Linking left ventricular function and mural architecture: what does the clinician need to know?

The myocardium has a unique architecture, which converts the linear pull of a striated but involuntary muscle into a constrictive action. The left ventricle has also to balance the need to restrict the diameter of its chamber, thereby minimising mural tension, while providing at the same time a wall thick enough to achieve systemic pressure within the cavity. The precise architectural arrangement of the cardiomyocytes that fulfils these requirements is currently a topic of considerable debate. There is a divide between proponents of a counter-wound, single myocardial band,1 and those who describe an arrangement of clefts around thinner lamellar units.2 ,3 In seeking to contribute to this debate, we present here a description of the changes that occur in surface geometry of the ventricle. We will show how the strain indexes of the wall, including mural thickening, are mathematically bound together by this geometry, irrespective of the internal architecture of the wall. We will then relate these indexes to demonstrable features of cardiomyocytic orientation and function.4 In so doing, we provide a relatively simple explanation for left ventricular (LV) twist that does not rely on the presence of a unique myocardial band. We will also reinforce the observation of MacIver and Townsend that hypertrophy of the left ventricle can falsely normalise its ejection fraction (EF) despite falling contractility.5 We conclude by addressing other significant aspects of mural architecture. Initially, we will regard the LV myocardium as a structure of fixed mass and so, at physiological pressures, of fixed volume. It envelops the cavity, and its surfaces are illustrated in figure 1. The magnitudes of changes in the inner and outer dimension of the wall, and of the distance between them, which is the mural thickness, are linked mathematically by the geometry of this very …