While viral infection of human hearts can result in damage to the organ, viruses can also be used to treat failing hearts. By Michael Lim
MY first patient with inflammation of the heart as a result of a viral infection (viral myocarditis or VM) was a 15-year-old schoolgirl who had symptoms of fever, cough and runny nose. She continued to go to school and felt increasingly breathless. When her symptoms became unbearable, she was taken to the hospital by her parents and was found to have an enlarged heart on the chest X-ray.
Further investigations showed an enlarged heart with poor heart-pumping function. Fortunately for her, she was responsive to medical treatment and did not require a heart transplant.
Getting a fever, cough and runny nose as a result of a viral infection is very common. While most recover uneventfully, what is not commonly known is that the viruses can enter the blood stream in some cases. Once the virus enters the blood stream, it can infect the heart muscle cells causing cell death and activation of the body’s immune response.
This may cause the body to develop antibodies to the virus and some heart cell proteins. As the immune response slows down, the damaged heart tissue is replaced by scar tissue. The heart chambers may dilate and the heart pump weaken resulting in a permanently swollen and damaged heart (dilated cardiomyopathy).
While adenoviruses, enteroviruses and parvoviruses are the most common viruses associated with VM, other associated viruses include the human herpes virus, Epstein-Barr virus and even Hepatitis C virus.
While the exact incidence of VM is not certain, one study suggests that it is the cause of sudden death in close to 9 per cent and is also identified in 9 per cent of routine postmortem examinations. Most of those with VM may not have symptoms but if there is shortness of breath, chest pain or abnormal heart rhythm, the presence of VM must be considered. The common tests used for the diagnosis of VM has limitations.
Commonly available blood tests to detect damage of heart muscle such as troponin I or cardiac enzymes have a sensitivity of only about 50 per cent. Other commonly used tests include electrocardiography to look for changes in the electrical pattern of the heart and to detect abnormal heart rhythms , and echocardiography using ultrasound techniques to assess heart chamber dilatation and damaged pump function (dilated cardiomyopathy).
For many decades, the diagnosis of VM was dependent on taking a biopsy of the heart muscle. Unfortunately, in the real world, it is estimated that about 17 biopsies of the inner wall of the heart (endomyocardial biopsy) is required to diagnose VM with 80 per cent sensitivity. In real world practice, this is impractical and rarely done, and hence many experts have moved towards non-invasive methods to diagnose VM and to assess the damage to the heart muscle.
The current recommendations from an American College of Cardiology Foundation/American Heart Association/European Society of Cardiology (ACCF/AHA/ESC) scientific statement support a limited role for endomyocardial biopsy in the evaluation of patients with cardiomyopathy.
The most significant development in the diagnosis of VM is the use of magnetic resonance imaging (MRI) of the heart. Developments in Heart MRI technology in recent years has made this the investigation of choice for those suspected to have VM. What it means is that with the use of Heart MRI, for those with viral infections, the presence of VM can be determined more accurately in a safe and non-invasive manner.
While most patients can be managed with medical treatment, those with acute swelling of the heart may require special devices to provide temporary support to the heart. After recovery from VM, a period of avoidance from aerobic exercises is essential; the duration being dependent on the severity of damage to the heart.
For those with dilated cardiomyopathy, fluid restriction may be required. Contrary to expectations, those who had severe fulminant (sudden) VM with compromise of blood pressure at presentation had a better long term outcome than those who had milder non-fulminant VM. In one study over 11 years, more than 90 per cent with fulminant VM were alive compared to 45 per cent for those with non-fulminant VM.
While viral infection of human hearts can result in swelling and damage of the hearts, the irony is that viruses are also used to treat failing hearts of any underlying aetiology. A decrease in the level of a protein pump, SERCA2a, which is required for contraction of heart muscle cells, is associated with decreased pump function of the heart.
The damaged heart cell is like a car with a flat battery (impaired SERCA2a pump). To get the car started again, a new battery must be added to get the car to function well again. The gene for production of SERCA2a has been identified but the challenge is to insert the “battery” into the heart muscle cell. For this, laboratory altered adenoviruses which carry the SERCA2a gene have been used to infect the heart muscle cells and transfer the SERCA2a gene into failing heart muscle cells. Increased SERCA2a production by adenoviral gene transfer in viable human heart cells has been shown to reverse the contractile abnormalities of failing hearts. This technique has tremendous promise for those with failing hearts.
In a way, the relationship between viruses and the heart is like a love-hate relationship. Although viral infections are mostly harmless, they should not be taken lightly if they are associated with shortness of breath, chest pain or abnormal heart rhythm. While viral infections can potentially damage hearts, the appropriate use of viruses as a carrier for genes has brought new hope to those who have weak and failing hearts.
The relationship between viruses and the heart is like a love hate relationship. Although viral infections are mostly harmless, they should not be taken lightly if they are associated with shortness of breath, chest pain or abnormal heart rhythm.