BackgroundAtrial fibrillation is associated with higher mortality. Identification of causes of death and contemporary risk factors for all‐cause mortality may guide interventions.Methods and ResultsIn the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET AF) study, patients with nonvalvular atrial fibrillation were randomized to rivaroxaban or dose‐adjusted warfarin. Cox proportional hazards regression with backward elimination identified factors at randomization that were independently associated with all‐cause mortality in the 14 171 participants in the intention‐to‐treat population. The median age was 73 years, and the mean CHADS 2 score was 3.5. Over 1.9 years of median follow‐up, 1214 (8.6%) patients died. Kaplan–Meier mortality rates were 4.2% at 1 year and 8.9% at 2 years. The majority of classified deaths (1081) were cardiovascular (72%), whereas only 6% were nonhemorrhagic stroke or systemic embolism. No significant difference in all‐cause mortality was observed between the rivaroxaban and warfarin arms (P=0.15). Heart failure (hazard ratio 1.51, 95% CI 1.33–1.70, P<0.0001) and age ≥75 years (hazard ratio 1.69, 95% CI 1.51–1.90, P<0.0001) were associated with higher all‐cause mortality. Multiple additional characteristics were independently associated with higher mortality, with decreasing creatinine clearance, chronic obstructive pulmonary disease, male sex, peripheral vascular disease, and diabetes being among the most strongly associated (model C‐index 0.677).ConclusionsIn a large population of patients anticoagulated for nonvalvular atrial fibrillation, ≈7 in 10 deaths were cardiovascular, whereas <1 in 10 deaths were caused by nonhemorrhagic stroke or systemic embolism. Optimal prevention and treatment of heart failure, renal impairment, chronic obstructive pulmonary disease, and diabetes may improve survival.Clinical Trial Registration URL: https://www.clinicaltrials.gov/. Unique identifier: NCT00403767.

SUMMARY A case is reported in which a congenital aneurysm of the right coronary sinus of Valsalva ruptured and dissected into the interventricular septum. M-mode and cross-sectional echocardiographic examination allowed accurate preoperative assessment of the pathologic anatomy, which was confirmed by angiography, surgery and autopsy. Dissection of the interventricular septum by a congenital sinus of Valsalva aneurysm is a rare lesion, has a poor prognosis, and can be diagnosed noninvasively with echocardiography.CONGENITAL ANEURYSM of the sinus of Valsalva is frequently encountered in clinical practice. Recent studies have emphasized the wide variety of clinical manifestations of this lesion, depending on its location and course.'-' In this report we present a case in which a ruptured right coronary sinus of Valsalva aneurysm took an unusual course, dissecting into the muscular interventricular septum. We believe this to be the first report of the preoperative diagnosis of this condition.Case Report A 16-year-old black male presented to the University of Cincinnati Hospital emergency room for evaluation of left-sided chest pain related to slight trauma that occurred 2 days before. Physical examination revealed systolic and diastolic murmurs, and an ECG revealed complete left bundle branch block. A chest x-ray was interpreted as normal. The patient was referred for further cardiac evaluation.The patient was the product of a normal pregnancy, labor and delivery with no history of perinatal cyanosis or respiratory difficulties. His subsequent growth and development were unremarkable. There was no history consistent with rheumatic fever or heart disease. Specifically The findings of the initial diagnostic evaluation in May 1979 were consistent with severe aortic regurgitation. Cardiac catheterization was refused. During the ensuing 6 months, the patient developed vague chest pain and progressive exertional dyspnea. Two weeks before admission, the patient developed increasing orthopnea and a nocturnal nonproductive cough. One week later, dyspnea increased, accompanied by several episodes of syncope. He was admitted to the University of Cincinnati Hospital, Cincinnati General Division in November 1979 for evaluation of congestive heart failure.Physical examination revealed a tall, slender adolescent black male in mild respiratory distress. There were no stigmata of Marfan's syndrome. The blood pressure was 110/50 mm Hg in both arms. The heart rate was 110 beats/min and cervical venous pressure was normal. The carotid upstrokes were brisk, with rapid emptying. Auscultation of the lungs revealed bibasilar end-inspiratory rales. On cardiac examination, the apical impulse was in the fifth intercostal space 1 cm lateral to the midclavicular line. Prominent apical and parasternal lifts were palpated. In addition, there was a diastolic thrill along the left sternal border. The first heart sound was decreased in intensity; the second heart sound was single.

The effects of the low-fat-low-cholesterol diet and lovastatin on lipoprotein levels were independent and additive. However, the reduction in LDL cholesterol produced by the diet was small, and its benefit was possibly offset by the accompanying reduction in the level of HDL cholesterol.

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