What is cardiomyopathy?

Cardiomyopathy refers to a group of diseases that affect the heart muscle (myocardium). In cardiomyopathy, the heart muscle becomes weakened, enlarged, thickened, or stiffened, leading to impaired function and potentially causing heart failure, arrhythmias (irregular heartbeats), or other complications. There are several types of cardiomyopathy, including:


  • Dilated Cardiomyopathy (DCM): In DCM, the heart chambers become dilated and weakened, leading to decreased pumping ability and systolic dysfunction. This results in decreased blood flow to the body and can lead to heart failure.


  • Hypertrophic Cardiomyopathy (HCM): HCM is characterized by abnormal thickening (hypertrophy) of the heart muscle, particularly of the left ventricle. This can obstruct blood flow out of the heart and increase the risk of arrhythmias and sudden cardiac death.


  • Restrictive Cardiomyopathy (RCM): RCM is characterized by stiffness of the heart muscle, which impairs the heart’s ability to fill with blood properly during the relaxation phase of the cardiac cycle. This can lead to heart failure and other complications.


  • Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC): ARVC is a rare form of cardiomyopathy where the muscle tissue in the right ventricle is replaced by fat and fibrous tissue, leading to arrhythmias and potential risk of sudden cardiac death.


  • Unclassified Cardiomyopathies: There are other types of cardiomyopathies that do not fit neatly into the above categories, such as noncompaction cardiomyopathy or stress-induced cardiomyopathy (Takotsubo cardiomyopathy).



What is the relationship between cardiomyopathy and oxidative stress?

Oxidative stress has been implicated in the development and progression of cardiomyopathy. Several factors contribute to oxidative stress in the heart, including increased production of reactive oxygen species (ROS), decreased antioxidant defenses, mitochondrial dysfunction, inflammation, and ischemia/reperfusion injury.


In cardiomyopathy, the imbalance between ROS production and antioxidant defenses can lead to oxidative damage to lipids, proteins, and DNA within cardiac cells. This oxidative damage can disrupt cellular function, impair myocardial contractility, promote cell death (apoptosis and necrosis), and contribute to the structural and functional changes observed in cardiomyopathy.


Moreover, oxidative stress can exacerbate underlying cardiovascular risk factors and pathological processes associated with cardiomyopathy, such as inflammation, fibrosis, hypertrophy, and endothelial dysfunction. In turn, these processes can further increase ROS production and perpetuate a vicious cycle of oxidative stress and cardiac injury.