This study investigated the differences in LV longitudinal systolic function of HCM patients relative to healthy subjects, with 4 main findings. First, in HCM patients decreased regional LV peak systolic longitudinal strain appeared not only in hypertrophied LV myocardium, but also in non-hypertrophied myocardium. Clockwise longitudinal rotation was found in the HCM patients, and the interventricular septum thickness at end-diastole positively correlated with the peak longitudinal systolic strain of the different layers. Finally, the area under the ROC curve values for the subendocardial, midmyocardial and subepicardial layers were 0.923, 0.938, 0.948, respectively. The sensitivity was higher for peak longitudinal systolic strain of the midmyocardial layer (97.2%) than for the subendocardial and subepicardial layers (94.4% and 91.7%). Specificity was higher for the peak longitudinal systolic strain of the subepicardial layer (88.9%) than for the subendocardial and midmyocardial layers (80.6% and 83.3%). Cut-off values for the subendocardial, midmyocardial and subepicardial layers were −19.43%, −16.33% and −15.33%.
HCM is a very common and important cardiac disease. LV hypertrophy, myocardial fibrosis, and fiber disarray in the LV myocardium has been reported as the major structural myocardial abnormalities in HCM patients [4], and systolic function is damaged thereby. LV hypertrophy is the result of compensatory myocardial function.
Systolic function by conventional measurements, such as LVEF, cannot detect cardiac myocardium impairment; microscopic abnormalities result in intrinsic functional abnormalities [24]. Cardiac function has been determined based on velocity, strain, strain rate, degrees of rotation, and torsion using 2D–STE in many heart diseases, including cardiomyopathy, coronary heart disease, and hypertension [8, 25,26,27,28]. However, to measure the peak systolic strain of the subendocardial, midmyocardial, and subepicardial layers is a novel method for adjudging myocardium function. One of the innovations of the present study was to use 2D–STE to measure the peak systolic longitudinal strain of the subendocardial, midmyocardial, and subepicardial layers in HCM patients, and then evaluate longitudinal systolic function in HCM patients relative to that of healthy individuals.
In the present study, the peak systolic longitudinal strain of the subendocardial, midmyocardial, and subepicardial layers in both HCM and healthy individuals was: subendocardial > middle myocardial > subepicardial. A normal myocardium consists of the subendocardium, middle, and subepicardium fibers. Longitudinally oriented fibers of the subendocardium and subepicardium lead to longitudinal contraction, and middle wall fibers that are circumferentially oriented lead to circumferential shortening. Differences in contraction of the subepicardial and subendocardial layers lead to high subendocardial strain. The subendocardial region is responsible for most of the longitudinal deformation.
The present result was consistent with previous studies [4, 21]. By detecting the peak systolic longitudinal strain of the subendocardial, midmyocardial, and subepicardial layers, our data showed attenuation of longitudinal systolic function of the LV myocardium in HCM patients. Popovic et al. [29] also demonstrated that myocardial fibrotic lesions in the LV myocardium were associated with reduced longitudinal strain in HCM patients, and fibrotic lesions and wall thickening were predictors of lower longitudinal strain. Kofflard et al. [30] considered that the decrease in coronary flow reserve in HCM patients predisposed to myocardial ischemia. According to the research, they found that in HCM patients, hemodynamic (LV end-diastolic pressure, LV outflow tract gradient), echocardiographic (indexed LV mass) and histological (% luminal area of the arterioles) changes are responsible for a decrease in coronary flow reserve. Because of these changes, the systolic function in HCM patients was impaired. From our present results, we conclude that longitudinal function was damaged in HCM patients, and longitudinal strain of the different myocardial layers can sensitively reflect cardiac systolic function.
The different orientation of the ventricular muscle fibers led to the different motion of the heart. In the short-axis view, when viewed from the apex, the LV apex rotates counterclockwise, whereas the base rotates clockwise in systole period. However, when a normal heart is viewed from the long-axis view, the motion can be described as shortening of its long axis and thickening of its walls [31, 32].
Longitudinal rotation, first discussed by Popovic et al. [31], refers to rotational motion in the longitudinal direction. Some researchers [28, 32] have found longitudinal rotation in patients with dilated cardiomyopathy, primary hypertension, and other heart diseases. In the present study, clockwise longitudinal rotation was found in HCM patents. The curves of normal subjects showed longitudinal rotations <3°, around the zero baseline for a small angle movement. However, in HCM patients, clockwise longitudinal rotation was found in the heart. The segmental rotation motion in HCM patients also differed from that of the healthy control subjects. In the normal subjects, the lateral wall rotated counter-clockwise, whereas the septum wall rotated clockwise, the rotation degrees were similar, but the direction was the opposite.
In the HCM patients of the present study, the rotational motion of the septum, apex, and the lateral wall of LV also differed from that of the controls. Differences in the segmental and global longitudinal rotation were associated with the unique distribution of myocardium disarray in the HCM patients. The myocardial hypertrophy and fibrosis of these patients was probably responsible for the global and regional abnormalities of the LV myocardial mechanics. When the heart contracted, the abnormal balance of the various myocardial layers resulted in aberrant differences in rotational degrees and the direction of global longitudinal rotation. We also considered that neural and humoral regulation mechanisms may underlie the orientation of the longitudinal rotation. Further researches are necessary to confirm this hypothesis.
In the present study, the IVSD of the HCM patients was found to correlate positively with the peak longitudinal systolic strain of the subendocardial, midmyocardial, and subepicardial layers; thickening of the IVSD in HCM patients was consistent with its systolic function. We therefore conclude that obvious thickening of the IVSD reflects impaired longitudinal systolic function.
The ROC analysis for detecting the accuracy of the peak longitudinal systolic strain showed that the area under ROC curve values for subendocardial, midmyocardial and subepicardial layers were 0.923, 0.938, 0.948. The sensitivity was higher for peak longitudinal systolic strain of midmyocardial layer (97.2%) than for the subendocardial and subepicardial layers (94.4% and 91.7%). Specificity was higher for peak longitudinal systolic strain of subepicardial layer (88.9%) than for the subendocardial and midmyocardial layers (80.6% and 83.3%). From ROC analysis, we knew that using 2D–STE for detecting the peak longitudinal systolic strain of HCM is accurately. The results also showed that the LV function was impaired in HCM patients.