Cause of Death and Predictors of All-Cause Mortality in Anticoagulated Patients With Nonvalvular Atrial Fibrillation : Data From ROCKET AF

M. Kaste on työryhmän ROCKET AF Steering Comm jäsen.Background-Atrial fibrillation is associated with higher mortality. Identification of causes of death and contemporary risk factors for all-cause mortality may guide interventions. Methods and Results-In 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= 75 years (hazard ratio 1.69, 95% CI 1.51-1.90, P Conclusions-In a large population of patients anticoagulated for nonvalvular atrial fibrillation, approximate to 7 in 10 deaths were cardiovascular, whereasPeer reviewe

Arterial stiffness and central hemodynamics in treated hypertensive subjects according to brachial blood pressure classification

BACKGROUND: International recommendations have classified brachial blood pressure (BP) in subgroups enabling better cardiovascular risk stratification. Central BP is an independent predictor of cardiovascular risk, differing from brachial BP through the predominant influence of arterial stiffness and wave reflections. Central BP has never been studied in relation to international guidelines for brachial BP classification. METHODS: In 580 chronically treated hypertensive subjects we measured: carotid-femoral pulse wave velocity (PWV), carotid artery augmentation index (AI) and carotid blood pressures, using applanation tonometry and pulse wave analysis, and using brachial BP for carotid pressure wave calibration. RESULTS: For each given brachial value, carotid systolic blood pressure (SBP) and PP were significantly lower than the corresponding brachial SBP and PP. This pressure amplification was significantly lower in the 'optimal' and 'normal' BP ranges (6.8-7.4 mmHg) than in the higher BP ranges (10.1-11.3 mmHg), mainly depending on heart rate (HR) and PWV levels. PWV gradually increased as a function of brachial BP classification and was a significant predictor of this classification independently of age, drug treatment, atherosclerotic lesions and even mean BP. Finally, PWV was a highly sensitive marker of the effective BP control throughout all decades of age. CONCLUSION: Under chronic antihypertensive therapy, central BP does not strictly parallel the corresponding brachial BP classification, depending on differences in aortic stiffness and HR. Whether aortic PWV might predict the brachial BP classification and/or the presence of effective BP control, as suggested in this study, needs further confirmation. © 2008 Lippincott Williams & Wilkins, Inc

Arterial stiffness and orthostatic blood pressure changes in untreated and treated hypertensive subjects

Carotid-femoral pulse wave velocity (PWV), an integrated marker of segmental aortic stiffness, was recently proposed as one of the underlying mechanisms inducing orthostatic hypotension in the elderly with marked arterial rigidity. We examined the relationship between PWV (Complior; Colson, Paris, France) and orthostatic blood pressure (BP) changes, measured repeatedly, over a wide range of age and arterial stiffness. Sixty-nine hypertensive subjects (age, 37 to 76 years; 39 untreated and 30 treated) were studied. BP, in both sitting and erect position, was measured at two occasions a few weeks apart, and in between PWV was assessed by means of pulse wave analysis. In untreated hypertensive subjects, the orthostatic alterations in systolic, but not in diastolic blood pressure (DBP), were inversely related to PWV, independently from age, gender, mean BP, and diabetes mellitus. The greater the aortic stiffness the larger was the systolic blood pressure (SBP) decrease during upraises. On the contrary, no such association was found between PWV and orthostatic changes of BP in treated hypertensive subjects. These results suggest the presence of a pathophysiological association between arterial stiffening and BP postural changes. Antihypertensive drug treatment, as well as other factors that have not been evaluated in the present study, might have modulated this association. However, it might be argued that a causal association between arterial stiffness - disturbed baroreflex sensitivity - postural BP changes, even in subjects without pronounced vascular aging or orthostatic hypotension, is implied. © 2008 American Society of Hypertension