Pericardial fat volume is highly associated with paroxysmal and persistent AF independent of traditional risk factors including left atrial enlargement. Whether pericardial fat plays a role in the pathogenesis of AF requires future investigation.

Objectives We sought to determine whether left atrial (LA) dysfunction predicts heart failure (HF) hospitalization in subjects with preserved baseline ejection fraction (EF). Background Among patients with preserved EF, factors leading to HF are not fully understood. Cross-sectional studies have demonstrated LA dysfunction at the time of HF, but longitudinal data on antecedent atrial function are lacking. Methods We performed resting transthoracic echocardiography in 855 subjects with coronary heart disease and EF≥50%. Left atrial functional index (LAFI) was calculated as [(LA emptying fraction × left ventricular outflow tract-velocity time integral)/(indexed LA end systolic volume)], where LA emptying fraction was defined as (LA end systolic volume - LA end diastolic volume)/LA end systolic volume. We used Cox models to evaluate the association between LAFI and HF hospitalization. Results Over a median follow-up of 7.9 years, 106 participants (12.4%) were hospitalized for HF. Rates of HF hospitalization were inversely proportional to quartile of LAFI: Q1: 47 per 1000 person-years; Q2: 18.3; Q3: 9.6; and Q4: 5.3 (p<0.001). Each standard deviation decrease in LAFI was associated with a 2.6-fold increased hazard of adverse cardiovascular outcomes (unadjusted HR: 2.6, 95% CI 2.1–3.3, p<0.001), and the association persisted even after adjustment for clinical risk factors, NT-proBNP, and a wide range of echocardiographic parameters (adjusted HR: 1.5, 95% CI 1.0–2.1, p=0.05). Conclusions LA dysfunction independently predicts HF hospitalization in subjects with coronary heart disease and preserved baseline EF. LAFI may be useful for HF risk stratification, and LA dysfunction may be a potential therapeutic target.

Background We sought to evaluate the prognostic performance of the CHADS2 score for prediction of ischemic stroke/TIA in subjects with coronary heart disease (CHD) without atrial fibrillation (AF). Methods In 916 non-anticoagulated outpatients with stable CHD and no AF by baseline electrocardiogram, we calculated CHADS2 scores (congestive heart failure, hypertension, age ≥ 75, diabetes (1 point each), and prior stroke or transient ischemic attack (TIA) (2 points)). The primary outcome was time to ischemic stroke or TIA over a mean follow-up of 6.4 ± 2.3 years. Results Over 5821 person-years of follow-up, 40 subjects suffered an ischemic stroke/TIA (rate 0.69 per 100 person-years, 95% CI 0.50-0.94). Compared to subjects with low (0-1) CHADS2 scores, those with intermediate (2-3) and high (4-6) CHADS2 scores had an increased rate of stroke/TIA, even after adjustment for age, tobacco, antiplatelet therapy, statins, and angiotensin inhibitors (CHADS2 score 2-3: HR 2.4, 95% CI 1.1-5.3, p=0.03, CHADS2 score 4-6: HR 4.0, 95% CI 1.5-10.6, p=0.006). Model discrimination (c-statistic = 0.65) was comparable to CHADS2 model fit in published AF-only cohorts. Conclusions The CHADS2 score predicts ischemic stroke/TIA in subjects with stable CHD and no baseline AF. The event rate in non-AF subjects with high CHADS2 scores (5-6) was comparable to published rates in AF patients with moderate CHADS2 scores (1-2), a population known to derive benefit from stroke prevention therapies. These findings should inform efforts to determine whether stroke prevention therapies or screening for silent AF may benefit subjects with stable CHD and high CHADS2 scores.

A growing body of evidence supports an association between vitamin D and cardiovascular disease. However, the mechanisms underlying this association are unknown. From 2000 to 2002, we identified 946 participants with stable cardiovascular disease in San Francisco, California, and followed them prospectively for cardiovascular events (heart failure, myocardial infarction, stroke, or cardiovascular death). We then examined the extent to which the association was attenuated by adjustment for poor health behaviors, comorbid health conditions, and potential biological mediators. During a median follow-up period of 8.0 years (through August 24, 2012), 323 subjects (34.1%) experienced a cardiovascular event. Following adjustment for sociodemographic factors, season of blood measurement, health behaviors, and comorbid conditions, 25-hydroxyvitamin D levels under 20 ng/mL remained independently associated with cardiovascular events (hazard ratio = 1.30, 95% confidence interval: 1.01, 1.67). However, after further adjustment for potential biological mediators, the independent association was no longer present (hazard ratio = 1.11, 95% confidence interval: 0.85, 1.44). Parathyroid hormone, a potentially modifiable biological factor downstream from 25-hydroxyvitamin D, was responsible for the majority of this attenuation. These findings highlight the need for randomized controlled trials to determine whether vitamin D supplementation in persons with deficiency could be beneficial for the primary or secondary prevention of cardiovascular events.