Thomas A. Burkart
University of Florida
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Journal of the American College of Cardiology | 2009
Joseph D. Mishkin; Sherry J. Saxonhouse; Gregory W. Woo; Thomas A. Burkart; William M. Miles; Jamie B. Conti; Richard S. Schofield; Samuel F. Sears; Juan M. Aranda
Multiple clinical trials support the use of implantable cardioverter-defibrillators (ICDs) for prevention of sudden cardiac death in patients with heart failure (HF). Unfortunately, several complicating issues have arisen from the universal use of ICDs in HF patients. An estimated 20% to 35% of HF patients who receive an ICD for primary prevention will experience an appropriate shock within 1 to 3 years of implant, and one-third of patients will experience an inappropriate shock. An ICD shock is associated with a 2- to 5-fold increase in mortality, with the most common cause being progressive HF. The median time from initial ICD shock to death ranges from 168 to 294 days depending on HF etiology and the appropriateness of the ICD therapy. Despite this prognosis, current guidelines do not provide a clear stepwise approach to managing these high-risk patients. An ICD shock increases HF event risk and should trigger a thorough evaluation to determine the etiology of the shock and guide subsequent therapeutic interventions. Several combinations of pharmacologic and device-based interventions such as adding amiodarone to baseline beta-blocker therapy, adjusting ICD sensitivity, and employing antitachycardia pacing may reduce future appropriate and inappropriate shocks. Aggressive HF surveillance and management is required after an ICD shock, as the risk of sudden cardiac death is transformed to an increased HF event risk.
Pacing and Clinical Electrophysiology | 2007
Thomas A. Burkart; Jordana Kron; William M. Miles; Jamie B. Conti; Mario D. Gonzalez
Sustained atrial fibrillation and atrial flutter during pregnancy are uncommon arrhythmias that can significantly complicate normal prenatal care. Direct current external cardioversion is the current method of terminating these arrhythmias. In practice, however, this technique is sometimes considered undesirable by both physician and patients due to the need for deep sedation or anesthesia. In the present study, we describe the use of ibutilide to safely terminate symptomatic persistent atrial flutter in a patient during her 24th week of pregnancy.
Current Treatment Options in Cardiovascular Medicine | 2010
Thomas A. Burkart; Jamie B. Conti
Opinion statementThis article reviews the appropriate evaluation and management of cardiac arrhythmias in the pregnant patient. Any treatment strategy in this patient population has the inherent potential to adversely affect the health of the unborn child. As such, there is no room for empiric therapy in these patients. Adequate arrhythmia documentation is paramount, preferably by noninvasive means. The decision to treat should be based on symptom severity and the risk to both mother and fetus posed by potentially recurring arrhythmia episodes throughout the pregnancy. Minimal symptoms in the setting of a structurally normal heart call for a conservative approach. Less is better. If pharmacologic therapy is justified, drugs with historically demonstrated safety profiles in pregnancy should be tried first. The safety profiles of virtually all drugs used to treat cardiac arrhythmias during human pregnancy are based solely on an accumulation of past clinical experience. Newer antiarrhythmics therefore carry a largely unknown risk. Most inherent rhythm disorders manifest long before a woman reaches childbearing age. Women with previously diagnosed arrhythmias frequently experience a recurrence or worsening of their arrhythmia during the pregnancy. Counseling of these individuals and perhaps preemptive treatment by means such as arrhythmia ablation prior to a planned pregnancy would seem optimal.
The Journal of Thoracic and Cardiovascular Surgery | 2010
Thomas M. Beaver; William M. Miles; Jamie B. Conti; Alexander Kogan; Thomas A. Burkart; Gregory W. Woo; Sherry J. Saxonhouse
CLINICAL SUMMARY A 31-year-old echocardiography technician experienced tachycardia after pregnancy 3 years before presentation. The patient reported symptoms of dizziness, shortness of breath, and fatigue. An echocardiogram revealed an ejection fraction of 65% and mild mitral valve prolapse. Twentyfour-hour Holter monitoring showed a resting heart rate between 70 and 175 beats/min with rare premature ventricular complexes and rare atrial premature complexes with no evidence of sinoatrial or atrioventricular nodal block. Metoprolol, atenolol, sotalol, digoxin, and amiodarone therapy had failed. Prior catheter-based ablation attempts had mapped the focus of tachycardia laterally at the superior vena cava and right atrial junction. The catheter ablation attempts were able to modify the heart rate; however, they were aborted because of proximity of the right phrenic nerve. Subsequently, she was referred for a minimally invasive thoracoscopic isolation of the sinus node using a dry bipolar radiofrequency energy clamp (AtriCure, West Chester, Ohio). Port sites were placed at the fifth interspace in the anterior axillary line and the sixth interspace in the posterior axillary line, and a 5-cm incision was made in the mid-axillary third interspace. The pericardium was opened, and adhesions from the catheter ablations were found lateral to the superior vena cava in the vicinity of the phrenic nerve. An isoproterenol infusion (4 mg/min) was started, which elevated the resting heart rate to 140 beats/min. The superior vena cava was then dissected free and the entire sinoatrial node complex was encircled with the radiofrequency clamp, which was applied multiple times with no change in the resting heart rate, although pacing confirmed transmural ablation lines (Figure 1). Subsequently, a reference electrode was sutured medial to the superior vena cava at the right atrial junction (Figure 2),
Journal of Cardiovascular Pharmacology and Therapeutics | 2000
Thomas A. Burkart; Anne B. Curtis
From the University of Florida, Gainesville, FL. Reprint requests: Anne B. Curtis, MD, Department of Medicine, University of Florida, P.O. Box 100277, Gainesville, FL 32610. Atrial fibrillation is the most prevalent and possibly the oldest described sustained cardiac arrhythmia seen in the adult population (1). One to 2 million Americans are estimated to suffer from atrial fibrillation. The prevalence rises sharply from 0.5% of the population <60 years of age to more than 10% of the population >80 years of age (2). Men have 1.5 times the risk of developing atrial fibrillation compared to women (3). Table 1 lists conditions commonly associated with the development of atrial fibrillation. Organic heart disease is found in 70%-80% of all patients with atrial fibrillation, with the most common association by autopsy reports being prior myocardial infarction, followed by coronary artery disease without infarction, rheumatic heart disease, and hypertensive heart disease (4-6). Hyperthyroidism and congestive heart failure are also among the more frequently implicated associated disorders. Lone atrial fibrillation (ie, occurring in the absence of structural heart disease) accounts for 5%-30% of the total population with atrial fibrillation (7). The Framingham Study has provided long-term data demonstrating a 1.5-1.8 rise in the risk of mortality in patients with atrial fibrillation compared with those without this arrhythmia. Serious thromboembolic events in the presence of atrial fibrillation are a major contributor to this rise in mortality, with atrial fibrillation being implicated in 15% of all strokes (8). Atrial fibrillation may also lead to impaired cardiac function as a result of the loss of atrial contractile function, loss of atrioventricular (AV) synchrony, rapid and irregular ventricular contraction, and the development of a rate-related cardiomyopathy (9). It may also serve to aggravate other underlying cardiac conditions such as congestive heart failure and angina. Treatment options for atrial fibrillation have evolved dramatically, with implantable devices and ablative therapies now available in addition to
Critical pathways in cardiology | 2016
David E. Winchester; Thomas A. Burkart; Calvin Y. Choi; Matthew McKillop; Rebecca J. Beyth; Phillipp Dahm
OBJECTIVE Training in quality improvement (QI) is a pillar of the next accreditation system of the Accreditation Committee on Graduate Medical Education and a growing expectation of physicians for maintenance of certification. Despite this, many postgraduate medical trainees are not receiving training in QI methods. We created the Fellows Applied Quality Training (FAQT) curriculum for cardiology fellows using both didactic and applied components with the goal of increasing confidence to participate in future QI projects. METHODS AND RESULTS Fellows completed didactic training from the Institute for Healthcare Improvements Open School and then designed and completed a project to improve quality of care or patient safety. Self-assessments were completed by the fellows before, during, and after the first year of the curriculum. The primary outcome for our curriculum was the median score reported by the fellows regarding their self-confidence to complete QI activities. Self-assessments were completed by 23 fellows. The majority of fellows (15 of 23, 65.2%) reported no prior formal QI training. Median score on baseline self-assessment was 3.0 (range, 1.85-4), which was significantly increased to 3.27 (range, 2.23-4; P = 0.004) on the final assessment. The distribution of scores reported by the fellows indicates that 30% were slightly confident at conducting QI activities on their own, which was reduced to 5% after completing the FAQT curriculum. An interim assessment was conducted after the fellows completed didactic training only; median scores were not different from the baseline (mean, 3.0; P = 0.51). CONCLUSION After completion of the FAQT, cardiology fellows reported higher self-confidence to complete QI activities. The increase in self-confidence seemed to be limited to the applied component of the curriculum, with no significant change after the didactic component.
Current Sports Medicine Reports | 2015
Katherine M. Edenfield; Ashley N. Stern; Michael Dillon; Thomas A. Burkart; James R. Clugston
Introduction Vasovagal syncope (VVS), also known as neurocardiogenic syncope and vasodepressor syncope, is a frequent and usually benign form of syncope that results from an errant reflex arc of cardiac mechanoreceptors (4,19). It is considered a subset of neurally mediated (reflex) syncope (17). While VVS is common, it rarely occurs during exercise (5). An athlete who presents with exertional syncope should not be diagnosed with VVS until a thorough cardiac evaluation excludes arrhythmias and structural heart disease. The 36th Bethesda Conference Guidelines do not restrict athletes with VVS from returning to participation (12,20). We describe a case of exertional syncope in a collegiate swimmer, which, after thorough workup, was attributed to VVS. The athlete was allowed to return to swimming with individual supervision. To our knowledge, this is the first reported case of VVS during swimming competition.
Texas Heart Institute Journal | 2018
Michael R. Kaufmann; Matthew McKillop; Thomas A. Burkart; Mark Panna; Jamie B. Conti; William M. Miles
Direct-current cardioversion is an important means of managing arrhythmias. During treatment, carefully synchronizing energy delivery to the QRS complex is necessary to avoid ventricular fibrillation caused by a shock during the vulnerable period of ventricular repolarization, that is, a shock on the T wave. The presence of an accessory pathway and ventricular preexcitation can lead to difficulty in distinguishing the QRS complex from the T wave because of bizarre, wide, irregular QRS complexes and prominent repolarization. We present the cases of 2 patients who had iatrogenic ventricular fibrillation from inappropriate T-wave synchronization during direct-current cardioversion of preexcited atrial fibrillation. Our experience shows that rapidly recognizing the iatrogenic cause of VF and immediate treatment with unsynchronized defibrillation can prevent adverse clinical outcomes.
Journal of the American College of Cardiology | 2014
Adisson Fortunel; Zheng Donghang; Mohammad Al-Ani; Thomas A. Burkart; William M. Miles; Matthew McKillop; Alexandra Lucas
background: Cryoballoon ablation (CB) for atrial fibrillation (AF) activates inflammation that may lead to increased atrial fibrosis, thrombosis, and recurrent arrhythmia. Two viral anti-inflammatory proteins, M-T7 (a chemokine/glycosaminoglycan inhibitor) and Serp-1 (a serine protease inhibitor) have proven anti-inflammatory activity in animal models. Serp-1 also reduced markers of myocardial damage in patients after coronary stent implant. In this study, we examined the systemic inflammatory response to AF ablation and the potential to modify inflammatory cell activation after ablation using these viral proteins.
Journal of the American College of Cardiology | 2014
Mohammad Al-Ani; Zheng Donghang; Adisson Fortunel; Thomas A. Burkart; William M. Miles; Alexandra Lucas; Matthew McKillop
Activation of innate immune responses after atrial fibrillation (AF) ablation may lead to collateral atrial myocardial damage, fibrosis, and recurrent arrhythmia. The extent of the inflammatory response to cryoballoon ablation (CB) is not yet well defined. Non-specific inflammation suppression with