Dedication: A Tribute to Dr. Norman Alpert. Preface. Acknowledgments. nI: Heart Failure and Therapies. 1. Pathophysiology of Heart Failure: Role of Oxygen Free Radicals; J. Kalra. 2. Therapeutics in Congestive Heart Failure: From Hemodynamics to Neurohormones; S.R. Goldsmith. 3. Dilated Cardiomyopathies and Congestive Heart Failure; B. Maisch, et al. 4. The Failing SHHF Rat Heart; R.A. Altschuld, et al. 5. Increased Expression of Na+-Ca2+ Exchanger in the Myocardium. Impact on Contractility and Arrhythmogenesis in Heart Failure; W. Schillinger, G. Hasenfuss. 6. Sarcoplasmic Reticulum Proteins and Potential Targets for Gene Therapy of Heart Failure; J.M.J. Lamers, et al. 7. Sarcoplasmic Reticulum Gene Expression of Ca2+-Cycling Proteins as a Target for the Treatment of Heart Failure; T. Netticadan, et al. 8. Effects of the Beta-Adrenoceptor Blocker Carvedilol in Children with Myocardial Failure; H. Scholz, et al. 9. The Contractile and Neurohormonal Roles of Phospholamban in Heart Failure; R. Dash, E.G. Kranias. 10. Annexins: Roles in the Regulation of Ca2+ Handling Proteins During Heart Failure; E. Camors, et al. 11. Modulators of Myofibrillar Function: Implications in Myocardial Failure; P. Vanburen, et al. nII: Remodeling and Heart Failure. 12. Structural Remodeling of Cardiac Myocytes in Hypertrophy and Progression to Failure; A.M. Gerdes, Xuejun Wang. 13. Three-Dimensional Imaging of Microvascular Morphology and Remodeling in Acute and Chronic Myocarditis; A. Takeda, et al. 14. Alterations in Hemodynamic and Neurohumoral Responses to Exercise in Swine with Left Ventricular Remodeling Early After Myocardial Infarction. Role of Blunted NO Bioavailability? D.B. Haitsma, et al. 15. Sheep Models of Postinfarction Left Ventricular Remodeling; L.H. Edmunds, et al. 16. Echocardiographic Characterizatoin of the Cardiovascular Phenotype in Mouse Models; B.D. Hoit. 17. A Novel Role for Cytokine Signaling in Cardiac Remodeling; K. Yamauchi-Rakihara, et al. 18. Effects of Angiotensin II Receptor Blockade and Angiotensin Converting Enzyme Inhibitor on Ventricular Remodeling After Myocardial Infarction: With Special References to Sarcoplasmic Reticulum and its mRNA; E. Geshi, et al. 19. The Effect of Bradykinin on the Remodeling of Pressure-Overloaded Myocardium; S. Mochizuki, et al. 20. Catecholamines and Cardiac Remodeling; H.-G. Zimmer. 21. Matrix Degradative Enzyme Activities on Cardiac Remodeling in Heart Failure; N. Makino, et al. 22. On Atrial Remodeling and Drug Treatment of Atrial Fibrillation; L. Szekeres. nIII: Biology of Heart Failure. 23. Infarct Scar. Living Tissue; K.T. Weber. 24. The Use of Bone Marrow Mesenchymal Stem Cells to Repair the Infarcted Heart; S. Tomita, et al. 25. Role of Na+/CA2+ Exchange in Contraction and Relaxation in Immature Ventricular Myocytes; S. Srivstava, et al. 26. Is an Intracrine Renin-Angiotensin System Involved in the Control of Cardiovascular Function? W.C. de Mello, R.N. Re. 27. Structural Substrates Involved in the Development of Severe Arrhythmias in Hypertensive Rat and Aged Guinea Pig Hearts; N. Tribul
According to the World Health Report (2000 http:/ /www. who. int/whr), of the 55 million deaths worldwide in 1999, more than 16 million were secondary to car diovascular complications. With the prospect of world population increasing from the current level of 6 billion to 9 billion by the middle of this century, the burden of cardiac disease is going to increase astronomically. Furthermore, scientists are being challenged not only to reduce mortality, but also to improve quality of life. Thus, more than ever, intellectuals from different disciplines including biology, sociology, informatics and health care have to join forces to meet the mandate. The World Heart Congress with a focus on "Frontiers in Cardiovascular Health" held in Winnipeg during July 6-11, 2001, made a unique attempt to bring these specialists together to brainstorm and map out the course of action for cardiovascular research and health in the next century. Anytime there is a relative increase in the workload on the heart, there are adap tive myocardial as well as humoral responses. When these adaptations or remodel ing at the organ, subcellular or gene level, become inadequate for a proper tissue perfusion, the condition of heart failure ensues. Prevention of the factors leading to the relative increase in workload as well as a better understanding of the adap tive responses and their failure are some of the hopes to combat the morbidity and mortality due to heart failure.
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