Atrial fibrillation practice patterns among cardiac electrophysiologists and cardiologists

Background: Treatment paradigms for atrial fibrillation (AF) are highly variable. This study explores the management practices for AF between general cardiologists and electrophysiologists in an academic institution.Methods: One hundred and eighty eight patients with AF who had primary outpatient evaluation by either a cardiologist (n = 94) or electrophysiologist (n = 94) in 2008 were selected from the Northwestern electronic medical record and included in the study. Chart review was used to determine the type of therapy, methods of monitoring AF, antiarrhythmic drug use patterns and outcome.Results: Patients seen by cardiologists vs. electrophysiologists were older (70.3 ± 11.8 vs. 65.3 ± 10.3, p = 0.002) and had more diabetes (21.3% vs. 10.6%, p = 0.046), renal disease (29.0% vs. 9.2%, p = 0.001) and coronary artery disease (40.4% vs. 23.4%, p = 0.01). A rate control strategy was used more often (80.9% vs. 54.3%, p < 0.001), and antiarrhythmics were prescribed less (10.6% vs. 31.9%, p < 0.001) by cardiologists than electrophysiologists. Antiarrhythmic choices were amiodarone (33.3%), sotalol (20.0%), flecainide (13.3%), propafenone (13.3%), and dofetilide (23.3%) for electrophysiologists, and were limited to amiodarone (80%) and sotalol (20%) for cardiologists. After a mean follow-up of 14.0 ± 11.6 and 12.8 ± 11.1 months (p = 0.44) for patients managed by cardiologists and electrophysiologists, mortality was 13.8% and 6.4% (p = 0.09), respectively. Long-term ambulatory electrocardiogram monitoring was used more frequently by electrophysiologists (74.4%) than by cardiologists (55.6%, p = 0.15).Conclusions: Practice patterns for treatment of AF significantly differ between electrophysiologists and cardiologists. Understanding specialist treatment patterns will help optimize individualized therapy for treatment of AF

Efficacy and tolerability of dronedarone for patients with atrial fibrillation

Background: Dronedarone is a new antiarrhythmic drug used in the treatment of atrial fibrillation (AF). We investigate its efficacy and tolerability in clinical practice.Methods: We identified 208 patients treated with dronedarone for AF at the Northwestern outpatient practice. Charts were reviewed for clinical efficacy and reasons for discontinuation of the drug.Results: The average age was 65.2 ± 10.8 years, 37% females. Paroxysmal, persistent andpermanent AF were noted in 46.2%, 51.9%, and 1.9%, respectively. Average ejection fraction was 56.3 ± 9.1%, 12.8% had a history of congestive heart failure, and 10.3% had valvularheart disease. Dronedarone was discontinued in 25 patients after curative catheter or surgical ablation procedure. Of the remaining 183 patients, dronedarone was discontinued in 48.6% after a mean duration of 6.2 ± 6.3 months because of in efficacy (26.2%), side effects (6%), and other reasons (16.4%). For those remaining on dronedarone (n = 94), after a mean of 11.6 ± 6.6 months, clinical efficacy (resolution of or patient-reported improvement in symptoms) was noted in 45.4% patients. On dronedarone therapy, 57.4% had no AF on follow-up (overallefficacy of 29.5%). To evaluate efficacy, ECG only or long-term monitoring were performed in 62.7% and 37.3%, respectively, and found no AF in 69.2 and 48.4%, respectively. There were 3 deaths and 2 transient ischemic attacks (TIA) off dronedarone vs. 1 death, 1 TIA and 2 strokes on dronedarone.Conclusions: Dronedarone has a significant discontinuation rate due to both inefficacy and side effects in clinical practice. Nevertheless, it has moderate clinical efficacy and tolerability in an outpatient population of patients with AF

Diabetes mellitus and sudden cardiac death: What are the data?

Diabetes mellitus has long been linked to an increased risk of sudden cardiac death. However, the magnitude of this association, and the mechanism accounting for this phenomenon, have not been precisely defined. In this review, we evaluate the epidemiological data pertaining to the association between diabetes mellitus and sudden cardiac death and discuss various proposed mechanisms that may account for this relationship. Potential factors contributing to the increased risk of sudden cardiac death observed in patients with diabetes mellitus include silent myocardial ischemia, autonomic nervous system dysfunction, abnormal cardiac repolarization, hypoglycemia, a hypercoaguable state secondary to diabetes mellitus, diabetic cardiomyopathy, and impaired respiratory response to hypoxia and hypercapnea. We conclude that diabetes mellitus does appear to be associated with an increased risk of sudden cardiac death. Although this increased risk is relatively modest, given the large number of diabetic patients worldwide, the absolute number of sudden cardiac deaths attributable to diabetes mellitus remains significant. Little evidence exists to support any specific mechanism(s) accounting for this association. Further investigation into the pathophysiology of sudden cardiac death in diabetes mellitus may yield improved risk stratification tools as well as identify novel therapeutic targets. (Cardiol J 2010; 17, 2: 117-129

Cukrzyca a nagły zgon sercowy - jakie są wyniki badań?

Cukrzycę od dawna wiązano ze zwiększonym ryzykiem nagłego zgonu sercowego (SCD). Jednak nie do końca określono stopień zwiększenia ryzyka oraz mechanizmy przyczyniające się do opisywanego zjawiska. W niniejszej pracy oceniono dane epidemiologiczne dokumentujące związek między występowaniem cukrzycy a SCD oraz przedyskutowano różne proponowane mechanizmy, które mogą się przyczyniać do zaistnienia opisywanej zależności. Do potencjalnych czynników zwiększających ryzyko SCD obserwowane u chorych na cukrzycę należą: nieme niedokrwienie mięśnia sercowego, dysfunkcja autonomicznego układu nerwowego, nieprawidłowa repolaryzacja komórek mięśnia sercowego, hipoglikemia, stan nadkrzepliwości wtórny do cukrzycy, kardiomiopatia cukrzycowa oraz upośledzona odpowiedź na niedotlenienie i hiperkapnię. Według autorów niniejszej pracy, wydaje się, że cukrzyca wiąże się ze zwiększonym ryzykiem SCD. Chociaż w wartościach względnych stopień zwiększenia ryzyka jest umiarkowany, to biorąc pod uwagę olbrzymią liczbę pacjentów chorych na cukrzycę na całym świecie, bezwzględna liczba SCD, które można powiązać z cukrzycą, jest istotna. Wciąż brakuje dowodów, które mogłyby potwierdzać jakikolwiek specyficzny mechanizm(y) przyczyniający się do opisywanego związku. Przyszłe badania dotyczące patofizjologii SCD u chorych na cukrzycę mogą dostarczyć użytecznych narzędzi stratyfikacji ryzyka oraz pomóc w identyfikacji nowych celów terapeutycznych. (Folia Cardiologica Excerpta 2010; 5, 4: 206-219

Personalizing sudden death risk stratification in dilated cardiomyopathy: past, present and future

Results from the DANISH Study (Danish Study to Assess the Efficacy of ICDs in Patients with Nonischemic Systolic Heat Failure on Mortality) suggest that, for many patients with dilated cardiomyopathy (DCM), implantable cardioverter defibrillators (ICD) do not increase longevity. Accurate identification of patients who are more likely to die of an arrhythmia and less likely to die from other causes is required to ensure improvement in outcomes and wise use of resources. Until now, left ventricular ejection fraction (LVEF) has been used as a key criterion for selecting patients with DCM for an ICD for primary prevention purposes. However, registry data suggest that many patients with DCM and an out-of-hospital cardiac arrest do not have a markedly reduced LVEF. Additionally, many patients with reduced LVEF die from non-sudden causes of death. Methods to predict a higher or lower risk of sudden death include the detection of myocardial fibrosis (a substrate for ventricular arrhythmia), microvolt T-wave alternans (MTWA; a marker of electrophysiological vulnerability) and genetic testing. Mid-wall fibrosis is identified by late gadolinium enhancement cardiovascular magnetic resonance imaging in around 30% of patients and provides incremental value in addition to LVEF for the prediction of SCD events. MTWA represents another promising predictor, supported by large meta-analyses that have highlighted the negative predictive value of this test. However, neither of these strategies has been routinely adopted for risk stratification in clinical practice. More convincing data from randomized trials are required to inform the management of patients with these features. Understanding of the genetics of DCM and how specific mutations affect arrhythmic risk is also rapidly increasing. The finding of a mutation in LMNA, the cause of around 6% of idiopathic DCM, commonly underpins more aggressive management due to the malignant nature of the associated phenotype. With the expansion of genetic sequencing, the identification of further high-risk mutations appears likely, leading to better informed clinical decision-making as well as providing insight into disease mechanisms. Over the next 5-10 years we expect these techniques to be integrated into the existing algorithm to form a more sensitive, specific and cost-effective approach to the selection of DCM patients for ICD implantation

QT-RR HYSTERESIS IS CAUSED BY DIFFERENTIAL AUTONOMIC STATES DURING EXERCISE AND RECOVERY

QT-RR hysteresis is characterized by longer QT intervals at a given RR interval while heart rates are increasing during exercise and shorter QT intervals at the same RR interval while heart rates are decreasing during recovery. It has been attributed to a lagging QT response to different directional changes in RR interval during exercise and recovery. Twenty control subjects (8 males, age 51 ± 6 yr), 16 subjects with type 2 diabetes (12 males, age 56 ± 8 yr), 71 subjects with coronary artery disease (CAD) and preserved left ventricular ejection fraction (LVEF) (≥50%) (51 males, age 59 ± 12 yr), and 17 CAD subjects with depressed LVEF (<50%) (13 males, age 57 ± 10 yr) underwent two 16-min exercise tests followed by recovery. In session 2, parasympathetic blockade with atropine (0.04 mg/kg) was achieved at end exercise. QT-RR hysteresis was quantified as: 1) the area bounded by the QT-RR relationships for exercise and recovery in the range of the minimum RR interval at peak exercise to the minimum RR interval + 100 ms and 2) the difference in QT interval duration between exercise and recovery at the minimum RR interval achieved during peak exercise plus 50 ms (ΔQT). The effect of parasympathetic blockade was assessed by substituting the QT-RR relationship after parasympathetic blockade. QT-RR hysteresis was positive in all groups at baseline and reversed by parasympathetic blockade (P < 0.01). We conclude that QT-RR hysteresis is not caused by different directional changes in RR interval during exercise and recovery. Instead, it is predominantly mediated by differential autonomic nervous system effects as the heart rate increases during exercise vs. as it decreases during recovery

Atrial Myopathy Underlying Atrial Fibrillation

While AF most often occurs in the setting of atrial disease, current assessment and treatment of patients with AF does not focus on the extent of the atrial myopathy that serves as the substrate for this arrhythmia. Atrial myopathy, in particular atrial fibrosis, may initiate a vicious cycle in which atrial myopathy leads to AF, which in turn leads to a worsening myopathy. Various techniques, including ECG, plasma biomarkers, electroanatomical voltage mapping, echocardiography, and cardiac MRI, can help to identify and quantify aspects of the atrial myopathy. Current therapies, such as catheter ablation, do not directly address the underlying atrial myopathy. There is emerging research showing that by targeting this myopathy we can help decrease the occurrence and burden of AF

Siegert pseudostates: completeness and time evolution

Within the theory of Siegert pseudostates, it is possible to accurately calculate bound states and resonances. The energy continuum is replaced by a discrete set of states. Many questions of interest in scattering theory can be addressed within the framework of this formalism, thereby avoiding the need to treat the energy continuum. For practical calculations it is important to know whether a certain subset of Siegert pseudostates comprises a basis. This is a nontrivial issue, because of the unusual orthogonality and overcompleteness properties of Siegert pseudostates. Using analytical and numerical arguments, it is shown that the subset of bound states and outgoing Siegert pseudostates forms a basis. Time evolution in the context of Siegert pseudostates is also investigated. From the Mittag-Leffler expansion of the outgoing-wave Green's function, the time-dependent expansion of a wave packet in terms of Siegert pseudostates is derived. In this expression, all Siegert pseudostates--bound, antibound, outgoing, and incoming--are employed. Each of these evolves in time in a nonexponential fashion. Numerical tests underline the accuracy of the method

Cardiac Troponin Assessment Following Atrial Fibrillation Ablation: Implications for Chest Pain Evaluation

Background: The range of elevation of troponin I (tI) that is within expected limits from left atrial radiofrequency ablation for atrial fibrillation (AF) is not well described, though such information may be of clinical value. Objectives: Identify the expected range of tI values post-atrial fibrillation (AF) ablation. Methods: 31 patients undergoing AF ablation had a single tI level drawn the day following the procedure. Clinical variables were also collected, such as ablation type and radiofrequency (RF) time. Results: Paroxysmal AF was present in 23 patients, and 8 had chronic AF. The average RF time was 2627.8 ± 737.5 seconds. The mean RF power was 61.7 ± 4.3W (range 55-70W). The mean RF temperature limit was 53.6 ± 2.0°C (range 50-55°C). There was no clinical or electrocardiographic evidence of coronary ischemia in this population. The mean tI the following day was 3.21 ± 1.5 (range 1.48-8.41). There was no correlation between RF time, ablation type, ablation catheter size, and ablation temperature or ablation power and tI levels. Conclusions: Troponin I elevation post-ablation was ubiquitous. Knowledge of expected post-ablation tI levels may be helpful in the evaluation of post-procedure chest pain