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Circulation. 2005;111:3015

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(Circulation. 2005;111:3015.)
© 2005 American Heart Association, Inc.

Issue Highlights


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    ALDOSTERONE SYNTHASE INHIBITOR AMELIORATES ANGIOTENSIN II–INDUCED ORGAN DAMAGE, by Fiebeler et al.
 
Aldosterone has been shown to contribute to angiotensin II–induced end-organ damage, and clinical studies have confirmed the benefit of adding aldosterone antagonists to angiotensin-converting enzyme inhibitor agents to prevent adverse remodeling. Angiotensin II increases circulating levels of aldosterone levels as well as de novo tissue synthesis of aldosterone by stimulating aldosterone synthase (CYP11B2); however, it is unknown which source of aldosterone plays a greater role in tissue remodeling and damage. In these studies, Fiebeler et al examine this question by utilizing both FAD286, a novel CYP11B2 inhibitor, and adrenalectomy in transgenic rats overexpressing human renin and angiotensinogen genes. Using these models, they are able to isolate the source of aldosterone that modulates some of the adverse cardiac and renal effects associated with hyperaldosteronism. See p 3087.


*    LONG-TERM RESPONSE TO CALCIUM CHANNEL BLOCKERS IN IDIOPATHIC PULMONARY ARTERIAL HYPERTENSION, by Sitbon et al.
 
Characteristics of patients with idiopathic pulmonary arterial hypertension (IPAH) who benefit from long-term calcium channel blockers (CCBs) are unknown. Sitbon and colleagues performed acute pulmonary vasodilator testing with epoprostenol or nitric oxide during initial right heart catheterization in 557 IPAH patients. Acute responders were treated initially with oral CCB. Long-term CCB responders were defined as those being in functional class I or II after at least 1 year on CCB monotherapy. Among the 70 patients (12.6%) who displayed acute pulmonary vasoreactivity and received CCB therapy, 38 (6.7%) improved long term. Long-term CCB responders had less severe disease at baseline and displayed a more pronounced fall in mean pulmonary artery pressure during acute vasodilator testing. Of note, long-term CCB responders represented less than 10% . . . [Full Text of this Article]


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