BackgroundEchocardiographic left atrial (LA) strain parameters have been associated with atrial fibrillation (AF) in prior studies. Our goal was to determine if strain measures [peak systolic longitudinal strain (LAS) and stiffness index (LASt)] changed after cardioversion (CV); and their relation to AF recurrence.Methods and results46 participants with persistent AF and 41 age-matched participants with no AF were recruited. LAS and LASt were measured before and immediately after CV using 2D speckle tracking imaging (2DSI). Maintenance of sinus rhythm was assessed over a 6-month follow up. Mean LAS was lower, and mean LASt higher, in participants with AF before CV as compared to control group (11.9 ± 1.0 vs 35.7 ± 1.7, p<0.01 and 1.31 ± 0.17 vs 0.23 ± 0.01, p<0.01, respectively). There was an increase in the mean LAS immediately after CV (11.9 ± 1.0 vs 15.9 ± 1.3, p<0.01), whereas mean LASt did not change significantly after CV (p=0.62). Although neither LAS nor LASt were independently associated with AF recurrence during the follow-up period, change in LAS after cardioversion (post-CV LAS – pre-CV LAS) was significantly higher among individuals who remained in sinus rhythm when compared to individuals with recurrent AF (3.6 ± 1.1 vs 0.4 ± 0.8, p=0.02).ConclusionsLAS and LASt differed between participants with and without AF, irrespective of the rhythm at the time of echocardiographic assessment. Baseline LAS and LASt were not associated with AF recurrence. However, change in LAS after CV may be a useful predictor of recurrent arrhythmia.

The relations of measures of arterial stiffness, pulsatile hemodynamic load, and endothelial dysfunction to atrial fibrillation (AF) remain poorly understood. To better understand the pathophysiology of AF, we examined associations between noninvasive measures of vascular function and new-onset AF. The study sample included participants aged ≥45 years from the Framingham Heart Study offspring and third-generation cohorts. Using Cox proportional hazards regression models, we examined relations between incident AF and tonometry measures of arterial stiffness (carotid–femoral pulse wave velocity), wave reflection (augmentation index), pressure pulsatility (central pulse pressure), endothelial function (flow-mediated dilation), resting brachial arterial diameter, and hyperemic flow. AF developed in 407/5797 participants in the tonometry sample and 270/3921 participants in the endothelial function sample during follow-up (median 7.1 years, maximum 10 years). Higher augmentation index (hazard ratio, 1.16; 95% confidence interval, 1.02–1.32; P =0.02), baseline brachial artery diameter (hazard ratio, 1.20; 95% confidence interval, 1.01–1.43; P =0.04), and lower flow-mediated dilation (hazard ratio, 0.79; 95% confidence interval, 0.63–0.99; P =0.04) were associated with increased risk of incident AF. Central pulse pressure, when adjusted for age, sex, and hypertension (hazard ratio, 1.14; 95% confidence interval, 1.02–1.28; P =0.02) was associated with incident AF. Higher pulsatile load assessed by central pulse pressure and greater apparent wave reflection measured by augmentation index were associated with increased risk of incident AF. Vascular endothelial dysfunction may precede development of AF. These measures may be additional risk factors or markers of subclinical cardiovascular disease associated with increased risk of incident AF.

Atrial fibrillation (AF) is a common complication of acute myocardial infarction (AMI) and contributes to high rates of in-hospital adverse events. However, there are few contemporary studies examining rates of AF in the contemporary era of AMI or the impact of new-onset AF on key in-hospital and post-discharge outcomes. We examined trends in AF among 6,384 residents of Worcester, Massachusetts who were hospitalized with confirmed AMI during 7 biennial periods between 1999 and 2011. Multivariate logistic regression analysis was used to examine associations between occurrence of AF and various in-hospital and post-discharge complications. The overall incidence of AF complicating AMI was 10.8%. Rates of new-onset AF increased from 1999 to 2003 (9.8% to 13.2%), and declined thereafter. In multivariable adjusted models, patients developing new-onset AF following AMI were at higher risk for inhospital stroke [Odds Ratio (OR) 2.5, 95% Confidence Interval (CI) 1.6–4.1], heart failure [OR 2.0, 95% CI 1.7 to 2.4], cardiogenic shock [OR 3.7, 95% CI 2.8–4.9] and death [OR 2.3, 95% CI 1.9 to 3.0] than patients without AF. Development of AF during hospitalization for AMI was associated with higher rates of readmission within 30-days after discharge [21.7% vs. 16.0%], but no significant difference was noted in early post-discharge 30-day all-cause mortality rates [8.3% vs. 5.1%]. In conclusion, new-onset AF following AMI is strongly related to in-hospital complications of AMI as well as higher short-term readmission rates.

Atrial fibrillation (AF) is an increasingly prevalent condition and the most common sustained arrhythmia encountered in ambulatory and hospital practice. Several clinical risk factors for AF include age, sex, valvular heart disease, obesity, sleep apnea, heart failure, and hypertension (HTN). Of all the risk factors, HTN is the most commonly encountered condition in patients with incident AF. Hypertension is associated with a 1.8-fold increase in the risk of developing new-onset AF and a 1.5-fold increase in the risk of progression to permanent AF. Hypertension predisposes to cardiac structural changes that influence the development of AF such as atrial remodeling. The renin angiotensin aldosterone system has been demonstrated to be a common mechanistic link in the pathogenesis of HTN and AF. Importantly, HTN is one of the few modifiable AF risk factors, and guideline-directed management of HTN may reduce the incidence of AF.

Anthracycline-based chemotherapeutics have long been recognized as effective agents for treating a wide range of malignancies. However, their use is not without significant adverse cardiotoxic side effects. Strategies for prevention involve limiting free-radical production and subsequent cardiac myocyte damage. Dexrazoxane remains the most widely studied cardioprotective medication. Alternative agents may reduce cardiotoxicity but may still cause significant cardiovascular problems. The role of β-blockers and angiotensin-converting enzyme inhibitors in the treatment of heart failure is well proven. The role of these medications in the prevention and treatment of chemotherapy-induced cardiotoxicity is not well established.