Our Focus on Cardiac Disorders
Why is Edgewise Focusing on Hypertrophic Cardiomyopathy?
Patients can experience limited efficacy, inconvenient dosing, and undesirable safety concerns with currently available treatments
Our team of muscle disease experts is dedicated to giving patients better alternatives though the development of novel therapies
Our drug candidates, including EDG-7500, are designed to offer alternative treatment options that can potentially alter the course of cardiac diseases
Healthy Heart vs. Heart with HCM
oHCM Heart Healthy Heart nHCM Heart
About Hypertrophic Cardiomyopathy
HCM, or Hypertrophic Cardiomyopathy, is a common form of inherited heart disease, is chronic and progressive in nature and can be deadly. With time, disease progression can increase the risk of heart failure, stroke, and atrial fibrillation.
People with HCM may experience breathlessness, irregular heartbeats, chest pain, tiredness, dizziness, or even fainting. These symptoms are caused by excessive contraction and thickening (hypertrophy) of the left ventricular wall- the heart’s primary pumping chamber. Symmetrical wall thickening is observed in non-obstructive HCM (nHCM). In contrast, obstructive HCM (oHCM) is characterized by asymmetrical wall thickening that is localized to the septal wall of the left ventricle.
Over time, the thickened muscle stiffens, causing the heart to be unable to properly relax and fill with blood (also known as diastolic dysfunction). Nearly all HCM patients exhibit some degree of diastolic dysfunction, a common feature of other cardiovascular diseases such as heart failure with preserved ejection fraction (HFpEF).
As many as 700,000 individuals in the U.S. have HCM, but a significant portion may not know they have it. HCM is a severe disease that can be diagnosed at any age.
Keep Reading To Learn More About oHCM and nHCM
Two major forms of HCM include obstructive (oHCM) and non-obstructive (nHCM) hypertrophic cardiomyopathy. oHCM pathology is observed in two thirds, while nHCM is present in one third of all individuals with HCM.
In oHCM, as the left ventricle (LV) contracts (systole) to eject oxygenated blood from the heart into systemic circulation, the mitral valve makes physical contact with the hypertrophied septal wall. This contact underlies the basis of the obstructed ejection of blood through the LV outflow tract (LVOT) creating a pressure difference, or gradient (LVOT-G) between the LV cavity and systemic circulation. Most common tool to measure LVOT-G is via Doppler echocardiography. The limitation of blood pumped by the heart causes several of the symptoms that oHCM patients experience.
The hypertrophy is more symmetrically distributed in the LV walls in nHCM and the mitral valve does not make contact with the LV wall during contraction. Therefore, nHCM patients do not develop LVOT obstruction nor pressure gradient. Due to LV hypertrophy and stiffness, LV relaxation is impaired and LV filling with blood (diastole) is significantly reduced. This LV impairment is termed diastolic dysfunction.
The diastolic dysfunction present in oHCM and nHCM patients leads to an increase in left atrial pressure and enlargement of the left atrium (LAE). The severity of LAE, a hallmark of cardiac structure remodeling, is a key predictor of adverse outcomes, which is assessed by echocardiography.