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.
akotsubo cardiomyopathy is a novel heart syndrome characterized by a transient left ventricular (LV) dysfunction with chest pain, ECG changes and not a high increase in cardiac enzymes, mimicking an acute myocardial infarction. 1,2 Because of the specific abnormalities of the LV contraction (ie, preserved basal function with apical akinesis or dyskinesis) the disease is also called as 'transient left ventricular apical ballooning' or 'ampulla cardiomyopathy '. 2,3 The general prognosis is considered to be rather favorable, 2-6 although some investigators have reported cases with various complications including death. [7][8][9] We present a case of takotsubo cardiomyopathy in a female patient who suffered a fatal LV free wall rupture and the results of a comprehensive histopathologic investigation.
Case ReportAn 81-year-old woman with hypertension started to feel chest pains after a quarrel with her son. Next day stomach pains and diarrhea appeared but the chest pain became intermittent, and the symptoms were accompanied by general fatigue. On the third day she was admitted to hospital because of chest discomfort at rest and ECG signs of ST-segment elevation myocardial infarction (MI) (Fig 1A). She had no history of prior angina or MI and no family history of heart disease and sudden death. On admission her heart rate was 104 beats/min, and blood pressure was 150/90 mmHg. Auscultation of the heart and lungs was normal, abdominal and neurological examination findings were negative, and there was no peripheral edema. Immediate coronary angiography did not reveal any significant coronary artery stenosis ( Figs 2A,B); the TIMI frame counts for the left anterior descending, circumflex and right coronary arteries were 29, 20 and 26 frames, respectively. However, ventriculography revealed a balloon-like LV motion abnormality with akinesis from the mid to apical portions and hyperkinesis of the base (Figs 2C,D). The LV end-systolic and end-diastolic pressureas were 150 mmHg and 15 mmHg, respectively, and there was no pressure gradient from the apex and midportion to the outflow tract; other hemodynamic data and the laboratory data on admission are shown in Table. After angiography the patient reported pain relief and was taken to the intensive care unit; however, the ECG recording showed no restoration of normal ST-segment (Fig 1B). The woman was stable during the first 40 h of admission, with no hemodynamic or arrhythmic problems, and she was given -blocker (metoprolol), angiotensin-converting enzyme inhibitor (ramipril) and aspirin; her blood pressure was within normal limits. She occasionally complained of chest discomfort; her creatine kinase-MB was maximal on admission and gradually diminished in further examinations, but the ST segment remained elevated ( Figs 1C,D). After 40 h of admission she reported a sudden pain in the epigastric region and the symptoms of acute abdomen soon appeared (C-reactive protein reached 267 mg/dl). After surgical consultation the woman was taken to the operation room for urgent surger...
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