Publication Database

The role of subendocardial form and function in heart failure with preserved ejection fraction (2018)

Art

Poster

Autoren

Beyhoff, N.

Lohr, D.

Foryst-Ludwig, A.

Smeir, E.

Klopfleisch, R. (WE 12)

Schreiber, L. M.

Kintscher, U.

Kongress

Heart Failure 2018 & World Congress on Acute Heart Failure

Vienna - Austria, 26. – 29.05.2019

Quelle

European journal of heart failure

Bandzählung: 20

Heftzählung: Suppl. S1

Seiten: 332 – 333

ISSN: 1388-9842

Sprache

Englisch

Verweise

URL (Volltext): https://onlinelibrary.wiley.com/doi/epdf/10.1002/ejhf.1197

DOI: 10.1002/ejhf.1198

Kontakt

Institut für Tierpathologie

Robert-von-Ostertag-Str. 15
14163 Berlin
+49 30 838 62450
pathologie@vetmed.fu-berlin.de

Abstract / Zusammenfassung

Background:
The subendocardium is highly susceptible to injury and is thereforeconsidered to be the earliest myocardial layer affected during cardiovascular disease development. Several studies have postulated the involvement of subendocardialdamage in heart failure with preserved ejection fraction (HFpEF), especially atsubclinical state. However, morphologic-functional studies regarding the impact ofsubendocardial status in HFpEF are currently lacking.

Purpose:
To identify the role of subendocardial damage in HFpEF.

Methods:
129/Sv mice were injected with a high-dose of Isoproterenol (ISO) to induce isolated subendocardial damage, or saline as appropriate control. Animals
were challenged with a graded exercise test protocol to determine exercise capacity. Two weeks after final treatment with ISO/saline, comprehensive echocardiographic examinations and gene expression analyses were performed. Myocardial microstructure was assessed by histologic analyses and diffusion tensor magnetic resonance imaging (Picture).

Results:
ISO-treatment led to pronounced fibrotic lesions, predominantly in the subendocardial layer, which was accompanied by increased atrial natriuretic peptide levels (p < 0.05 vs. control). Left-ventricular ejection fraction and fractional shortening were comparable among both groups. Global Longitudinal Strain and -Strain Rate were markedly impaired due to ISO-treatment, whereas radial and circumferential strain values remained unaffected. Subendocardial fibrosis induced a moderate diastolic dysfunction and increased estimated filling pressures in the absence of lung congestion or reduced exercise capacity.

Conclusion(s):
Isolated subendocardial fibrosis alone is able to induce several characteristics of HFpEF, however, does not lead to heart failure symptoms or signs under experimental conditions. Diagnostic assessment of subendocardial form and function may contribute to early assessment of cardiac damages in subclinical patients at risk to develop HFpEF, and may consequently improve prevention of functional impairment.