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Background: Appropriate cardiac hypertrophy (CH) is necessary in several clinical settings, such as pulmonary artery banding in the two-stage arterial switch operation for transposition of the great arteries. Pressure-overload CH, however, produces ventricular dysfunction due to structural and molecular changes. Case presentation A previously healthy young man in his late 20s was presented to the emergency department with a 2-day history of persistent pleuritic chest pain and shortness of breath associated with diaphoresis, restlessness, palpitations, vomiting and polydipsia. He denied fever, cough or other constitutional symptoms. Hypertrophy is the cumulative effect of increased protein synthesis, suppressed protein degradation, or both 5-7. Data show that clenbuterol acts to induce mild cardiac hypertrophy in cardiac myocytes via paracrine signalling involving fibroblast-derived IGF-1. Cardiac Fibroblast Introduction To date, the only effective treatment for severe end-stage heart failure has been cardiac transplantation. High-dose clenbuterol (a selective β 2-adrenergic agonist) has been proposed to promote myocardial recovery during left ventricular assist device (LVAD) support, but its effects on cardiac and skeletal muscle are largely unknown. Clenbuterol is known to produce skeletal 12 and cardiac hypertrophy, to affect EC coupling and cellular metabolism, 13 gene expression and myocardial function 14–16 in normal hearts
Hypertrophy is the cumulative effect of increased protein synthesis, suppressed protein degradation, or both 5-7. Purpose Chronic administration of pharmacological levels of β2-agonists have been shown to have toxic effects on the heart; however, no data exist on cardiac function after chronic clenbuterol administration. Clenbuterol (Clen), a beta(2)-agonist, is known to produce skeletal and myocardial hypertrophy. This compound has recently been used in combination with left ventricular assist devices for the treatment of end-stage heart failure to reverse or prevent the adverse effects of unloading-induced myocardial atrophy. Methods: Cardiac hypertrophy was induced in 7-week-old Sprague-Dawley rats by daily injections of clenbuterol for 3 weeks. Thyroxine and isoproterenol were also used to produce cardiac hypertrophy to serve as positive controls for physiological and pathological hypertrophy, respectively. Ical unloading using left ventricular assist device (LVAD) support is combined with pharmacological therapy aimed at maximizing reverse remodeling and then followed by the use of the 2 adrenergic agonist clenbuterol to stimulate physio-logical hypertrophy and improve cardiac function (the Harefield Protocol). The combination of anabolic steroids and clenbuterol can be the cause of myocardial infarction, even with a normal coronary artery in angiogram due to coronary spasm [ 31 ] www.asiancupid.eu/activity/p/139779/
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