Chaim Yosefy

BACKGROUND: Tricuspid regurgitation (TR) is an important predictor of morbidity and mortality in heart failure. We aimed to examine the 3D geometry of the tricuspid valve annulus (TVA) in patients with functional TR, comparing them with patients with normal tricuspid valve function and relating annular geometric changes to functional TR. METHODS AND RESULTS: TVA shape was examined by real-time 3D echocardiography in 75 patients: 35 with functional TR and 40 with normal tricuspid valve function (referent group). The 3D shape of the TVA was reconstructed from rotated 2D planes, and the annular plane was computed by least-squares fitting. Annular area and mediolateral, anteroposterior, and high (superior)-low (inferior) distances were calculated. TR was assessed by vena contracta width. The normal TVA has a bimodal pattern (high-low distance=7.23+/-1.05 mm). High points were located anteroposteriorly, and low points were located mediolaterally. With moderate or greater TR (vena contracta width 5.80+/-2.62 mm), the TVA became dilated (17.24+/-4.75 versus 9.83+/-2.18 cm2, P<0.0001, TR versus referent), more planar with decreased high-low distance (4.14+/-1.05 mm), and more circular with decreased ratio of mediolateral/anteroposterior (1.11+/-0.09 versus 1.32+/-0.09, P<0.0001, TR versus referent). CONCLUSIONS: The normal TVA has a bimodal shape with distinct high points located anteroposteriorly and low points located mediolaterally. With functional TR, the annulus becomes larger, more planar, and circular. These changes in annular shape with TR have potentially important mechanistic and therapeutic implications for tricuspid valve repair.

Lifestyle factors, including nutrition, play an important role in the etiology of Cardiovascular Disease (CVD). This position paper, written by collaboration between the Israel Heart Association and the Israel Dietetic Association, summarizes the current, preferably latest, literature on the association of nutrition and CVD with emphasis on the level of evidence and practical recommendations. The nutritional information is divided into three main sections: dietary patterns, individual food items, and nutritional supplements. The dietary patterns reviewed include low carbohydrate diet, low-fat diet, Mediterranean diet, and the DASH diet. Foods reviewed in the second section include: whole grains and dietary fiber, vegetables and fruits, nuts, soy, dairy products, alcoholic drinks, coffee and caffeine, tea, chocolate, garlic, and eggs. Supplements reviewed in the third section include salt and sodium, omega-3 and fish oil, phytosterols, antioxidants, vitamin D, magnesium, homocysteine-reducing agents, and coenzyme Q10.

BACKGROUND: Mitral valve prolapse (MVP) is a common disorder associated with mitral regurgitation, endocarditis, heart failure, and sudden death. To date, 2 MVP loci have been described, but the defective genes have yet to be discovered. In the present study, we analyzed a large family segregating MVP, and identified a new locus, MMVP3. This study and others have enabled us to explore mitral valve morphological variations of currently uncertain clinical significance. METHODS AND RESULTS: Echocardiograms and blood samples were obtained from 43 individuals who were classified by the extent and pattern of displacement. Genotypic analyses were performed with polymorphic microsatellite markers. Evidence of linkage was obtained on chromosome 13q31.3-q32.1, with a peak nonparametric linkage score of 18.41 (P<0.0007). Multipoint parametric analysis gave a logarithm of odds score of 3.17 at marker D13S132. Of the 6 related individuals with mitral valve morphologies not meeting diagnostic criteria but resembling fully developed forms, 5 carried all or part of the haplotype linked to MVP. CONCLUSIONS: The mapping of a new MVP locus to chromosome 13 confirms the observed genetic heterogeneity and represents an important step toward gene identification. Furthermore, the genetic analysis provides clinical lessons with regard to previously nondiagnostic morphologies. In the familial context, these may represent early expression in gene carriers. Early recognition of gene carriers could potentially enhance the clinical evaluation of patients at risk of full expression, with the ultimate aim of developing interventions to reduce progression.