FT011 Prevents fibrosis (blue strain) from developing following heart disease

Diabetic Cardiomyopathy

Congestive cardiac failure (CHF) is a major and growing public health problem in industrialized nations, estimated to reach prevalence in the US of 10 million by 2007. The ability to non-invasively assess cardiac systolic function with echocardiography has brought with it the realization that approximately 40% of hospitalizations for heart failure occur in patients with preserved left ventricular systolic function. Diabetic patients are particularly prone to developing CHF with preserved systolic function even in the absence of either demonstrable ischemia or elevated blood pressure, as a consequence of a diabetic cardiomyopathy.

Diabetic patients are particularly prone to developing congestive heart failure (CHF) with preserved systolic function even in the absence of either demonstrable ischemia or elevated blood pressure, as a consequence of a diabetic cardiomyopathy. Such failure may be a consequence of changes in the visco-elastic properties of the heart, and are potentially mediated by inflammatory processes leading to matrix accumulation and fibrosis, which contribute to impaired ventricular filling in the later, passive phase of diastolic relaxation. Despite current therapeutic strategies, these pathological processes continue, resulting in increased morbidity and mortality in CHF patients. This indicates a clear unmet clinical need to develop new therapeutic agents. Accordingly, strategies that directly target pathological accumulation of ECM have been advocated as potential therapies for the treatment and prevention of kidney and heart failure.