Cost and Outcomes

The cost of AF to the health care system as a whole is difficult to measure. The staggering cost of hospital admissions and outpatient visits for the treatment of AF itself must be considered, as well as the cost of complications directly related to the disease, especially those of debilitating strokes. In an attempt to estimate only a portion of total costs, Geraets et al. (7) found that between 1985 and 1990 patients with AF had an average length of stay of 5 d per admission, with an average cost of $4800 per admission, adding up to an annual expense of one billion dollars in the United States alone. More recently, Dell'Orfano et al. (8) found that in patients admitted via the emergency department, the length of stay was 4 d, but the average cost was approx $6,700 per admission. These figures, of course, do not take into account the annual cost of over 75,000 strokes believed to be directly attributable to AF.

Based on these data, it is clear that a cost-effective strategy of treating patients with AF must be found. However, studies have not determined which of the many approaches to therapy is the most cost-effective.

Anticoagulation of patients with AF has clearly been shown to provide health benefits at a decreased cost (9). The cost-effectiveness of other aspects of AF therapy remains uncertain. For example, the optimal strategy following cardioversion remains unclear. In a study by Eckman et al. (10), cardioversion followed by aspirin therapy alone yielded a gain in quality-adjusted life years (QALYs) of 1.2 yr at a cost of $10,800 per QALY. On the other hand, cardioversion followed by amiodarone and warfarin therapy, although the most effective therapy in the model, yielded a gain of 2.3 QALYs at the relatively high cost of $92,400 per QALY.

Another management option of uncertain cost-effectiveness is the use of transesopha-geal echocardiography to expedite cardioversion, rather than the traditional approach of waiting for at least 3 wk of therapeutic anticoagulation prior to the restoration of normal sinus rhythm. One study suggests that this is an effective approach to therapy, especially in patients admitted to the hospital and at a high risk of hemorrhagic complications (11). Another issue which has spawned much debate, is whether hospitalization is needed for the initiation of antiarrhythmic therapy for acute pharmacological cardioversion or immediately following electrical cardioversion. Some studies, especially in Europe, suggest that this is not necessary for all antiarrhythmic drugs (12). Unfortunately, all of these cost-effective analyses use decision-analysis models, which make several important assumptions (based on sometimes limited data) to obtain their conclusions. It is uncertain how applicable these models and their conclusions are to cohorts of "real" patients. The relative merit of maintaining sinus rhythm over rate control alone, for example, is being evaluated by several large multicenter trials in the United States and Europe. More studies are needed to establish the most cost-effective strategies for the management of this disease, bearing in mind that the well-being and safety of the patient should always be the top priority.

In terms of long-term outcomes, most longitudinal studies have demonstrated an increase in total and cardiovascular mortality in patients with AF compared to those without it (13,14). However, whether the increased mortality is causally related to the presence of AF, or whether AF is simply a marker of advanced cardiovascular disease, remains to be established. Contradictory data can be found in the literature in this regard in all patients, including those post-myocardial infarction (MI) (15,16) and those with congestive heart failure (CHF) (17,18).

Although there is some controversy on whether AF confers an increased mortality risk, there is no doubt that it increases the risk of cerebral thromboembolic events (19). Epidemiological and clinical studies have shown a 4-5% risk per yr, which constitutes a four-to-fivefold increased risk compared to the population at large. The risk is clearly increased in all subsets of patients, except for those who are of a young age and have "lone" AF. "Lone" AF is defined as AF in the absence of any structural heart disease, including hypertension. For example, Kopecky et al. (20) found that in Olmsted County, MN, patients less than 60 yr old and with no structural heart disease (including no hypertension), had a risk of a cerebral thromboembolic event of only 1.3% after 15 yr of follow-up. Based on these and other studies, it is now widely believed that young patients without structural heart disease do not need chronic anticoagulation with warfarin.

Despite the increased risk of stroke and the possible increase in total mortality, AF is often considered a benign rhythm. Physicians often tend to settle for rate-control management, especially in patients with minimal symptoms. However, one should consider other important effects of AF on both atrial and ventricular tissue. Recently, for example, the concept of "atrial remodeling" was elucidated in an elegant study by Wijffels et al. (21). In a goat model, the authors demonstrated that paroxysms of AF lead to persistent AF through a progressive shortening of the atrial refractory periods. They also showed that the longer these episodes were allowed to persist, the more difficult it was to maintain a normal sinus rhythm post-cardioversion. Atrial dilatation and chronically elevated left atrial pressures have also been shown to occur when AF becomes persistent (22,23). "Atrial stunning" is a delay in the return of atrial mechanical function post-cardioversion; the return of atrial mechanical systole may lag from a few hours to 6 wk after restoration of sinus rhythm. This effect on atrial mechanical function can be associated with significant morbidity if the patient is not appropriately anticoagulated post-cardioversion.

The effects of AF on the ventricular tissue can be dramatic. A reduction in left ventricular function, and an improvement in function after restoring sinus rhythm, has been demonstrated in several studies (24). This entity has been termed a "tachycardia mediated cardiomyopathy" because the poor left ventricular function results primarily from poor ventricular rate control, and the process is usually reversible by restoring sinus rhythm. However, an improvement in left ventricular function has also been shown in patients with a well-controlled ventricular response, raising the possibility that other mechanisms, such as the irregularity of the rhythm (25), may contribute to the ventricular dysfunction.

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