Interferon-Beta May Have Disease Modifying Effect in Patients With B19-Positive Inflammatory Cardiomyopathy: Presented at HF2008

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Title: Interferon-Beta May Have Disease Modifying Effect in Patients With B19-Positive Inflammatory Cardiomyopathy: Presented at HF2008
URL: http://www.pslgroup.com/dg/223B7A.htm
Doctor's Guide
June 17, 2008

By Chris Berrie

MILAN, Italy -- June 17, 2008 -- Interferon (IFN)-beta treatment reduces endothelial cell damage induced by B19 vasculotropic parovirus (B19) in patients with B19-positive inflammatory cardiomyopathy, according to a study presented here at the Heart Failure 2008 (HF2008) Congress.

Endothelial cells are B19-specific targets, and B19 persistence is associated with endothelial dysfunction, impaired microvascular perfusion, and atypical angina, said principal investigator Caroline Schmidt-Lucke, MD, Department of Cardiology and Pulmonology, Charité Medical University, Berlin, Germany.

Dr. Schmidt-Lucke and colleagues therefore conducted their study to determine whether IFN-beta therapy would affect endothelial cell apoptosis and endothelial regeneration in patients with myocardial persistence of B19, she said in a presentation on June 15.

The 23 patients included 9 patients in a noninfected control group, 5 patients in the B19-infected control group (B19 controls), and 9 in the B19-infected group who were treated with IFN-beta (B19+IFN-beta).

Baseline clinical characteristics of the B19 controls and B19+IFN-beta patients were mainly New York Heart Association (NYHA) functional class 1/2 (80%, 78%, respectively), with mixed atypical angina (20%, 78%), arrhythmias (20%, 44%), and fatigue (60%, 78%).

The haemodynamic and echocardiographic measures were similar across the B19 groups, respectively, for left-ventricular ejection fraction (about 50% both; non-B19 controls, 60%) and left ventricular end diastolic pressure (17.0 and 7.3 mm Hg). Laboratory analysis showed 316 and 300 copies of B19 per mcg DNA, respectively.

Treatment with IFN-beta was administered subcutaneously 3 times weekly, with uptitration from 4 times 106 U IFN-beta, through 8 times 106 U during the second week, to 16 times 106 U after the fourth week. The full treatment period was up to 24 weeks.

Endothelial dysfunction was measured by ultrasound using flow-mediated dilatation at baseline and at various time points throughout the study. All B19 patients showed significantly reduced endothelial dysfunction at baseline (P = .015). After 6 months of treatment and continuing to 12 months, flow-mediated dilatation was significantly improved (P = .012).

"On the other hand," said Dr. Schmidt-Lucke, "B19 patients who did not receive this treatment showed persistently low flow-mediated dilatation [P = .003], indicating that [IFN-beta] improved endothelial function."

Mature apoptotic endothelial cells determined by cytometry and fluorescence microscopy analysis showed that B19 patients had almost 6-fold higher levels at baseline versus controls (P = .004) that were significantly reduced to control levels after IFN-beta treatment (P = .008).

"Much to our surprise, we saw that in these patients with atypical angina, the circulating endothelial progenitor cells were markedly significantly increased compared to controls [P = .03]," Dr. Schmidt-Lucke said. "These counts normalised after [IFN-beta] treatment, and continued to normalise 6 months after."

Finally, B19 DNA was significantly increased in both bone marrow and circulating endothelial progenitor cells in B19 patients compared with controls (both P < .05).

Thus, B19 infection is associated with endothelial dysfunction, systemic endothelial apoptosis, and impaired endothelial regeneration, with IFN-beta acting as a disease-modifying treatment in B19-induced vascular injury, the researchers concluded.

[Presentation title: Interferon-Beta Improves Endothelial Damage and Normalises the Numbers of Endothelial Progenitor Cells in Parovirus B19 Positive Inflammatory Cardiomyopathy. Abstract O192]

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