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J Am Coll Cardiol, 2007; 49:31-32, doi:10.1016/S0735-1097(07)00201-X
© 2007 by the American College of Cardiology Foundation
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INSIDE THIS ISSUE OF JACC

Inside This Issue of JACC


    Atherosclerosis
 Top
 Atherosclerosis
 Valvular Heart Disease
 Atrial Fibrillation
 Atrial Fibrillation
 
Limited Utility for Measuring LDL Particle Size.   Several lines of evidence suggest that small, dense low-density lipoprotein (LDL) particles are more highly atherogenic than larger-sized particles, yet the traditional lipid profile cannot discern whether elevated levels of LDL reflect small or large particles. El Harchaoui and colleagues compared the ability of LDL particle number (LDL-P), LDL particle size (LDL-S), and several established cardiovascular risk factors to predict the first cardiac event in almost 3,000 subjects. LDL-S correlated inversely with risk for coronary artery disease, and LDL-P was more predictive than LDL alone; however, after adjusting for high-density lipoprotein cholesterol (HDL-C) and triglycerides, neither test was superior. This study confirms that LDL-P and LDL-S add additional information to cardiovascular risk, but little additional information compared to non–HDL-C. See page 547.


    Valvular Heart Disease
 Top
 Atherosclerosis
 Valvular Heart Disease
 Atrial Fibrillation
 Atrial Fibrillation
 
Rosuvastatin Decreases Rate of AS Progression.   Because degenerative aortic stenosis (AS) shares many of the same risk factors as coronary artery disease, statins may slow the degeneration of the valve. Moura and colleagues studied 121 patients with aortic valve areas of 1.0 to 1.5 cm2. Approximately one-half met NCEP-ATP III guidelines for statin therapy and they received rosuvastatin 20 mg/day for the next 18 months; the other patients did not receive any statin therapy. Serial echocardiograms showed that rosuvastatin significantly decreased the shrinking in aortic valve area (–0.1 vs. –0.05 cm2/year). This preliminary study suggests that statins may be effective in slowing the progression of AS. See pages 554 and 562.


    Atrial Fibrillation
 Top
 Atherosclerosis
 Valvular Heart Disease
 Atrial Fibrillation
 Atrial Fibrillation
 
Both Obesity and Sleep Apnea Are Risk Factors for AF.  
Figure 1
Obesity is known to be a risk factor for atrial fibrillation (AF), but it is unknown if the related condition of obstructive sleep apnea (OSA) is also a risk factor. Gami and colleagues performed a retrospective cohort study of over 3,500 adults who underwent a polysomnography and were followed for a new incidence of AF. Independent predictors of incident AF included both body mass index and a decrease in nocturnal oxygen saturation. This study suggests that both obesity and OSA are risk factors for new-onset AF. See page 565. See figure.


    Atrial Fibrillation
 Top
 Atherosclerosis
 Valvular Heart Disease
 Atrial Fibrillation
 Atrial Fibrillation
 
KCNQ1 Mutation May Predispose to AF.  
Figure 2
The KCNQ1 gene, which forms the a-subunit of the channel that regulates the slow component of the delayed rectifier K+ current, was sequenced by Otway and colleagues in 50 families with potentially familial atrial fibrillation (AF). One missense mutation was identified in a family with a high prevalence of hypertension. Atrial fibrillation was present only in older individuals who had developed atrial dilatation and carried the mutant gene. In vitro transfection studies suggest that the function of the mutant channel is normal at baseline, but when cells are stretched with hypotonic saline, the mutant channels demonstrated several differences from the wild-type cells. These data suggest that this KCNQ1 mutation alone is insufficient to cause AF, but may predispose to AF when the atrium becomes dilated from chronic hypertension. See page 578. See figure.


Related Article

Value of Low-Density Lipoprotein Particle Number and Size as Predictors of Coronary Artery Disease in Apparently Healthy Men and Women: The EPIC-Norfolk Prospective Population Study
Karim El Harchaoui, Wim A. van der Steeg, Erik S.G. Stroes, Jan Albert Kuivenhoven, James D. Otvos, Nicholas J. Wareham, Barbara A. Hutten, John J.P. Kastelein, Kay-Tee Khaw, and S. Matthijs Boekholdt
J. Am. Coll. Cardiol. 2007 49: 547-553. [Abstract] [Full Text] [PDF]




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