Synopsis Aging is associated with an increased prevalence of cardiac arrhythmias, which contribute to higher morbidity and mortality in the elderly. The frequency of cardiac arrhythmias, particularly atrial fibrillation and ventricular tachyarrhythmia, is projected to increase as the population ages, greatly impacting health care resource utilization. Several clinical factors associated with the risk of arrhythmias have been identified in the population, yet the molecular bases for the increased predisposition to arrhythmogenesis in the elderly are not fully understood. Therefore, only limited therapeutic strategies directed at pathophysiological processes that enhance cardiac vulnerability to arrhythmias are available. This is further compounded by the paucity of outcome studies providing evidence on which optimal management guidelines can be formulated for the very elderly. This review highlights the epidemiology of cardiac dysrhythmias, changes incardiac structure and function associated with aging, and the basis for arrhythmogenesis in the elderly, the understanding of which is critical to formulate preventive strategies.

Vitamin K antagonists (VKAs) are the most widely used anticoagulants for stroke prevention in patients with atrial fibrillation (AF). Recently, the US FDA approved three novel anticoagulants that work through inhibition of coagulation cascade independent of Vitamin K-dependent enzymatic reactions and, therefore, should have less food-drug interactions. Since AF is a disease of the aging heart, it is important to assess safety and efficacy of these new anticoagulants in elderly patients. We reviewed age-related changes in pharmacokinetics and pharmacodynamics observed with senescence and the effects of these changes on novel anticoagulants, known and anticipated drug and food interactions, and challenges related to bleeding complications and temporary discontinuation prior to surgery or interventional procedure. Although advantageous to VKA in age groups represented in trials, there are lack of data on VKA usage in older-elderly patients; additional research and post-marketing analysis in older-elderly patients are needed.

Introduction: Atrial fibrosis alters myocardial electrophysiological properties, increasing susceptibility to postoperative atrial fibrillation (PoAF); however, its estimation is problematic. We hypothesized that a noninvasive approach using history of AF (HxAF), LA mechanics and serum biomarkers of collagen turnover provides a surrogate for the extent of interstitial atrial fibrosis to identify patients at risk for PoAF. Methods: In patients undergoing cardiac surgery from April-Dec 2013, concentrations of biomarkers reflecting collagen synthesis/degradation and extracellular matrix remodeling were determined in serum from preoperative blood using an enzyme-linked immunosorbent assay, and echocardiographic evaluation was performed using M-mode, 2D, Doppler and 3D speckle tracking. Results: Of 66 patients (68 ±11 y, 67% men), 15 had HxAF and 11 of 51 with no HxAF (22%) developed new onset PoAF. In patients with HxAF, biomarkers for collagen turnover were elevated (Fig A) and correlated with a reduction in LA ejection fraction and global and regional relaxation of the LA wall (p=0.01, Fig B). In patients with no HxAF, procollagen type III (PIIINP) was significantly different in those who developed PoAF (p=0.01) and correlated with reduction in contractility in the posterior LA roof (p=<0.001) with a prolonged time to peak end-diastolic volume (p=0.03). LA size or ventricular structure and function were not different between groups. Conclusion: Surrogate serum and imaging biomarkers correlate with the substrate abnormality that promotes AF. These results need to be validated in larger cohorts to assess the power of these parameters in predicting new onset PoAF.

No abstract

No abstract

No abstract

Postoperative atrial fibrillation (PoAF) is a common complication in up to 40% of patients after cardiac surgery, increasing morbidity, hospital stay and costs. The myocardial substrate underlying PoAF is not fully characterized. The objective was to assess the impact of atrial fibrosis on incident AF and define the fibrosis threshold level predictive of PoAF. Methods: Right atrial appendages removed from patients undergoing elective CABG with no history of AF or class III/IV heart failure were used to characterize the ratio of collagen to myocardium (Masson’s trichrome; NIH ImageJ software; Fig A), which was correlated with incident AF. Percentage burden of fibrosis predictive of PoAF with high sensitivity and specificity was determined by ROC curve. Results: Of 28 patients (67±10 years, 64% males), 15 had PoAF. There were no age, gender or comorbidity differences between groups. Compared to the group that remained in sinus rhythm, patients with PoAF had a significantly higher ratio of extracellular collagen to myocardium (45±16% vs. 5±4%, p <0.001; Fig B). A threshold ratio of 12.7% collagen to myocardium (ROC area under the curve 0.997; z statistic 137; P<0.0001) with 96% sensitivity and 97% specificity identified those with PoAF (Fig C). A classification system based on histological extent of atrial fibrosis is proposed for identifying patients at risk for PoAF (Fig D). Conclusion: Ongoing studies will confirm the predictive value of this new classification system for identifying the atrial substrate predisposing PoAF and correlate with preoperative cardiac imaging and circulatory serum biomarkers to provide a novel noninvasive tool to stratify patients at risk for PoAF.