Latent arterial hypertension in apparently lone atrial fibrillation

Introduction. Longitudinal studies on lone AF are rare and the incidence of hypertension in this population unknown. This study aimed at investigating the incidence of arterial hypertension in patients with apparently lone atrial fibrillation (AF). Methods and Results. Out of 292 consecutive patients presented with permanent or paroxysmal AF, 32 patients were diagnosed as having lone AF according to strict criteria. Three patients were subjected to ablation of the ligament of Marshall, 14 patients to pulmonary vein isolation, and the remainder were treated with beta blockade. Patients were followed-up for a 1-3 year period. During follow-up, 14 patients were diagnosed as having arterial hypertension. Thirteen of them had recurrent AF despite ligament of Marshall ablation (1 patient), pulmonary vein isolation (4 patients) and beta blockade (8 patients). Cox regression analysis revealed that the only significant predictor of development of hypertension was complete or partial response to antiarrhythmic therapy (beta = 3.82, S.E. = 1.22, exp(b) = 45.63, 95% C.I. = 4.17-499.2, p = 0.001), independent of age (beta = -0.01, p = 0.74), sex (beta = -0.91, p = 0.28), left ventricular ejection fraction (beta = 0.06, p = 0.52), left atrial size (beta = 0.58, p = 0.7) and kind of antiarrhythmic therapy (ablation or drug therapy) (beta = 1.36, p = 0.09). In patients with lone AF that did not respond at all to antiarrhythmic therapy, there was a 45.6 times higher risk of diagnosing hypertension during the next 3 years as compared to responders. Conclusion. Approximately 44% of patients with an initial diagnosis of lone AF may represent occult cases of arterial hypertension. In these patients hypertension may affect AF recurrence and treatment outcomes, regardless of the mode of antiarrhythmic therapy used

Drug-Induced Thrombophilic or Prothrombotic States: An Underestimated Clinical Problem That Involves Both Legal and Illegal Compounds

Vascular thrombosis, both arterial and venous, is a condition associated with significant morbidity and mortality. There are multiple risk factors for thrombosis, both congenital and acquired, and in the majority of cases, these risk factors are not modifiable. Over the past 2 decades, multiple drugs (both illegal and legal) have been associated with increased risk of thrombosis. However, due to limited scientific literature regarding the prothrombotic tendencies of these drugs, there is a concomitant limited understanding of the pathophysiology of drug-induced thrombosis. As drugs are one of the few modifiable risk factors for thrombosis, further study and dissemination of knowledge regarding drug-associated and drug-induced thrombosis are essential and have the potential to lead to decreased future incidence of thrombosis. The mechanisms at the basis of the thrombophilic activity of these drugs are variable and sometimes still ill recognized. Increased levels of clotting factors, reduction in coagulation natural inhibitors, decreased fibrinolysis, activated clotting factors, increased blood viscosity, endothelial damage, and increased platelet number and activation are the most frequent causes. Arterial steal or coronary arteries no flow has also been implicated. In some cases due to the intake of several drugs, more than one mechanism is present in a given patient. The purpose of the present review is to analyze all the drugs demonstrated to be potentially thrombotic. It is hoped that a prudent use or nonuse of these drugs might result in a reduction of thrombosis-associated diseases