Left ventricular hypertrophy in aortic valve stenosis: preventive or promotive of systolic dysfunction and heart failure?
- PMID: 15860517
- DOI: 10.1093/eurheartj/ehi290
Left ventricular hypertrophy in aortic valve stenosis: preventive or promotive of systolic dysfunction and heart failure?
Abstract
Aims: In aortic stenosis (AS), left ventricular (LV) hypertrophy is considered a compensatory response helping maintain systolic function. Recent research in experimental AS suggests, however, that LV hypertrophy is not necessary to sustain LV contractions but may in fact be maladaptive. The present work aimed to clarify the role of LV hypertrophy in AS-related heart failure (HF) in man.
Methods and results: We studied 137 adult patients with isolated AS undergoing pre-operative echocardiography and cardiac catheterization. HF was diagnosed by the European criteria and LV hypertrophy by sex-specific limits of echocardiographic LV mass. The higher the LV mass was, the poorer was the LV ejection fraction (beta=-0.26, P< 0.001, linear regression) and the greater the likelihood of HF independent of the severity of AS (P< 0.001, logistic regression). In the subgroup of critical AS (valve area <0.4 cm(2)/m(2), n=85), patients with absent LV hypertrophy (n=19) had better preserved ejection fraction (mean+/-SE, 64+/-3 vs. 57+/-2%, P=0.045) and less HF (16 vs. 48%, P=0.025) than patients with LV hypertrophy (n=66).
Conclusion: In isolated AS, increased LV mass predicts the presence of systolic dysfunction and HF independent of the severity of valvular obstruction. LV hypertrophy may be maladaptive rather than beneficial in AS in man.
Comment in
-
Iconoclasts topple adaptive myocardial hypertrophy in aortic stenosis.Eur Heart J. 2005 Sep;26(17):1697-9. doi: 10.1093/eurheartj/ehi344. Epub 2005 May 23. Eur Heart J. 2005. PMID: 15911565 No abstract available.
-
Left ventricular hypertrophy, apoptosis, and progression to heart failure in severe aortic stenosis.Eur Heart J. 2005 Dec;26(24):2747. doi: 10.1093/eurheartj/ehi623. Epub 2005 Oct 24. Eur Heart J. 2005. PMID: 16246825 No abstract available.
Publication types
MeSH terms
LinkOut - more resources
Full Text Sources
Medical
Research Materials
Miscellaneous