Double Blind Placebo Controlled Study of Cyclosporin A in Patients With Left Ventricular Hypertrophy Caused by Sarcomeric Gene Mutations
Cyclosporine A
Maladie de la valve aortique+9
+ Sténose aortique sous-valvulaire
+ Sténose de la valve aortique
Étude thérapeutique
Résumé
Date de début de l'étude : 1 décembre 1999
Date à laquelle le premier participant a commencé l'étude.Hypertrophic cardiomyopathy (HCM) is a genetic cardiac disease characterized by marked increase in cardiac mass caused by proliferation/hypertrophy of several cell types (myocytes, fibroblasts, smooth muscle cells, and endothelial cells). There is often associated left ventricular (LV) diastolic dysfunction and myocardial ischemia. The severity of the LV hypertrophy, diastolic dysfunction, and myocardial ischemia are important determinants of clinical course. In several animal models of LV hypertrophy, calcineurin has been implicated in the development of myocardial hypertrophy, leading to cardiac dilatation and failure. Inhibitors of calcineurin (Cyclosporin A and FK506) have been shown to prevent the development of cardiac hypertrophy in these animal models, where cardiac hypertrophy is related to sarcomeric dysfunction. We propose to study the ability of Cyclosporin A (CsA) to reduce LV mass, and to improve symptoms, LV diastolic function, and myocardial perfusion in HCM caused by sarcomeric gene mutations.
Protocole
Cette section fournit des détails sur le plan de l'étude, y compris la manière dont l'étude est conçue et ce qu'elle évalue.32 participants à inclure
Nombre total de participants que l'essai clinique vise à recruter.Traitement
Éligibilité
Les chercheurs recherchent des patients correspondant à une certaine description appelée critères d'éligibilité : état de santé général ou traitements antérieurs du patient.Tout sexe
Le sexe biologique des participants éligibles à s'inscrire.Volontaires sains non autorisés
Indique si les individus en bonne santé et ne présentant pas la condition étudiée peuvent participer.Conditions
Pathologie
Critères
Patients of either gender, aged 18-75 years, with HCM caused by sarcomeric gene mutations determined by existing protocols. LV wall thickness of greater than or equal to 20 mm measured in any LV segment by MRI. Severe symptoms refractory to medical treatment (New York Heart Association functional class III or IV). No LV outflow tract obstruction at rest greater than 30 mm Hg as determined by cardiac catheterization. No coronary artery disease (greater than 50% arterial luminal narrowing of a major epicardial vessel). No chronic atrial fibrillation. No bleeding disorder (PTT greater than 35 sec, pro time greater than 14 sec, platelet count less than 154 k/mm(3). No anemia (Hb less than 12.7 g/dl in males and less than 11.0 g/dl in females). No renal impairment (serum creatinine greater than 1.3 mg/dl). No hepatitis B or C; nor unexplained abnormal LFTs. No inability to estimate LV wall thickness. No positive urine pregnancy test. No pregnant or lactating female patients. No concurrent use of immunosuppressives or steroids. No diabetes mellitus. No history of malignancy other than skin tumors (squamous and basal cell) in the last 5 years. No condition that excludes the patient from undergoing an MRI test.
Centres d'étude
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National Heart, Lung and Blood Institute (NHLBI)
Bethesda, United StatesOuvrir National Heart, Lung and Blood Institute (NHLBI) dans Google Maps