At Cardiol, we believe in the application of science to develop therapies to improve the quality of life for people living with chronic inflammation, with an initial focus on heart failure.
Acute inflammation is a protective response of the body’s immune system to danger signals, including infections and damaged cells, to eliminate infection and repair damaged tissues. Inflammation leads to increased blood flow and permeability of blood vessels so that immune cells can access the site of infection or damage. Following tissue repair and elimination of the danger signal, it is vital that the initial inflammatory and reparative response be switched off. This is usually a result of the accumulated inflammatory cells undergoing cell death by apoptosis and their uptake by macrophages via efferocytosis, a process which induces an anti-inflammatory response, terminating the inflammation. A failure of this off switch results in ongoing chronic inflammation, which is seen in many disorders including heart failure.
One of the factors predisposing people to heart failure is older age. It is widely recognized that ageing is associated with an increase in low grade background inflammation, which, in turn, appears to result from a failure of efferocytosis of apoptotic cells. The effect of chronic inflammation in the heart is an increase in cell death of cardiomyocytes (heart muscle cells) and increased fibrogenesis (the laying down of scar tissue). The result is reduced heart function due to the weakening and stiffening of the heart muscle.
The rationale for using cannabidiol to treat patients with inflammatory heart conditions is based on extensive pre-clinical investigations by Cardiol and others in models of cardiovascular inflammation which have demonstrated that cannabidiol has significant anti-inflammatory and anti-fibrotic activity, as well as anti-ischemic, and anti-arrhythmic action, and that it improves myocardial function in models of heart failure. In pre-clinical models of cardiac injury, cannabidiol was shown to be cardio-protective by reducing cardiac hypertrophy, fibrosis, and the production of certain re-modelling markers, such as cardiac B-type Natriuretic Peptide (BNP), which is typically elevated in patients with heart failure. These data were accepted for presentation at the American College of Cardiology’s 69th Annual Scientific Session held virtually on March 28 – 30, 2020.