Background: Inflammation and matrix degradation may play a pathogenic role in chronic heart failure (CHF), and therefore, we examined whether thalidomide, a drug with potential immunomodulating and matrix-stabilizing properties, could improve left ventricular (LV) function in patients with CHF secondary to idiopathic dilated cardiomyopathy (IDCM) or coronary artery disease (CAD).
Methods And Results: Fifty-six patients with CHF and an LV ejection fraction (LVEF) <40% who were already on optimal conventional cardiovascular treatment were randomized to thalidomide (25 mg QD increasing to 200 mg QD) or placebo and followed up for 12 weeks. Our main findings were as follows: (1) During thalidomide treatment but not during placebo, there was a marked increase in LVEF (&7 EF units) along with a significant decrease in LV end-diastolic volume and heart rate.
Background: Congestive heart failure (CHF) is characterized by enhanced immune activation, which possibly plays a pathogenic role in this disorder. We therefore examined whether immunomodulation with thalidomide could improve cardiac performance in patients with CHF.
Methods: Nine patients with chronic symptomatic CHF and left ventricular ejection fraction (LVEF) <40%, who were receiving "optimal" conventional cardiovascular treatment, were given 200 mg thalidomide daily in an open design for a period of 6 weeks.
Objective: Heart failure is associated with alterations in contractile parameters and accompanied by abnormalities in intracellular calcium homeostasis. Sarcoplasmic reticulum Ca(2+) ATPase (SERCA2) and phospholamban (PLB) are important in intracellular calcium cycling. The aim of the present study was to examine mechanisms causing reductions in SERCA2 activity in the failing heart.
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