Strain is “stretching” in lay language, and “deformation” in technical terms, and can be used to measure and express myocardial deformation during contraction. Strain is a dimensionless quantity and is expressed as a percentage change in length from the original dimension. It is defined mathematically by the Lagrangian formula: E = L /( L o − L i ), where E is strain, L o is the original length of myocardium, L i is the length of myocardium after it is stretched, and L is the change in length ( L o − L i ). It is not possible to measure L i in a beating heart, so end-diastolic length is used. Contraction generally results in negative strain, while relaxation results in positive strain. There are different types of left ventricular (LV) myocardial strain: LV long-axis strain measured in the base-to-apex orientation, circumferential strain (generally measured as LV midwall strain) along the circumference of the minor LV axis, and radial strain as a measure of LV wall thickening. LV long-axis and circumferential strain is negative during systole, and radial strain is positive. These are overt simplifications, and it must be recognized that LV muscle fiber orientation is too complex to be resolved along different geometric planes cutting through the left ventricle. Normal systolic longitudinal strain is in the range of −20%, similar to the amount of sarcomeric shortening of the myocyte during its contraction. Contractility is better expressed in terms of the systolic stress-strain relationship. LV circumferential and longitudinal strain used to be obtained traditionally using contrast left ventriculography, but the computation was cumbersome. Cardiac magnetic resonance imaging with myocardial tagging permits one to measure systolic myocardial strain at a temporal resolution of about 50 msec. Ultrasonic methods such as tissue Doppler and speckle tracking permit the measurement of both systolic and diastolic strain and strain rate at a high temporal resolution in the range of 5 to 10 msec. These tools are quite user friendly and potentially powerful for the assessment of both regional systolic and diastolic function. Myocardial systolic wall stress is a measure of how much force the myocardium must overcome to contract. Systolic wall stress is proportional to LV systolic pressure and size and inversely proportional to LV wall thickness, following the principles of the Laplace equation, with geometric corrections for wall stresses in different myocardial fiber orientations. Higher wall stresses make it difficult for the myocardium to contract. Hence, a given strain value must be interpreted in the context of the operating wall stress. A strain value of 18% at a systolic wall stress of 150 g/cm 2 indicates better contractile function than the same strain at a systolic wall stress of 75 g/cm 2 .
In this issue of JASE , Iida et al. report newer insights regarding altered myocardial mechanics in patients with aortic regurgitation (AR), despite normal LV ejection fraction (EF), demonstrable by myocardial strain imaging. The salient findings of this study include reduced LV long-axis or meridional strain even in patients with moderate AR and reduced LV subendocardial circumferential and radial strain in patients with severe AR, with preservation of normal LV EF because of compensatory increases in subepicardial strain. Iida et al. describe the latter phenomenon as “transmural compensation,” a phenomenon of cross-fiber talk between different myocardial layers.
However, further examination of their data reveals additional interesting and important findings: (1) a lower LV EF for a given afterload measured as LV end-systolic wall stress, (2) probable exquisite afterload sensitivity of contractile performance of practically all myocardial fiber groups, manifested as a steeper slope of the stress-strain relationship compared with controls, (3) lower subendocardial strain for a given LV end-systolic wall stress, accompanied by an increased slope of the LV stress-strain relationship indicating impaired contractility, and (4) increased afterload sensitivity of subepicardial strain despite a higher strain value, indicating that this layer is operating under a higher catecholamine drive, bringing out its contractile reserve. “Compensation” by subepicardial myocardium may be a marker of neurohormonal surge or higher catecholaminergic drive, similar to the heart failure syndrome. Reduced global and longitudinal strain in moderate or severe AR, despite normal EF, has been reported in the past. But this study provides additional insights into myocardial layer–specific performance normalized for operating wall stress that the myocardium must overcome.
What are the implications of this study, and why is EF normal despite reduced myocardial strain? EF is a measure of change in LV cavity size during systole, and intuitively, this variable would be a weak measure of the extent of myocardial shortening. It depends on LV geometry and its preload, afterload, and contractile function. The EF could be preserved despite significant myocardial dysfunction in patients with LV hypertrophy, in whom radial strain could be exaggerated because of higher LV mass, aided by lower LV wall stress because of greater LV wall thickness and a smaller LV cavity size. Normal LV sarcomeric shortening is 15% to 20%, very similar to meridional strain, which is a measure of LV long-axis muscle shortening. Strain is also preload and afterload sensitive; hence, referencing strain to operating afterload, measured as corresponding systolic wall stress, makes it more objective. Systolic wall stress is the force the muscle fiber must overcome to contract. If the wall stress is high, even normal myocardium may contract less, and dysfunctional myocardium may exhibit normal strain in the presence of reduced wall stress. Hence, it is important to reference strain data to corresponding wall stress measures. In principle, systolic wall stress is directly proportional to systolic pressure and LV radius, and inversely proportional to LV wall thickness. Additional geometric corrections are made for LV geometry. Hence, a dilated left ventricle has greater wall stress even in the presence of normal systolic pressure and systolic wall thickness, while LV hypertrophy reduces the wall stress for a given LV size and systolic pressure.
LV long-axis, circumferential, and radial strain values are now easily obtainable with speckle-tracking echocardiography, along with corresponding wall stress data, and these measures give invaluable and accurate insights into LV contractile function. Accurate assessment of LV systolic mechanics can be obtained by normalizing strain to wall stress, examining strain over a range of wall stress data by afterload manipulation, and examining contractile reserve by infusing inotropes. Certainly, strain is a more direct measure of muscle fiber shortening and intuitively a more direct measure of LV systolic function than EF, but referencing to corresponding wall stress will indicate how much “lifting” the myocardial fibers are able to do. This is similar to a common analogy in which a person able to carry 100 lb for 10 yards is stronger than one who can carry only 50 lb for 10 yards. The ability to maintain a given strain despite an increase in wall stress indicates good contractile function, and in this case, a plot of strain against stress will have a fairly flat profile, or a near-zero slope ( Figure 1 , lower curve). Inotropic stimulation brings out contractile reserve. With inotropic stimulation, normal myocardium will exhibit a higher strain level for a given level of end-systolic wall stress, and LV contractile reserve would be diminished in the diseased myocardium ( Figure 1 , upper curve). If strain drops with increasing stress, it indicates reduced contractile function; the stress-strain relationship will have a steeper negative slope ( Figure 2 ). Afterload-matched LV EF, fractional shortening, velocity of fiber shortening, and end-systolic dimension and volume have been used in the past as more accurate measures of LV systolic function. But strain as a function of afterload would be a superior measure, as it provides a direct measure of performance of different sets and layers of myocardial fibers.
