M-mode and cross-sectional echocardiography revealed that left ventricular hypertrophy patterns differ by etiology, with nonuniform hypertrophy forming a continuum in hypertrophic cardiomyopathy.
M-mode and cross-sectional echocardiography can differentiate patterns of left ventricular hypertrophy and functional impairment based on the underlying etiology, such as pressure overload, volume overload, or primary cardiomyopathy.
1)Left ventricular hypertrophy in hypertension is almost symmetric. However, the interventricular septum is slightly thicker than the posterior wall. In aortic regurgitation and mitral regurgitation the posterior wall is thicker than the interventricular septum. The above situation suggests a difference between the influence of pressure overloading to the heart and that of volume overloading. Hypertrophy in congestive cardiomyopathy is similar to that in aortic regurgitation. 2) The interventricular septum was thickened in all the examined cases of hypertrophic cardiomyopathy. In some cases the interventricular septum was mass-like, bulging into the left ventricular cavity and in some cases into the right ventricular cavity. 3) In the posterior wall of the left ventricle, various degrees and extents of hypertrophy are observed, with and without hypertrophy of the papillary muscle. In some cases, only one of the anterolateral and posteromedial papillary muscles is hypertrophied, but not the other. These findings reveal that a nonuniform hypertrophy develops not only in the septum and free wall, but also even in the papillary muscles. In one examined case a muscle bundle was hypertrophied, occupying a large space in the narrow ventricular cavity, but not the papillary muscle. 4) Motion of the hypertrophied ventricle especially the maximum velocity of the thickened posterior wall during rapid filling, is generally slow. There is a trend that the thicker the posterior wall, the slower the maximum velocity in rapid filling. However, the posterior wall velocity in cases of hypertrophic cardiomyopathy in diastole is generally slower than that in cases of hypertensive heart, even if the posterior wall thickness is the same in both conditions. 5) The mitral SAM consists of echoes of the mitral chordae which are shifted forwards by the hypertrophied papillary muscles sticking out anteriorly into the left ventricular cavity in systole. 6) The hypertrophied and maloriented papillary muscles occupying a large space in the narrow cavity possibly play an essential role in developing the intraventricular pressure gradient in cases of hypertrophic obstructive cardiomyopathy. 7) The obstructive and nonobstructive forms of hypertrophic cardiomyopathy do not seem to be essentially different, but with various manifestations, depending upon the locality and extent of nonuniform inappropriate hypertrophy, form a continuum.
Nagata et al. (Mon,) conducted a review in Left ventricular hypertrophy. M-mode and Real-time Cross-sectional Echocardiography was evaluated on Anatomical and functional features of hypertrophied left ventricle. M-mode and cross-sectional echocardiography revealed that left ventricular hypertrophy patterns differ by etiology, with nonuniform hypertrophy forming a continuum in hypertrophic cardiomyopathy.