There has been a tendency to treat paroxysmal atrial fibrillation (PAF) in a similar way to sustained AF, but treatment objectives may be very different. We discuss current definitions, epidemiology, pathophysiology and natural history of PAF, and review evidence for its treatment and management. PAF comprises between 25% and 62% of cases of AF, with similar underlying causes to those in sustained AF. The main objective of management is prevention of paroxysms and long-term maintenance of sinus rhythm, and Class 1c drugs are highly effective, although beta-blockers are useful alternatives. If patients have severe coronary artery disease or poor ventricular function, amiodarone is probably the drug of choice. Although randomized controlled trials of thromboprophylaxis in patients with paroxysmal AF per se are lacking, the approach to patients with paroxysmal AF should be similar to that in patients with sustained AF, with warfarin for 'high risk' patients and aspirin for those at 'low risk'. Non-pharmacological therapeutic options, including pacemakers, electrophysiological techniques and the implantable atrial defibrillator, show great promise. Despite paroxysmal AF being a common condition, management strategies are limited by evidence from small randomized trials, with inconsistencies over the definition of the arrhythmia and the inclusion of only symptomatic subjects. Evidence for antithrombotic therapy is also based on epidemiological studies and subgroup analyses of the large randomized trials.

To investigate the hypothesis that abnormalities of thrombogenesis and endothelial damage/dysfunction are greater in malignant hypertension (MHT) compared with uncomplicated nonmalignant essential hypertension (EHT) > 160/90 mm Hg), we measured markers of endothelial function (von Willebrand factor) platelet activation (soluble P-selectin) and fibrinogen in 18 consecutive patients with MHT, 50 patients with untreated EHT, and 34 healthy control subjects. We also investigated whether there was any diurnal variation in the measured indices, as well as the effects of good blood pressure (BP) control after 6-month follow-up. Mean plasma fibrinogen and von Willebrand factor levels were both highest in the MHT group, intermediate in the nonmalignant hypertension group and lowest in the normotensive control subjects (P < .001). Similarly, mean soluble P-selectin levels were higher in both hypertensive groups compared to normotensive control subjects (P = .033). There was no significant diurnal variation in plasma fibrinogen, soluble P-selectin, and von Willebrand factor levels over the 24-h study period among the MHT patients. At 6-month follow-up and a reduction in mean BP, there was no significant change in mean plasma fibrinogen levels (P = .25), but both soluble P-selectin (P < .001) and von Willebrand factor (P = .0025) were significantly reduced. In conclusion, malignant hypertension is associated with abnormal endothelial damage (elevated von Willebrand factor), platelet activation (soluble P-selectin), and fibrinogen levels, which may be related to the pathogenesis of this condition, as well as the development of complications. These abnormalities do not undergo any significant diurnal variation and may be beneficially altered by BP reduction.

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