Introduction Hypertrophic left ventricular disease occurs in numerous conditions including hypertension, aortic stenosis, hypertrophic cardiomyopathy, Fabry disease, amyloid and heart failure with a normal ejection fraction. Many clinical studies have showed the presence of abnormal longitudinal and circumferential left ventricular regional function (strain, strain rate, peak shortening velocities etc) in patients with concentric left ventricular hypertrophy. In addition, there is significantly reduced radial strain in many of these conditions despite the apparent normal radial ‘function’ and ejection fraction. In order to improve understanding of the relationship between strain and wall thickening, this study assesses the effect of left ventricular end-diastolic wall thickness and circumferential/longitudinal strain on radial strain and wall thickening.

Methods The deformation characteristics of an isolated cube of myocardium 9×9×9 mm were assessed. The myocardial tissue was assumed to be a non-compressible elastomer. Circumferential (CS) and longitudinal strain (LS) were adjusted as follows, normal (–20%), moderately reduced (−15%) and severely reduced (–10%). The effect of changing end-diastolic wall thickness (EDWT) and LS/CS on radial strain (RS ie, relative wall thickening) and absolute wall thickening were calculated.

Results Increasing end-diastolic wall thickness, with constant LS and CS, increased end-systolic wall thickness and absolute wall thickening but radial strain remained constant. When LS & CS were reduced, end-systolic wall thickness, RS and absolute thickening decreased. However, in the presence of an increase in end-diastolic wall thickness, absolute wall thickening remained normal despite a reduction in radial strain (see abstract 089 table 1)

Conclusion LS & CS determine RS. However, absolute radial thickening is determined by both end-diastolic wall thickness and RS. Since, the external left ventricular circumference reduces by only 3% the absolute radial thickening determines most of the endocardial displacement and hence determines stroke volume. It is essential to differentiate between absolute and relative radial thickening when describing radial function. An increase in end-diastolic wall thickness with normal shortening must lead to an increased absolute thickening; in order for the absolute wall thickening to remain normal, myocardial shortening must be reduced. Myocardial strain has to be reduced proportionally to the degree of concentric hypertrophy otherwise the ejection fraction and stroke volume will be inappropriately increased. This study explains the geometric findings in hypertrophic heart disease regardless of the cause. A normal ejection fraction does not equate to normal deformation or even normal systolic function. The term ‘global systolic function’ is unhelpful, misleading and should be abandoned.