By Dr Michael Lim
Mon, May 30, 2011
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.
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).
Viruses
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.
http://health.asiaone.com/Health/Health%2BMatters/Story/A1Story20110530-281363.html
Autoantibodies against cardiac troponin I in patients presenting with myocarditis
Akira Matsumoria,
, 
, , Toshio Shimadab, Hiroaki Hattoric, Miho Shimadaa and Jay W. Masond
Received 19 August 2010;
revised 22 November 2010;
accepted 18 February 2011.
Available online 22 March 2011.
.
Summary
.
Background
.
2009
Myocarditis....
Autoantibodies against cardiac troponin I (cTnI) play an important role in the pathogenesis of experimental cardiomyopathy. We developed a new method to measure anti-cardiac troponin I autoantibody (Anti-cTnIAAB) in patients with myocarditis with or without HCV infection.
Methods
Patients with heart failure for up to 2 years, without a distinct cause, were enrolled in the Myocarditis Treatment Trial between 1986 and 1990. Frozen blood samples were available from 1315 to 2233 enrolled patients. Anti-cTnIAAB was determined by a two-step immunoassay.
Results
The mean (±SEM) value of serum Anti-cTnIAAB titer in the 1315 patients was 0.067 ± 0.003 arbitrary unit (AU), significantly higher than in 1115 healthy volunteers (0.053 ± 0.002 AU, P < 0.01). The mean Anti-cTnIAAB titer in 88 patients whose endomyocardial biopsies (EMB) satisfied the diagnostic Dallas criteria was 0.086 ± 0.010 AU, versus 0.066 ± 0.004 AU in 1227 patients whose EMB did not satisfy these criteria. The mean Anti-cTnIAAB in both groups was significantly higher than that measured in the healthy volunteers (P < 0.01). The mean Anti-cTnIAAB titer in the 88 patients with Dallas criteria-confirmed myocarditis tended to be higher than in the other 1227 patients. Among the 88 patients with Dallas criteria-confirmed myocarditis, the mean Anti-cTnIAAB titer in 5 patients infected with the hepatitis C virus infection (HCV) was significantly higher (0.146 ± 0.047 AU) than in 83 patients without HCV infection (0.082 ± 0.010 AU, P < 0.05).
Conclusions
Elevated autoantibody titers against cTnI were detected in patients with myocarditis, and were higher in HCV-infected patients. The presence of Anti-cTnIAAB might correlate with inflammation and viral infection of the heart.
Methods
Patients with heart failure for up to 2 years, without a distinct cause, were enrolled in the Myocarditis Treatment Trial between 1986 and 1990. Frozen blood samples were available from 1315 to 2233 enrolled patients. Anti-cTnIAAB was determined by a two-step immunoassay.
Results
The mean (±SEM) value of serum Anti-cTnIAAB titer in the 1315 patients was 0.067 ± 0.003 arbitrary unit (AU), significantly higher than in 1115 healthy volunteers (0.053 ± 0.002 AU, P < 0.01). The mean Anti-cTnIAAB titer in 88 patients whose endomyocardial biopsies (EMB) satisfied the diagnostic Dallas criteria was 0.086 ± 0.010 AU, versus 0.066 ± 0.004 AU in 1227 patients whose EMB did not satisfy these criteria. The mean Anti-cTnIAAB in both groups was significantly higher than that measured in the healthy volunteers (P < 0.01). The mean Anti-cTnIAAB titer in the 88 patients with Dallas criteria-confirmed myocarditis tended to be higher than in the other 1227 patients. Among the 88 patients with Dallas criteria-confirmed myocarditis, the mean Anti-cTnIAAB titer in 5 patients infected with the hepatitis C virus infection (HCV) was significantly higher (0.146 ± 0.047 AU) than in 83 patients without HCV infection (0.082 ± 0.010 AU, P < 0.05).
Conclusions
Elevated autoantibody titers against cTnI were detected in patients with myocarditis, and were higher in HCV-infected patients. The presence of Anti-cTnIAAB might correlate with inflammation and viral infection of the heart.
Keywords: Myocarditis; Cardiac troponin I; Autoantibody; Hepatitis C virus
....
2009
Myocarditis....
Other viruses implicated in myocarditis include influenza virus, echovirus, herpes simplex virus, varicella-zoster virus, hepatitis, Epstein-Barr virus, and cytomegalovirus. Hepatitis C, in particular, is becoming a major focus of research.
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