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Circulation. 2007;116:1525
doi: 10.1161/CIRCULATIONAHA.107.185633
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(Circulation. 2007;116:1525.)
© 2007 American Heart Association, Inc.

Issue Highlights


*    GROWTH DIFFERENTIATION FACTOR 15 FOR RISK STRATIFICATION AND SELECTION OF AN INVASIVE TREATMENT STRATEGY IN NON–ST-ELEVATION ACUTE CORONARY SYNDROME, by Wollert et al.
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*GROWTH DIFFERENTIATION FACTOR 15...
down arrowPATTERNS OF WEIGHT CHANGE...
down arrowCHANGE IN SALT INTAKE...
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A number of biomarkers have been shown to help in risk stratifying patients with non–ST-elevation acute coronary syndrome, but only cardiac-specific enzyme elevations have been shown to help in identifying those who benefit from early revascularization. Growth differentiation factor 15 is a member of the transforming growth factor β-cytokine family that is induced in the myocardium after ischemia and reperfusion. Prior studies have shown it to be elevated in non–ST-elevation acute coronary syndrome and to be independently related to mortality. This study was undertaken to determine if an elevated level of growth differentiation factor 15 would assist in risk stratification and help identify those patients who would benefit most from an early invasive strategy. On the basis of data from the Fast Revascularization during InStability in Coronary artery disease II (FRISC-II) trial, modest or highly elevated levels predicted a better outcome with an invasive strategy. In patients with normal levels of growth differentiation factor 15, an invasive strategy was not beneficial even in the presence of ST depression or elevated Troponin levels. This study suggests that growth differentiation factor 15 levels may help in risk stratification and in clinical decision making in patients with non–ST-elevation acute coronary syndrome. See p 1540.


*    PATTERNS OF WEIGHT CHANGE PRECEDING HOSPITALIZATION FOR HEART FAILURE, by Chaudhry et al.
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Among patients with chronic heart failure (HF), hospitalization for decompensation of symptoms is a substantial morbidity burden, as well as a major driver of the economic burden of HF. Disease management programs are increasingly used in an attempt to homogenize the applications of evidence-based care, as well as to respond to short-term clinical changes in a timely fashion. A major assumption driving these programs is that weight change represents fluid overload and justifies diuretic changes, though little actual data support that intuitive concept. In this issue of Circulation, Chaudhry and colleagues present data extracted from remote monitoring of HF patients using a case-control design to demonstrate that weight gain can be detected beginning even 30 days before heart failure hospitalization, with more significant divergence within a week of hospitalization. Moreover, an apparent "dose response" existed, in that greater weight gain was associated with greater risk of HF hospitalization. These data support an approach to such patients with aggressive treatment for presumed fluid overload, and they also support the hypothesis that congestion plays the major pathophysiological role in decompensation of HF patients. See p 1549 (editorial p 1526).


*    CHANGE IN SALT INTAKE AFFECTS BLOOD PRESSURE OF CHIMPANZEES: IMPLICATIONS FOR HUMAN POPULATIONS, by Elliott et al.
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In this issue of Circulation, Elliott and colleagues study 2 sets of chimpanzees, a cohort of 17 animals in Gabon and another cohort of 110 in Bastrop, Tex, with varying salt intake. In Gabon, the salt intake of the chimpanzees fluctuated annually from 75 to 35 to 120 mmol/d over the course of 3 years. In Bastrop, the animals were divided into 2 groups; 1 group received 250 mmol sodium/d for 2 years, while the sodium intake for the second group was halved during year 2 of the study. In both groups of chimpanzees, lower sodium intake was associated with lower systolic, diastolic, and mean arterial blood pressure. Unlike the previous human studies, these were single-variable experiments, and lifestyle and other potential risk factors, such as change in diet, alcohol intake, and cigarette smoking, were not present. Even though this study was not conducted in humans, these findings suggest that more effort is needed, by both the public and private sectors, to achieve a decrease in salt intake in the human population. See p 1563 (editorial p 1530).

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*    Images in Cardiovascular Medicine
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Pseudoaneurysm and Intracardiac Fistula Caused by an Infected Paclitaxel-Eluting Coronary Stent. See p e364.

Optical Coherence Tomography in the Setting of an Acute Anterior Myocardial Infarction. See p e366.


Figure 15432
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*    Correspondence
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*Correspondence
 
See p e368.


Related Articles:

Can We Predict and Prevent the Onset of Acute Decompensated Heart Failure?
Eugene E. Wolfel
Circulation 2007 116: 1526-1529. [Extract] [Full Text]

Eat Your Fruits and Vegetables But Hold the Salt
Paul R. Conlin
Circulation 2007 116: 1530-1531. [Extract] [Full Text]

Pseudoaneurysm and Intracardiac Fistula Caused by an Infected Paclitaxel-Eluting Coronary Stent
James J. Jang, Ashok Krishnaswami, Junming Fang, Mateo Go, and Valerie C. Kwai Ben
Circulation 2007 116: e364-e365. [Extract] [Full Text]

Optical Coherence Tomography in the Setting of an Acute Anterior Myocardial Infarction
Ravinay Bhindi, Shahzad M. Munir, and Keith M. Channon
Circulation 2007 116: e366-e367. [Extract] [Full Text]

Letter by Weidemann et al Regarding Article, "Global Diastolic Strain Rate for the Assessment of Left Ventricular Relaxation and Filling Pressure"
Frank Weidemann, Joerg M. Strotmann, and Bart Bijnens
Circulation 2007 116: e368. [Extract] [Full Text]

Growth Differentiation Factor 15 for Risk Stratification and Selection of an Invasive Treatment Strategy in Non–ST-Elevation Acute Coronary Syndrome
Kai C. Wollert, Tibor Kempf, Bo Lagerqvist, Bertil Lindahl, Sylvia Olofsson, Tim Allhoff, Timo Peter, Agneta Siegbahn, Per Venge, Helmut Drexler, and Lars Wallentin
Circulation 2007 116: 1540-1548. [Abstract] [Full Text]




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