Researchers are continually searching for more information on the potential causes, treatments and methods of preventing cardiomyopathy. Recent research includes:

• Researchers believe that many cases of idiopathic dilated cardiomyopathy (DCM), which account for about 50 percent of all DCM cases, may be genetically related. In recent years, a number of genes have been uncovered that are linked to DCM, including genes that code for heart and skeletal muscle. Scientists have also found that a significant number of people with dilated cardiomyopathy have autoantibodies in their bloodstream that target heart cells, and their family members also have these autoantibodies. This research may increase our ability to recognize people at greater risk for DCM and may one day even provide new treatment options.
  
  
• Researchers discovered the presence of a type of virus called Coxsackie B in heart tissue samples taken from patients with dilated cardiomyopathy who had previously been classified as having idiopathic DCM. In a significant number of patients, the virus was self-replicating. Further research may result in the use of antiviral agents to combat the Coxsackie B virus as part of the treatment of DCM.
  
  
• Studies have linked hypertrophic cardiomyopathy with irregularities in the connective tissue of the heart. Some autopsies have shown that patients with hypertrophic cardiomyopathy have increased amounts of connective tissue in their hearts. The connective tissue may be arranged in a disorganized and abnormal pattern, leading researchers to speculate that this pattern itself may be a cause of hypertrophic cardiomyopathy.
  

Clinical studies have also focused on a number of factors that may affect the development of cardiomyopathy in both children and adults. Other clinical studies have examined prevention and treatment of the disease. Clinical research studies include:

• Identifying factors that may raise or lower the risk of death in cardiomyopathy patients. Researchers have examined elements such as episodes of fainting, age of diagnosis, extent of muscle thickening and family history of sudden death. This research can help with evaluation, treatment and prognosis.
  
  
• Evaluating drugs that may decrease the extent of muscle thickening. Researchers are also studying the use of pacemakers, including the use of cardiac resynchronization therapy (CRT) to relieve symptoms and delay the need for heart transplantation. Both of these areas need additional studies to determine their effectiveness in patients. Although researchers have so far been stymied in their search for a truly artificial heart, some centers have experienced success with left ventricular assist devices (LVAD). These devices help failing hearts pump effectively. They were originally designed for use as a bridge to transplantation, but in recent years, physicians have used them for longer-term therapy with limited success.
  
  
• Assessing the use of implantable cardioverter defibrillators (ICDs) to prevent sudden cardiac death in patients with hypertrophic cardiomyopathy. They are focusing particularly on patients who are high risk for arrhythmias.
  
  
• Evaluating the use of enzyme therapy to improve cardiac and skeletal muscle function in infants.
  
  
• Examining the association of fatty acid oxidation disorders and cardiomyopathy. These are a group of inherited metabolic conditions that lead to an accumulation of fatty acids in the body and a decrease in cell metabolism. These conditions can cause recurrent episodes of hypoglycemia. Clinical studies are evaluating the disorders in terms of type, severity and treatment and their possible role in causing cardiomyopathy.