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Commencing Volume 19, Issue 1, MedReviews has ceased the publication of this journal. Reviews in Cardiovascular Medicine will continue to be published by IMRPress, Ltd. (www.imrpress.org)

Volume 5, No 2 - Spring 2004

Volume 5, No 2 - Spring 2004

Table of Contents

The Role of Aldosterone and Aldosterone-Receptor Antagonists in Heart Failure Treatment Review
Prolonged overactivation of neurohormonal mechanisms in heart failure produces deleterious effects on the cardiovascular system and leads to poor prognosis. Angiotensinconverting enzyme (ACE) inhibitors and ß-blockers have been shown to interrupt this excessive overactivity and improve survival. Activation of the renin-angiotensin system leads to increased synthesis of aldosterone in heart failure. Some aldosterone production is independent of ACEs; therefore, ACE inhibition does not entirely suppress the excessive formation of aldosterone. An excess of aldosterone in heart failure leads to sodium retention and myocardial fibrosis. The use of aldosterone antagonists, combined with standard therapy for heart failure, improves morbidity and mortality. [Rev Cardiovasc Med. 2004;5(2):71-81]
Stem Cell Transplantation in Myocardial Infarction Treatment Update
Congestive heart failure, which is most commonly caused by myocardial infarction, is the most frequent cause of hospitalization in the United States in patients over the age of 65. Although current pharmacotherapy can inhibit neurohormonal activation, this falls short of preventing left ventricular remodeling and the development of congestive heart failure. Stem cells are undifferentiated pluripotent cells that have the potential to proliferate and differentiate into cardiomyocytes. Cellular cardiomyoplasty, which is the replacement or regeneration of cardiomyocytes through cell transplantation, is a potential therapeutic approach to prevent left ventricular remodeling after myocardial infarction. The majority of the data on stem cell transplantation comes from preclinical animal studies. Although the results are interesting and perhaps safe, early phase I clinical studies are small and very preliminary. Data from large, randomized controlled trials are needed to clarify the short- and long-term effects of cellular cardiomyoplasty. [Rev Cardiovasc Med. 2004;5(2):82-98]
Ximelagatran: A Novel Oral Direct Thrombin Inhibitor for Long-Term Anticoagulation New Drug Review
The ideal anticoagulant agent would have a fixed oral dose without need for dose adjustment, a wider therapeutic window than that of warfarin, and acceptable bleeding risks without the need for routine coagulation monitoring. Ximelagatran is a new oral agent that, when converted to its active form, melagatran, directly inhibits thrombin, thus blocking its activity and modulating several of its key functions. For the prevention of venous thromboembolism after orthopedic surgery, treatment of venous thromboembolism, and prevention of stroke in patients with atrial fibrillation, clinical trials indicate that ximelagatran meets the criteria for a superior anticoagulant. [Rev Cardiovasc Med. 2004;5(2):99-103]
Severe Reversible Left Ventricular Systolic and Diastolic Dysfunction Due to Accidental Iatrogenic Epinephrine Overdose
Catecholamine-induced cardiomyopathy due to chronic excess of endogenous catecholamines has been recognized for decades as a clinical phenomenon. In contrast, reports of myocardial dysfunction due to acute iatrogenic overdose are rare. A 35-year-old woman whose cervix uteri was inadvertently injected with 8 mg of epinephrine developed myocardial stunning that was characterized by severe hemodynamic compromise, profound, albeit transient, left ventricular systolic and diastolic dysfunction, and only modestly elevated biochemical markers of myocardial necrosis. Our case illustrates the serious consequences of medical errors that can be avoided through improved medication labeling and staff supervision. [Rev Cardiovasc Med. 2004;5(2):130–133]