Numular headache is a chronic, mild to moderate, pressurelike pain in a circumscribed cranial area of approximately 2 to 6 cm in diameter. Pain usually is limited to the parietal region, although it may appear in any cranial site. It is a benign process of usually unknown origin.
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.
Atrial Fibrillation (AF) is one of the most frequent arrhythmias, especially in elderly patients. Cardiac overload increases the incidence of AF. Clinical presentation of atrial fibrillation can occur as nonsustained paroxysms, persistent episodes and in chronic-permanent form. The physio-pathological mechanisms are:• Circuit of multiple and anarchic re-entries • Atrial fibrillatory conduction • Re-entry circuit with fibrillatory conduction. Remodeling (electrical or structural) facilitates the appearance and persistence of AF: Neurovegetative changes and cytosolic Ca overload facilitate AF. Interstitial atrial fibrosis, in which Renin-Angiotensin System (RAS) hyperactivity is a main aspect of remodeling. There is clinical evidence that supports the antiatrial fibrillatory actions of RAS blockade. Potential mechanisms are: (a) direct modulation of ionic channels, (b) hemodynamic improvement, (c) reduction of atrial stretching, (d) antifibrotic effects. There is less clinical evidence with antialdosterone drugs, but theoretically these might also be useful. Keywords: atrial fibrillation, remodeling, renin-angiotensin systemAtrial fibrillation, pathophysiology, remodeling. Atrial fibrillation (AF) is one of the most frequent arrhythmias in adulthood, with its incidence increasing with age. The situations and pathologies that lead to hemodynamic or pressure overload are associated to AF. This can be present as nonsustained paroxysms, persistent episodes (reverted to Sinus Rhythm by medical treatments) and as chronic-permanent AF. It is referred to as 'isolated' when there is no structural cardiopathy or other morbid entities that can explain it. Three mechanisms have been described to explain its physiopathogenia [Nattel and Ehrlich, 2004]: a. Multiple, coexistent, anarchic re-entry circuits. AF settles down if the conditions are appropriate for them to appear and persist over time. These alterations involve refractoriness (reduction), velocity of conduction (delay), and an increase in heterogeneity of both properties [Moe and Abildskov, 1995;Cosio, 1994;Cosio and Arribas, 1989;Allessie, et al. 1985;Moe, 1962]. The quantity of atrial 'mass' (atrial volume) is also a determining factor. For hearts with big atria, AF is more frequent and lasting [Henry et al. 1976]. The persistence of the fibrillatory state depends on the number of the aforementioned re-entries circuits that are simultaneously present, at any determined moment. Few coexistent re-entries diminish the possibility of persistence.b. Rapid and continued ectopic activity, with 'fibrillatory conduction' in auricles, due to its impossibility to respond in an organized form.c. Only one circuit of re-entry with 'fibrillatory conduction,' with this 'fibrillatory conduction' also depending on the heterogeneity of refractoriness and atrial conductivity.An interrelationship may exist between these three mechanisms.An episode of AF needs a 'trigger' (premature beats, tachycardia) to initiate it, by interaction with 'modulators' (neurovegetative system, br...
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