Immunosuppression Improves LV Function in Virus-Negative Inflammatory Cardiomyopathy

Shelley Wood

September 03, 2008

September 3, 2008 (Munich, Germany) - A small study in patients with virus-negative inflammatory cardiomyopathy indicates that six months of immunosuppressive therapy can improve left ventricular function and results in a disappearance of inflammatory infiltrates. According to Dr Andrea Frustaci (La Sapienza University, Rome, Italy), who presented the results during the final hotline session of the European Society of Cardiology Congress 2008, the findings justify a strategy of first testing patients for persistent viral load and, if negative, proceeding with immunosuppressive therapy.

As he explained in his presentation, the role of immunosuppressive therapy in inflammatory cardiomyopathy has been debated because of controversial results in children and adults presenting with either cardiac arrhythmias or heart failure. Previous studies of immunosuppression in inflammatory cardiomyopathy have produced mixed results, but retrospective analyses of these studies have suggested that the key is to first distinguish between virus-negative patients and virus-positive patients, in whom antiviral agents may be effective but immunosuppression may be harmful.

For their study, Frustaci et al randomized 85 patients with active lymphocytic myocarditis and more than six months worth of LV dysfunction to immunosuppression (1 mg/kg daily prednisone for four weeks, followed by a 0.33 mg/kg daily dose for five months) and azathioprine (2 mg/kg daily for six months) or to placebo. At baseline, all patients had a mean left ventricular ejection fraction (LVEF) of 27% and most were in NYHA heart failure class 3 or 4.

At six months, however, 88% of patients in the immunosuppression group had improved LV diameter and contractility, defined as a >10% increase in EF and reduction in LV dimension, whereas LV function in the placebo group actually worsened over the study period. Even in patients in the immunosuppression group with the most advanced disease, left ventricular end diastolic dimension (LVEDD) improved by up to 90 mm.

Changes in LV Measurements Following Immunosuppressive Therapy

End point Baseline 6 mo
LVEF (%) 26.4 48.0
LVEDD (mm) 68.6 52.8

Lack of a response in 12% of patients in the immunosuppression group likely points to the presence of viruses that were not picked up in the initial screening or mechanisms of myocardial damage and inflammation not susceptible to immunosuppression, Frustaci concluded.

Dr Andre Keren (Hadassah University Hospital, Jerusalem, Israel), discussant for the trial, emphasized that Frustaci et al's study represents the first randomized trial of immunosuppression in patients with proven chronic myocardial inflammation but with virus-negative biopsies.

"The remarkable results of this report compare favorably with those of a previous randomized study of immunosuppression in chronic myocardial inflammation in which viral status was not evaluated," Keren said.

The choice of whether to incorporate immunosuppression into routine clinical practice will be enhanced, Keren noted, by ongoing multicenter studies of immunomodulatory therapy.


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