a vasovagal response was elicited in 5 of the 30 hypovolemics and in 4 of the 15 normovoiemic (16.7% and 26.7%, respectively, P = NS). In those who developed vasovagal response, the changes of heart rate and blood pressure during HUT were not significantly different between hypovolemics and normovolemics, neither at the endpoint (vasovagal response) nor immediately before the development of the vasovagal response. In patienis with nonvasovagal events, four types of hemodynamic responses to tilt were observed; normal blood pressure response associated with normal heart rate increase, normal blood pressure response in association with accentuated increase in heart rate, orthostatic hypotension with normal acceleration of heart rate, and orthostatic hypotension with accelerated increase in heart rate. The percent distribution of these responses were 44%, 20%. 0%, and 36% in the 25 nonvasovagal hypovoiemics versus 73%, 0%, 18%, and 9% in the 11 nonvasovagal normovolemics. The results demonstrate that supine total blood volume does not predict the occurrence of vasovagal response to HUT. However, accentuated orthostatic tachycardia was more prevalent in hypovolemics as compared to normovolemics with nonvasovagal response to tilt.
JAMA | 2002
Bruce L. Wilkoff; James R. Cook; Andrew E. Epstein; Leon Greene; Alfred P. Hallstrom; Henry H. Hsia; Steven P. Kutalek; Arjun Sharma; Brian Blatt; Barry Karas; James Kirchhoffer; Deborah Warwick; Mary Duquette; Jean Provencher; Maureen Redmond; John M. Herre; Robert Bernstein; Linette R. Klevan; Kathleen D. Barackman; Jennine Zumbuhl; Mina K. Chung; Fredrick J. Jaeger; David O. Martin; Andrea Natale; Walid Saliba; Robert A. Schweikert; Mark Niebauer; Patrick Tchou; Raquel Rozich; Marc Roelke