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/pdf/acc-aha-2005-guideline-update-for-the-diagnosis-and-4hik65ngbe.pdf

ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult

ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure).

Mariell Jessup, MD, FACC, FAHA, Chair [*][1]

William T. Abraham, MD, FACC, FAHA[†][2]

Donald E. Casey, MD, MPH, MBA[‡][3]

Arthur M. Feldman, MD, PhD, FACC, FAHA[§][4]

Gary S. Francis, MD, FACC, FAHA[§][4]

Theodore G. Ganiats, MD[∥][5]

Marvin A. Konstam, MD, FACC[¶][6]

Donna M.

/pdf/2009-focused-update-incorporated-into-the-acc-aha-2005-3z9lhvyqwq.pdf

2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: Developed in Collaboration With the International Society for Heart and Lung Transplantation

The clinical use of anthracyclines like doxorubicin and daunorubicin can be viewed as a sort of double-edged sword. On the one hand, anthracyclines play an undisputed key role in the treatment of many neoplastic diseases; on the other hand, chronic administration of anthracyclines induces cardiomyopathy and congestive heart failure usually refractory to common medications. Second-generation analogs like epirubicin or idarubicin exhibit improvements in their therapeutic index, but the risk of inducing cardiomyopathy is not abated. It is because of their janus behavior (activity in tumors vis-a-vis toxicity in cardiomyocytes) that anthracyclines continue to attract the interest of preclinical and clinical investigations despite their longer-than-40-year record of longevity. Here we review recent progresses that may serve as a framework for reappraising the activity and toxicity of anthracyclines on basic and clinical pharmacology grounds. We review 1) new aspects of anthracycline-induced DNA damage in cancer cells; 2) the role of iron and free radicals as causative factors of apoptosis or other forms of cardiac damage; 3) molecular mechanisms of cardiotoxic synergism between anthracyclines and other anticancer agents; 4) the pharmacologic rationale and clinical recommendations for using cardioprotectants while not interfering with tumor response; 5) the development of tumor-targeted anthracycline formulations; and 6) the designing of third-generation analogs and their assessment in preclinical or clinical settings. An overview of these issues confirms that anthracyclines remain "evergreen" drugs with broad clinical indications but have still an improvable therapeutic index.

/pdf/anthracyclines-molecular-advances-and-pharmacologic-4vygbx1i0b.pdf

Anthracyclines: Molecular Advances and Pharmacologic Developments in Antitumor Activity and Cardiotoxicity

Increasing evidence in both experimental and clinical studies suggests that oxidative stress plays a major role in the pathogenesis of both types of diabetes mellitus. Free radicals are formed disproportionately in diabetes by glucose oxidation, nonenzymatic glycation of proteins, and the subsequent oxidative degradation of glycated proteins. Abnormally high levels of free radicals and the simultaneous decline of antioxidant defense mechanisms can lead to damage of cellular organelles and enzymes, increased lipid peroxidation, and development of insulin resistance. These consequences of oxidative stress can promote the development of complications of diabetes mellitus. Changes in oxidative stress biomarkers, including superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase, glutathione levels, vitamins, lipid peroxidation, nitrite concentration, nonenzymatic glycosylated proteins, and hyperglycemia in diabetes, and their consequences, are discussed in this review. In vivo studies of the effects of various conventional and alternative drugs on these biomarkers are surveyed. There is a need to continue to explore the relationship between free radicals, diabetes, and its complications, and to elucidate the mechanisms by which increased oxidative stress accelerates the development of diabetic complications, in an effort to expand treatment options.

Diabetes, oxidative stress, and antioxidants: a review

Doxorubicin (Adriamycin) has been used in oncologic practice since the late 1960s. It held promise as a powerful drug in the fight against cancer. The tumors most commonly responding to doxorubicin when it is given as a single agent or in combination with other antitumor agents include breast and esophageal carcinomas; osteosarcoma, Kaposi's sarcoma, and soft-tissue sarcomas; and Hodgkin's and non-Hodgkin's lymphomas. Other cancers that are less responsive to doxorubicin but that are still treated with the drug because of its overall benefits include gastric, liver, bile-duct, pancreatic, and endometrial carcinomas. However, reports of fatal cardiotoxic effects of doxorubicin have . . .

Doxorubicin-Induced Cardiomyopathy

Subcellular effects of adriamycin in the heart: A concise review

Effects of an antioxidant, vitamin E, and a membrane stabilizing agent, zinc, were examined on the isoproterenol-induced changes in the rat myocardium. Isoproterenol treatment (80 mg/kg given over 2 days in two equal doses) caused arrhythmias and 25% mortality within 24 h of the last injection. The ultrastructural changes in the subendocardium and in focal areas of the subepicardium included swelling of mitochondria, loss of myofibrils, cell necrosis, fibrosis, and infiltration of the affected areas by polymorphonucleocytes. Both creatine phosphate and adenosine triphosphate levels were markedly decreased in hearts from isoproterenol-treated animals. Pretreatment of the animals with vitamin E (10 mg X kg-1 X day -1 for 2 weeks) or zinc (10 mg/kg ZnSO4, twice a day for 7 days) prevented these deleterious effects of isoproterenol. Animals maintained on vitamin E deficient diet for 8 weeks were found to be more sensitive to isoproterenol-induced changes and this increased sensitivity was reversed by a 2-week feeding of the animals on the normal diet coupled with vitamin E treatment. Based on the data obtained in this study it is proposed that catecholamine-induced changes may involve free radicals, which by promoting lipid peroxidation may increase membrane permeability and lead to the development of cardiomyopathy.

Role of free radicals in catecholamine-induced cardiomyopathy

The Utility of Cardiac Biomarkers, Tissue Velocity and Strain Imaging, and Cardiac Magnetic Resonance Imaging in Predicting Early Left Ventricular Dysfunction in Patients With Human Epidermal Growth Factor Receptor II–Positive Breast Cancer Treated With Adjuvant Trastuzumab Therapy

Pawan K. Singal

Papers

Doxorubicin-Induced Cardiomyopathy

Subcellular effects of adriamycin in the heart: A concise review

Role of free radicals in catecholamine-induced cardiomyopathy

The Utility of Cardiac Biomarkers, Tissue Velocity and Strain Imaging, and Cardiac Magnetic Resonance Imaging in Predicting Early Left Ventricular Dysfunction in Patients With Human Epidermal Growth Factor Receptor II–Positive Breast Cancer Treated With Adjuvant Trastuzumab Therapy

Role of oxidative stress in transition of hypertrophy to heart failure