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‘How wonderful that we have found a paradox. Now we have some hope of making progress.’
Neils Böhr (1885–1962)
Concentric remodelling (reduction of the diameter/thickness ratio) and hypertrophy (increase of mass—left ventricular hypertrophy; LVH) have been classically interpreted as the physiological mechanisms used by the left ventricle to compensate for chronic pressure overload.1 At the cellular level, increasing the number of contractile elements improves contractile force. At the organ level, a thicker myocardial wall reduces left ventricular radial, circumferential and meridional systolic stresses. Concentric remodelling and hypertrophy thus take advantage of Laplace's law to benefit systolic function. Even under extreme values of intraventricular pressure, overall systolic performance is maintained and pump function remains normal in terms of cardiac output and filling pressures. In the long term, if the systolic load is not relieved, this compensatory mechanism fails, hypertrophy switches towards eccentric remodelling, filling pressures rise and overt heart failure develops (a phase classically designated ‘afterload mismatch’). This has been the classic conception of the favourable ‘adaptive’ effects of left ventricular remodelling under increased systolic stress.1
In their article published in this issue of Heart, Cioffi et al2 (see page 301) analyse the prognostic value of LVH in a prospective cohort of patients with aortic valve stenosis (AS). The major finding of their study is related to adverse outcome if values are 110% higher than the values expected for wall stress, body size and gender. Importantly, such an inappropriate increase in left ventricular mass (LVM) was found in 59% of patients from an unselected cohort with asymptomatic AS. Multivariate analysis showed the independent predictive value of and inappropriate LVM, in addition to well established …
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