Changes in desmin expression in patients with cardiac diastolic dysfunction and preserved or reduced ejection fraction.
OBJECTIVE
Desmin regulates function of mitochondria, T-tubular system and cytosolic Ca(2+) transients. We investigated whether desmin remodeling correlates with diastolic dysfunction and whether progressive desmin abnormalities are accompanied by increasing diastolic dysfunction stages.


METHODS
Eighty five patients with idiopathic dilated cardiomyopathy and suspected myocarditis without confirmed cardiac tissue inflammation in histopathology assays were included and divided into groups: with preserved EF and reduced EF. After echocardiographic analysis of diastolic dysfunction we identified 2 preserved EF subgroups (normal diastolic function (NDF) and impaired relaxation (IR)) and 3 reduced EF subgroups (NDF, IR, and pseudonormalization). Patients with preserved EF and NDF formed the control group. Tissue desmin staining revealed 4 types of desmin expression: I - normal, with regular pattern of cross-section, IIA - increased with regular pattern, IIB - increased, with irregular pattern and presence of aggregates, III - decreased/lack desmin.


RESULTS
Desmin I was observed only in patients with NDF n=8 (100%) in preserved EF and reduced EF, desmin IIA in NDF n=8 (33%) in preserved EF and n=5 (33%) in reduced EF and IR n=16 (66%) in preserved EF and n=10 (66%) in reduced EF. Desmin IIB and III were observed in patients with reduced EF and diastolic dysfunction: IR and pseudonormalization n=9 (39%) and n=2 (29%); n=14 (61%) and n=5 (71%), respectively. Desmin was found to be an independent predictor of diastolic function parameters β=-0.63, R(2)=0.52 for E'; β=0.54, R(2)=0.42 for E/E'.


CONCLUSIONS
Increasing desmin abnormalities were correlated with diastolic dysfunction progression. Desmin expression represents a novel factor contributing or paralleling the development of diastolic dysfunction.
Department of Invasive Cardiology, Central Clinical Hospital of the Ministry of Internal Affairs, Warsaw, Poland. Electronic address: a.pawlak1@wp.pl.
Agnieszka
A
Pawlak
Department of Invasive Cardiology, Central Clinical Hospital of the Ministry of Internal Affairs, Warsaw, Poland; Mossakowski Medical Research Centre, Academy of Science, Warsaw, Poland.
Robert Julian
RJ
Gil
Department of Pathology, Central Clinical Hospital of Ministry of Internal Affairs, Warsaw, Poland.
Anna Maria
AM
Nasierowska-Guttmejer
Department of Cardiology, Medical University, Łódź, Poland.
Jarosław D
JD
Kasprzak
D000328:Adult; D009202:Cardiomyopathies / Q000378:metabolism / Q000503:physiopathology; D003893:Desmin / Q000378:metabolism*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009205:Myocarditis / Q000378:metabolism / Q000503:physiopathology; D020097:Natriuretic Peptide, Brain / Q000378:metabolism; D010446:Peptide Fragments / Q000378:metabolism; D020257:Ventricular Remodeling / Q000502:physiology
D003893:Desmin; D010446:Peptide Fragments; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain
Desmin; Diastolic dysfunction; NT-pro-BNP; Proteins; Ventricular remodeling