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(Circulation. 2004;110:2073.)
© 2004 American Heart Association, Inc.
Issue Highlights |
CORONARY ARTERY CALCIFICATION AND FAMILY HISTORY OF PREMATURE CORONARY HEART DISEASE: SIBLING HISTORY IS MORE STRONGLY ASSOCIATED THAN PARENTAL HISTORY, by Nasir et al.
Contemporary noninvasive imaging techniques allow a new window into the determinants and associations of subclinical atherosclerosis in large populations. In this issue of Circulation, Nasir and colleagues find, in >8000 asymptomatic subjects, that self-reported family history of premature coronary heart disease is associated with a significant increase in the prevalence and magnitude of coronary artery calcium (by electron beam CT imaging), a marker of subclinical atherosclerosis. Moreover, in a novel finding, sibling history of premature coronary heart disease is more powerfully associated with coronary artery calcium than parental history. In an accompanying editorial, O’Donnell discusses the importance of family history in the setting of growing access to genomic analyses and addresses the issue of self-reported versus validated family history. See pp 2074 and 2150.
SCN5A MUTATION ASSOCIATED WITH DILATED CARDIOMYOPATHY, CONDUCTION DISORDER, AND ARRHYTHMIA, by McNair et al.
Dissecting the molecular details of Nature’s ’experiments’: Research investigating the mechanisms by which some families have a unique predisposition to cardiovascular disorders continues to provide new insights into the molecular basis of disease. In this issue of Circulation, McNair et al show convincing evidence that a single base substitution in the cardiac sodium channel gene is the cause of one family’s autosomal dominant inheritance of progressive conduction system disease and cardiomyopathy. The point mutation leads to a single–amino acid substitution in the sodium channel, changing the charge of one segment of the protein and likely the voltage dependence of channel gating. This adds to a growing list of "channelopathies" and will help stimulate future research to develop novel therapeutic approaches for the treatment of cardiovascular disease. See p 2163.
EFFECT OF CANDESARTAN ON CAUSE-SPECIFIC MORTALITY IN HEART FAILURE PATIENTS: THE CANDESARTAN IN HEART FAILURE ASSESSMENT OF REDUCTION IN MORTALITY AND MORBIDITY (CHARM) PROGRAM, by Solomon et al.
The Candesartan in Heart Failure Assessment of Reduction in Mortality and Morbidity (CHARM) trial program demonstrated that the angiotensin receptor blocker candesartan caused a 12% reduction in cardiovascular mortality and a borderline 9% reduction in overall mortality. Most patients died suddenly (8.5%) or from worsening heart failure (6.2%). In this issue, Solomon et al provide the detailed analysis of the mode of death. For the overall trial, candesartan caused a 15% reduction in sudden death and a 22% reduction in death due to worsening heart failure but had no effect on the rate of myocardial infarction or stroke. The reductions in sudden and heart failure deaths were apparent in patients with systolic failure in the ‘Alternative‘ and ‘Added‘ component trials but not in the patients with preserved systolic function in the ‘Preserved‘ trial. See p 2180.
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Clinician Update
Prevention of Sudden Death in Hypertrophic Cardiomyopathy: But Which Defibrillator for Which Patient? See p e438.
Images in Cardiovascular Medicine
High-Resolution Images Obtained With Ultrasound and Magnetic Resonance Imaging of Pericarotid Fibrosis in Erdheim Chester Disease. See p e443.
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Related Articles:
Circulation 2004 110: 2163-2167.
Circulation 2004 110: 2180-2183.
Circulation 2004 110: e438-e442.
Circulation 2004 110: e443-e444.
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