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

Flecainide Toxicity Leading to Loss of Pacemaker Capture and Cardiac Arrest

An 86-year-old man with paroxysmal atrial fibrillation on flecainide, a class IC antiarrhythmic, presented with cardiac arrest. The patient had extremely wide QRS complexes with inconsistent pacemaker capture on electrocardiography. Due to cardiac failure and renal failure, the patient developed progressive flecainide toxicity, which led to pacemaker failure, and ultimately, death. (Level of Difficulty: Beginner.) [Display omitted

Abstract 17248: Statin Therapy Increases Coronary Artery Calcification Scores

Introduction: Coronary artery calcification (CAC) assessment is a noninvasive test to determine atherosclerotic burden. There has been a discordance with the well-known lipid lowering and cardiovascular protection of statins and the progression of CAC in small trials with narrow inclusion criteria. We performed a subgroup analysis of the Multi-Ethnic Study of Atherosclerosis (MESA) dataset to assess the impact of statins on patients with a baseline CAC score of 0. Hypothesis: Statin usage will cause patients to have a higher CAC scores despite lowering LDL and reducing cardiac mortality. Methods: A subgroup analysis (3235 patients) was performed on the MESA dataset to identify patients with a CAC score of 0 at baseline. Statin usage and cholesterol values were reviewed at 4 examination points. Multivariate regression was performed. Results: The number of patients using statins (Table 1) and lipid levels (Table 2) increased throughout the study as expected for an aging population. A consistently larger increase in CAC score was noted in patients receiving statins; this difference was demonstrated in all stratified groups by Framingham score (Table 3). Table 4 shows the results of multivariate linear regression. Excluding gender, statins had the largest impact on CAC; more than any established cardiovascular risk factor. Conclusion: This large subgroup analysis of the MESA dataset demonstrates that statins are associated with increasing CAC score. While this is in contrast to the well-established cardiovascular protection of statin therapy, it adds to the growing literature that statin use is associated with progression of CAC, even in low risk patients with baseline CAC of 0. One hypothesis for this finding is that statins promote coronary atheroma calcification which ultimately results in plaque stabilization and less likelihood for progression to unstable plaques. It is therefore necessary for clinicians to take into account statins when interpreting CAC scores

Abstract 17114: CHA 2 DS 2 -VASc Score is a Poor Predictor of Thromboembolic Events in Heart Failure Patients With and Without Atrial Fibrillation

Introduction: Recent evidence suggests that the CHA 2 DS 2 -VASc score could be used to predict thromboembolic events (TE) (both CVA and noncerebral thromboembolism) in heart failure (HF) patients without atrial fibrillation (AF). This non-American cohort study had several limitations. We performed a retrospective analysis using the national Veteran Affairs database to externally validate the findings. Hypothesis: The CHA 2 DS 2 -VASc score can be used equally to predict TE in HF patients with or without AF. Methods: A retrospective cohort of the national Veteran’s Affairs database was used to identify HF patients discharged between 2002-2010. Rates for TE were calculated at both 1 and 5 years. C-statistics were calculated to test the performance of CHA 2 DS 2 -VASc in predicting the rate of TE in HF patients with and without AF. Patients who developed AF during the follow-up period (crossovers) and those on anticoagulation where excluded. Negative predictive value was calculated using cutoff value of 1. Results: A total of 77,601 patients were included in this analysis: 51,667 without AF and 15,630 with AF. 10,294 crossover patients were excluded. Baseline characteristics and medications are listed in Table 1. Event rates are reported in Table 2—there is a small trend towards higher incidence with increasing score in both groups. However, C-statistics were overall poor but similar for predicting TE in both groups (Table 3) Conclusion: Our analysis suggests CHA 2 DS 2 -VASc is a poor predictive model for TE in HF with or without AF. We found that previous conclusions regarding the predictive ability of CHA 2 DS 2 -VASc are not generalizable to our large American cohort. Like previously published studies, we show that the predictive ability of CHA 2 DS 2 -VASc was similar in both HF patients with or without AF, despite excluding patient receiving anticoagulation. This suggests that AF may not be the main predictor of TE in HF patients. There is a need for better predictive models for TE in HF

The CHA2DS2-VASc Score for Risk Stratification of Stroke in Heart Failure With-vs-Without Atrial Fibrillation

A recent study suggested that the CHA2DS2-VASc score can risk stratify heart failure (HF) patients without atrial fibrillation (AF) for stroke. We performed a retrospective analysis using the national Veteran Affairs database to externally validate the findings. Crude incidence rates of end points were calculated. A Cox proportional model was used to study the association between the CHA2DS2-VASc score and outcomes. In HF patients with AF (n = 17,481) and without AF (n = 36,935), the 1 year incidence rate for ischemic stroke, thromboembolism, thromboembolism (without MI), and death were 2.7 and 2.0%; 10.3 and 7.9%; 4.1 and 3.1%; and 19.2 and 26.0%, respectively, with higher rates with increasing CHA2DS2-VASc scores both with and without AF. CHA2DS2-VASc score predicted strokes in HF patients without AF (1-year C-statistic 0.62, 95% CI 0.60-0.64; NPV 85.4%, 95% CI 83.4-87.4%) with similar predictive ability to those with AF (C-statistic 0.59, 95% CI 0.56-0.62; NPV 86.4%, 95% CI 82.6-90.2%). Among patients with HF, there was an increased risk of stroke, thromboembolism, and death with increasing CHA2DS2-VASc scores regardless of AF status. Our findings support the use of the CHA2DS2-VASc score as a prognostic tool in HF