Aims So far, little has been known on whether myocardial inflammatory infiltration influences heart failure (HF) progression. Thus, the aim of this study was to test the impact of intramyocardial infiltration on clinical outcomes.
Methods Biopsy samples from 358 patients with stable HF secondary to dilated cardiomyopathy were studied. Immunohistochemistry for lymphocyte (CD3) and macrophage (CD68) markers was performed and counted. After a 1-year follow-up, patients were classified as improved based on the predefined definition of improvement. The clinical data were collected from 324 patients (90.5%).
Results According to the predefined definition of improvement, 133 patients improved (41.0%) but 191 remained unchanged or deteriorated (58.9%). After a 12-month follow-up, the OR with 95% CI of counts of myocardial inflammatory CD68-positive ≥4 cell/high power field (HPF) compared with CD68-positive <4 cell/HPF for lack of improvement was 1.91 (1.65–2.54). However, the number of CD3 positive cell infiltration had no impact on clinical outcome after a 1-year follow-up. In the baseline study, a reasonably negative correlation was found between the number of CD68 positive cells and troponin T (r=−0.39; p<0.001 by Spearman’s r). This was corroborated with a low negative correlation between these cells and myocardial form of creatine kinase (CK-MB) fraction (r=−0.27; p=0.006). There was no correlation between CD3 and CD68 positive cells (Spearman’s r; r=−0.17, p=0.16).
Conclusions The current results provide evidence that high macrophage counts may be a predisposing factor for HF progression.
- cardiovascular diseases
Data availability statement
All data relevant to the study are included in the article.
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Handling editor Dhirendra Govender.
Contributors ER-W: substantial contributions to conception and design of, or acquisition of data or analysis and interpretation of date. JN: acquisition of date. KK: acquisition of date. EN-K: revising it critically for important intellectual content. RW: final approval of the version to be submitted.
Funding This study was supported by a grant from Medical University of Silesia No: KNW-1-044/N/5/0.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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