Background Narrower retinal arterioles and wider retinal venules have been associated with negative cardiovascular outcomes. We investigated whether retinal vessel calibers are associated with cardiovascular outcomes in long-term follow-up and provide incremental value over the 2013 American College of Cardiology/American Heart Association pooled cohort equations (PCE) in predicting Atherosclerotic Cardiovascular Disease Events (ASCVE). Methods 10,470 men and women without prior ASCVE or heart failure (HF) in the Atherosclerosis Risk in Communities (ARIC) study underwent retinal photography at visit 3 (1993–1995). Results During a mean follow up of 16 years, there were 1779 incident CHD events, 548 ischemic strokes, 1395 HF events and 2793 deaths. Rates of all outcomes were higher in those with wider retinal venules and narrower retinal arterioles. Subjects with wider retinal venules [hazard ratio (HR) 1.13 (95% CI: 1.08–1.18), HR 1.18 (1.07–1.31) and HR 1.10 (1.00–1.20) per standard deviation (SD) increase] and narrower retinal arterioles [HR 1.06 (1.01–1.11), HR 1.14 (1.03–1.26) and HR 1.13 (1.03–1.24) per SD decrease] had a higher risk of death and stroke in both sexes as well as incident CHD in women but not men (interaction p=0.02) after adjustment for the PCE risk-score variables. The association between retinal vessel caliber and HF was non-significant after adjustment for systolic blood pressure. Among women with PCE-predicted 10-year ASCVE risk <5% (overall risk 3.9%), women in the narrowest arteriolar quartile had a 10-year event-rate of 5.6% compared to 2.8% for the widest quartile (5.0% vs. 3.4% for wider vs. narrower venules). Retinal vessel caliber reclassified 21% of low-risk women (11% of all women) as intermediate-risk (>5%). Conclusions Narrower retinal arterioles and wider retinal venules conferred long-term risk of mortality and ischemic stroke in both genders and CHD in women. These measures serve as an inexpensive, reproducible biomarker that added incremental value to current practice guidelines in ASCVE risk prediction in low-risk women.

BackgroundSleep apnea (SA) is associated with an increased risk of atrial fibrillation (AF). We sought to determine the effect of SA on cardiac structure in patients with AF, whether therapy for SA was associated with beneficial cardiac structural remodelling, and whether beneficial cardiac structural remodelling translated into a reduced risk of recurrence of AF after pulmonary venous isolation (PVI).Methods and ResultsA consecutive group of 720 patients underwent a cardiac magnetic resonance study before PVI. Patients with SA (n=142, 20%) were more likely to be male, diabetic, and hypertensive and have an increased pulmonary artery pressure, right ventricular volume, atrial dimensions, and left ventricular mass. Treated SA was defined as duration of continuous positive airway pressure therapy of >4 hours per night. Treated SA patients (n=71, 50%) were more likely to have paroxysmal AF, a lower blood pressure, lower ventricular mass, and smaller left atrium. During a follow‐up of 42 months, AF recurred in 245 patients. The cumulative incidence of AF recurrence was 51% in patients with SA, 30% in patients without SA, 68% in patients with untreated SA, and 35% in patients with treated SA. In a multivariable model, the presence of SA (hazard ratio 2.79, CI 1.97 to 3.94, P<0.0001) and untreated SA (hazard ratio 1.61, CI 1.35 to 1.92, P<0.0001) were highly associated with AF recurrence.ConclusionsPatients with SA have an increased blood pressure, pulmonary artery pressure, right ventricular volume, left atrial size, and left ventricular mass. Therapy with continuous positive airway pressure is associated with lower blood pressure, atrial size, and ventricular mass, and a lower risk of AF recurrence after PVI.

Perfusion findings in (82)Rb PET/CT are strong MACE outcome predictors. MBF quantification has an added value allowing further risk stratification in patients with normal and abnormal perfusion images.

Background Anthracyclines are cardiotoxic; however, there are limited data characterizing the serial changes in cardiac structure and function after anthracyclines. The aim of this study was to use cardiac magnetic resonance (CMR) to characterize anthracycline-induced cardiotoxicity (AIC) in mice. Methods and Results This was a longitudinal CMR and histological study of 45 wild-type male mice randomized to doxorubicin (DOX, n=30, 5 mg/kg of DOX/week for 5 weeks) or placebo (n=15). A CMR was performed at baseline and at 5, 10 and 20 weeks after randomization. Measures of primary interest included left ventricular ejection fraction (LVEF), myocardial edema (multi-echo short-axis spin-echo acquisition) and myocardial fibrosis (Look-Locker gradient-echo). In DOX-treated mice vs. placebo, there was an increase in myocardial edema at 5 weeks (T2 values of 32±4 vs. 21±3 msec, P < 0.05); followed by a reduction in LVEF (54±6 vs. 63±5%, P < 0.05) and an increase in myocardial fibrosis (extracellular volume of 0.34±0.03 vs. 0.27±0.03, P < 0.05) at 10 weeks. There was a strong association between the early (5 weeks) increase in edema and the sub-acute (10 weeks) increase in fibrosis (r = 0.90, P < 0.001). Both the increase in edema and fibrosis predicted the late DOX-induced mortality in mice (P < 0.001). Conclusions Our data suggest that, in mice, AIC is associated with an early increase in cardiac edema and a subsequent increase in myocardial fibrosis. The early increase in edema and sub-acute increase in fibrosis are strongly linked and are both predictive of late mortality.