Circulation. 2006;114:183
(Circulation. 2006;114:183.)
© 2006 American Heart Association, Inc.
Issue Highlights
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PLASMA PHOSPHOLIPID TRANS FATTY ACIDS, FATAL ISCHEMIC HEART DISEASE, AND SUDDEN CARDIAC DEATH IN OLDER ADULTS: THE CARDIOVASCULAR HEALTH STUDY, by Lemaitre et al.
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Higher dietary consumption of
trans fatty acids has been associated
with elevated risk of coronary heart disease. Data are limited,
however, regarding variation in coronary risk according to the
type of
trans fatty acid, eg,
trans-isomers of oleic acid (
trans-18:1)
versus
trans-isomers of linoleic acid (
trans-18:2). In this
issue of
Circulation, Lemaitre and colleagues conducted a nested
case-control study using data from elderly participants in the
Cardiovascular Health Study. The investigators compared plasma
trans-18:1 and
trans-18:2 levels (collected 3 years before occurrence
of events) in 214 individuals (cases) with fatal coronary heart
disease with plasma levels of these
trans fatty acids in 214
matched controls. They report that higher plasma
trans-18:2
levels were associated with greater risk of fatal ischemic heart
disease and sudden cardiac death in multivariable analyses that
adjusted for clinical and lifestyle risk factors including plasma
levels of n-3 polyunsaturated fatty acids. In contrast, higher
levels of
trans-18:1 were associated with lower risk. These
observations suggest that different types of
trans-isomers in
the diet may influence coronary risk differentially. If confirmed,
these findings suggest that current efforts at decreasing
trans fatty acid intake in foods should take into consideration their
trans-18:2 content. See p
209.
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PREVALENCE, CLINICAL PROFILE, AND SIGNIFICANCE OF LEFT VENTRICULAR REMODELING IN THE END-STAGE PHASE OF HYPERTROPHIC CARDIOMYOPATHY, by Harris et al.
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A minority of patients with hypertrophic cardiomyopathy (HCM)
enter a phase known as "end-stage," thought to be represented
by systolic dysfunction, left ventricular dilation, and thinning
of previously hypertrophied walls. In this issue of
Circulation,
Harris and colleagues provide results of the largest group of
end-stage patients reported to date, culled from a large multicenter
cohort of over 1200 HCM patients. These data demonstrate a far
more diverse pattern of left ventricular (LV) remodeling than
has been appreciated—including a significant number of
patients who, despite an abnormal ejection fraction, still maintain
normal LV cavity size and/or persistently hypertrophied LV walls.
Furthermore, the clinical course appears largely unfavorable,
with a substantial number of sudden arrhythmic deaths as well
as heart failure events or transplantations occurring over a
short period following clinical recognition. This study provides
broader insight into the prevalence, morphology, and clinical
course of this unique subset of HCM patients, with the hope
of earlier disease recognition and with implications for aggressive
treatment interventions. See p
216.
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ANGIOTENSIN II TYPE I RECEPTOR BLOCKADE PREVENTS ALCOHOLIC CARDIOMYOPATHY, by Cheng et al.
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The mechanism responsible for alcoholic cardiomyopathy is not
known. Cheng et al caused myocardial dysfunction in dogs by
feeding them alcohol once daily accounting for 33% of daily
calorie intake. Alcohol caused activation of the renin-angiotensin
system (RAS) at virtually all levels, including increased plasma
angiotensin, renin activity, myocardial angiotensin-converting-enzyme
activity and cardiac myocyte angiotensin II type 1 receptor
expression. Alcohol was also associated with abnormalities in
myocardial contractility, and at the isolated myocyte level,
with reduced shortening, prolonged relaxation, and decreased
calcium transient amplitude. Treatment with the angiotensin
receptor blocker ibresartan reduced the activation of the RAS
and corrected the functional abnormalities at the myocardial
and isolated myocyte levels. These observations thus implicate
the RAS in the pathophysiology of alcoholic myocardial dysfunction,
and suggest a potentially useful therapeutic role for the angiotensin
receptor blocker. See p
226.
Visit http://circ.ahajournals.org:
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Clinician Update
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Acute Pulmonary Embolism: Part II: Treatment and Prophylaxis.
See p
e42.
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Images in Cardiovascular Medicine
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Hereditary Hemorrhagic Telangiectasia With Pulmonary Arteriovenous
Fistulas. See p
e48.
Iatrogenic Left Ventricle-to-Coronary Venous Fistula. See p e50.
Epicardial Radiofrequency Catheter Ablation of Ventricular Tachycardia in the Vicinity of Coronary Arteries Is Facilitated by Fusion of 3-Dimensional Electroanatomical Mapping With Multislice Computed Tomography. See p e51.
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Correspondence
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See p
e53.
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