Heart Failure (HF) is a chronic condition that affects more than 26 million people globally. Over five million adults in the U.S. suffer from HF and it remains a leading cause of death and hospitalization, with associated healthcare costs exceeding $30 billion annually. People with HF suffer from shortness of breath, rapid heart rate, edema, reduced exercise capacity, often struggle with simple daily activities, and are frequently hospitalized. For many, these symptoms significantly reduce quality of life.
In a healthy heart, the left ventricle (lower left chamber) relaxes to fill with blood from the atrium (upper left chamber). Once filled, the left ventricle pumps the blood to the body. In heart failure, there is insufficient output from the heart. In heart failure with reduced ejection fraction (HFrEF), also known as systolic heart failure, this results from reduced contraction of the left ventricle such that not enough blood is pumped into the circulation. In heart failure with preserved ejection fraction (HFpEF), also known as diastolic heart failure, the left ventricle becomes stiff and does not relax normally. As a result, it cannot fill properly, and pressure begins to increase in the left heart chambers and in the lungs. The increased pressure in the lungs is the cause of shortness of breath.
HFpEF is associated with several co-morbidities including obesity, hypertension, diabetes, and older age. It is thought that HFpEF involves activation of the coronary micro-vascular endothelium (the lining of the small blood vessels in the heart) driven by a systemic pro-inflammatory state resulting from these co-morbidities. This systemic inflammation-induced endothelial dysfunction and activation leads to leakage of inflammatory cells from the circulation into the cardiac tissue. The subsequent production of a series of cytokines and increased oxidative stress leads to increased fibrosis, stiffness, and may impair cardiac contractile cell function.
There have been no significant treatment advances in HFpEF in the past 20 years; the primary therapy remains diuretics. Cardiol is dedicated to improving patients’ outcomes with innovative nanotherapeutics that target anti-inflammatory drugs to areas of cardiac tissue having significant inflammation and increased fibrosis.