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.

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The basics of pathogenesis, clinic and diagnosis of myocardial reperfusion syndrome are considered. Myocardial reperfusion syndrome is defined. Its relevance as one of the most poorly studied and formidable complications of cardiac reperfusion in myocardial infarction with elevation of the S-T segment has been explained. A brief review of the historical review of this problem and such types of manifestations of myocardial reperfusion syndrome as: diastolic myocardial dysfunction, post-reperfusion disturbances of the heart rhythm, the phenomenon of no-reflow and irreversible damage to the myocardium are briefly reviewed. The modern views on the pathological physiology of diastolic myocardial dysfunction, post-reperfusion damage to the myocardium, and the no-reflow phenomenon are analyzed. A review of current views on the pathological physiology of the development of post-reperfusion disturbances in heart rhythm is carried out. The clinical picture and the effect on the hemodynamics of such a manifestation of myocardial reperfusion syndrome as diastolic myocardial dysfunction are described. A brief description of the clinical picture of irreversible post-reperfusion damage to the myocardium is given. The clinical picture and types of post-reperfusion rhythm disturbances are described. The diagnostics of the no-reflow phenomenon has been analyzed in detail, the coronary angiographic scales for assessing thrombolysis in myocardial infarction and for assessing myocardial perfusion are graphically shown. A description of the basics of diagnosing post-reperfusion disturbances in heart rhythm, diastolic myocardial dysfunction, and post-reperfusion irreversible damage to the myocardium is given. A brief description of the known in the world literature predictors of the development of myocardial reperfusion syndrome is presented.