Because of the lack of a clinical method for assessing the transmural myocardial function, few studies on the heterogeneity during the myocardial contraction/relaxation sequence inside the human ventricular wall have been reported, despite the fact that the importance of the pathophysiology in the transmural heterogeneity has been stressed in previous experimental studies. We studied the transmyocardial functional heterogeneity of the basal anteroseptal segment in normal subjects (n = 8, 40.0 +/- 12.8 year, male), adopting the novel high resolution Doppler measurement "Phased Tracking Method". Each transmural layer of 0.75 mm thickness showed functional heterogeneity (physiological transmural functional heterogeneity), namely larger thickening occurred in the left ventricular endocardial side (right side 1/3: 26.1 +/- 5.2% of the total wall thickness, middle 1/3: 31.9 +/- 2.7%, left side 1/3: 42.1 +/- 6.4%) and the peak thickening shifted smoothly in time from the middle layers to the left subendocardial side during the contraction period. We concluded that transmural functional heterogeneity does exist in normal subjects as well as in the experimental animals of previous reports. Smooth and coordinate myocardial layer contraction across the ventricular wall (physiological transmural functional heterogeneity) is fundamental to maintain the normal ventricular function.
Using the Phased Tracking Method (Doppler frequency: 3 MHz, PRF: 9 kHz), we examined the transmural response to mitral inflow in ten hypertrophic cardiomyopathy (HCM) patients to determine if transmural physical heterogeneity could be a determinant factor of the left ventricular end-diastolic pressure (LVEDP) elevation in HCM. In normal and AS patients, no heterogeneity in the transmural response of the vertical velocity at each preset point (0.75mm-intervals in depth) and the change in each transmural layer thickness across the septum to the mitral inflow was observed. In HCM, the magnitude and the timing of the velocity at each preset point showed remarkable variation among myocardial layers across the septum. The "passive thickening" by atrial inflow was observed at several layers by these temporal and amplitude heterogeneities of transmural velocity distribution. The % of layers showing "passive thickness" during the atrial contraction period was strongly correlated to LVEDP. We concluded that the transmural heterogeneity plays an important role in the LVEDP elevation in HCM patients.
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