(Circulation. 2006;114:e13.)
© 2006 American Heart Association, Inc.
Correspondence |
University Hospital of North Staffordshire, Keele University Medical School, Stoke-on-Trent, UK
Aurigemma et al1 have attempted to reconcile the recent findings that ventricular long-axis function in systole is reduced in diastolic heart failure (DHF) with the standard concept that systolic function is entirely normal in this condition. They question the relevance of long-axis function mainly because annular velocities are within normal limits in some patients. However, DHF is episodic and often requires a triggering factor, such as an ischemic episode, arrhythmia, etc. No study to date has measured regional ventricular function in DHF on admission. Furthermore, ventricular long-axis function in systole is abnormal in all the conditions considered to be risk factors for DHF, including ischemic heart disease, hypertension, and diabetes, despite a normal ejection fraction.2 Mitral annular velocities are more powerful predictors of outcome in a variety of cardiac diseases and they correlate better with brain natriuretic peptide levels in heart failure than does ejection fraction.3,4 Therefore, these measurements are of some significance. Strain and strain rate are more sensitive as the authors suggest, but recent studies have shown that both are reduced in early diabetic myocardial disease, left ventricular hypertrophy, and myocardial infarction despite a normal ejection fraction.5
The authors do not discuss the role of ventricular suction, which is a major factor in normal early diastolic filling, when the majority of left ventricle filling occurs. Suction is dependent on the stored energy generated by the previous systolic contraction and may be more influenced by impaired long-axis systolic function (and torsion). Global hemodynamics alone will not detect these abnormalities of ventricular form and function.
Obviously, abnormal regional systolic function is not the entire explanation for DHF, but like in systolic heart failure, it is likely that there is a mixture of abnormalities. I have provided elsewhere an alternative explanation that takes into account the different phenotypes of systolic and diastolic heart failure and the important role of remodeling (a more useful classifier than ejection fraction), which incorporates the findings on long-axis function into a more coherent scheme.2 Dichotomizing heart failure patients on the basis of the left ventricular ejection fraction alone is not sensible, given the complexities of ventricular function and the remodeling process. Although apparently more neat, the old concept of heart failure that divides heart failure into 2 clear types based on the left ventricular ejection fraction, which Aurigemma and colleagues have so resolutely defended, fails to accommodate the information that is emerging from the new imaging technologies. Surely, it is time to move on.
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2. Sanderson JE. Heart failure with a normal ejection fraction. Heart. December 30, 2005. DOI: hrt.2005.074187v1. Available at: http://heart.bmjjournals.com/cgi/rapidpdf/hrt.2005.074187v1. Accessed February 7, 2006.
3. Wang M, Yip GWK, Zhang Y, Ho PY, Tse MK, Lam KW, Sanderson JE. Peak early diastolic annular velocity by tissue Doppler imaging adds independent and incremental prognostic value. J Am Coll Cardiol. 2003; 41: 820826.
4. Vinereanu D, Lim PO, Frenneaux MP, Fraser AG. Reduced myocardial velocities of left ventricular long-axis contraction identify both systolic and diastolic heart failure: a comparison with brain natriuretic peptide. Eur J Heart Fail. 2005; 7: 512519.
5. Zhang Y, Chan AKY, Yu CM, Yip GWK, Fung JWH, Lam WMM, So NM, Wang M, Wu EB, Wong JT, Sanderson JE. Strain rate imaging differentiates transmural from non-transmural myocardial infarction: a validation study using delayed-enhancement magnetic resonance imaging. J Am Coll Cardiol. 2005; 46: 864871.
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