The effect of beta-blocker therapy on clinical outcome in patients with Marfan's syndrome: A meta-analysis
Section snippets
Background
The major causes of mortality and morbidity in Marfan's patients are the cardiovascular complications of aortic dissection and rupture [1]. In the late 1960s it was reported that blood pressure lowering medication improves survival in patients in the general population with acute dissection of aortic aneurysms [2], [3], [4], [5], [6]. This therapy then began to be utilized for the prophylactic treatment of patients with aortic root dilatation related to Marfan's syndrome. It has been reported
Search
We searched Medline database from 1965, with the latest electronic search on July 10, 2005 for publications of long-term follow-up of patients with Marfan's syndrome. Keywords included Marfan's syndrome and outcome or beta-blockade or beta-adrenergic blockade or cardiovascular surgery. Language of publication did not influence article selection. Titles and abstracts were screened to exclude ineligible studies. References from these studies and from related review articles or editorials were
Study selection and characteristics
Seventeen studies, which included relevant long-term follow-up data, were considered for inclusion in the study. Ten were excluded because of incomplete or redundant information. One study had no control group.
A total of 6 studies were thus included. All studies based the diagnosis on internationally established clinical criteria for Marfan's syndrome. The study by Salim et al. [10] used genetic information to confirm the diagnosis in one sub-group of patients. Clinical data from the six
Discussion
Clinical use of beta-blocker therapy and other anti-hypertensive agents for dissecting aortic aneurysms began in the late 1960s. This treatment was instituted after the observation that patients with aortic dissection or rupture had a high incidence of hypertension (75%) [4]. Studies with turkeys demonstrated that propanolol appeared to prevent aortic rupture at a dose which did not significantly alter mean arterial pressure but did decrease cardiac impulse [17], [18]. This finding suggested
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