Circulation. 2005;111:3015
(Circulation. 2005;111:3015.)
© 2005 American Heart Association, Inc.
Issue Highlights
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ALDOSTERONE SYNTHASE INHIBITOR AMELIORATES ANGIOTENSIN II–INDUCED ORGAN DAMAGE, by Fiebeler et al.
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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.
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LONG-TERM RESPONSE TO CALCIUM CHANNEL BLOCKERS IN IDIOPATHIC PULMONARY ARTERIAL HYPERTENSION, by Sitbon et al.
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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% of IPAH patients evaluated
in a pulmonary vascular referral center. These data suggest
that routine administration of CCB as first-line therapy in
IPAH patients may be ill advised. See p
3105.
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APOLIPOPROTEIN E MIMETIC PEPTIDE DRAMATICALLY LOWERS PLASMA CHOLESTEROL AND RESTORES ENDOTHELIAL FUNCTION IN WATANABE HERITABLE HYPERLIPIDEMIC RABBITS, by Gupta et al.
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Elevated high-density lipoprotein (HDL) levels are associated
with a reduction in the frequency of cardiovascular events.
To develop new drugs for the treatment of atherosclerosis, investigators
have been evaluating the therapeutic properties of HDL components
in both animal models of vascular disease and patients with
coronary atherosclerosis. However, some of these agents are
structurally complex and difficult to produce. In this issue
of Circulation, Gupta et al analyze the atheroprotective properties
of a synthetic peptide containing the arginine-rich receptor-binding
domain of ApoE fused to an amphipathic helical peptide that
possesses ApoA-I–like properties. A single administration
of the dual-domain peptide dramatically reduces plasma cholesterol
levels and improves vascular reactivity in a dyslipidemic rabbit
model. These improvements coincide with a reduction in markers
of oxidative stress that are associated with vascular inflammation.
These data suggest that this HDL-mimetic peptide could make
‘good‘ cholesterol better and have utility for the
treatment of atherosclerosis. See p
3112.
Visit http://www.circ.ahajournals.org:
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Cardiology Patient Page
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How to Respond to an Implantable Cardioverter-Defibrillator
Shock. See p
e380.
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Images in Cardiovascular Medicine
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Reversible Right Ventricular Hypertrophy Due to Cardiac Sarcoidosis.
See p
e383.
Three-Dimensional Imaging in Rupture of Papillary Muscle After Acute Myocardial Infarction. See p e385.
Angiosarcoma of the Pericardium: A Fatal Disease. See p e388.
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Correspondence
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See p
e390.
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Aldosterone Synthase Inhibitor Ameliorates Angiotensin II–Induced Organ Damage
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ALDOSTERONE SYNTHASE INHIBITOR...
LONG-TERM RESPONSE TO CALCIUM...