BSH detected by routine echocardiography is prominent in older individuals. In our study, the majority of participants with concentric remodeling were from the BSH group. BSH was independently correlated with RWT, but not with LVMI. The subgroup analysis showed no interaction between BSH and age, sex, BMI, diabetes mellitus, CHD, stroke, or smoking status.
The mechanism leading to BSH may be associated with Laplace’s law. The larger the vessel radius, the larger the wall tension required to withstand pressure. The basal IVS has the largest radius in the human heart; thus, it would be expected to experience the greatest inward wall stress. The basal septum is the last part of the ventricle to be electrically activated, and contractions from other myocardial segments further increase wall stress in the basal septum. Moreover, the load created by pressure from the right ventricle exerts additional stress on the septum [1]. Longitudinal shortening is more pronounced in the basal IVS than at other sites in patients with hypertension [9].
Previous studies have indicated that the basal IVS is locally thickened in many patients with essential hypertension, which is recognized early in these subjects [10]. This localized thickening decreases in response to antihypertensive treatment [11]. Thus, BSH might be valuable to detect masked hypertension in the general population [3]. Central blood pressure correlates with basal SWT, but not with mid-SWT [12]. Thus, stricter blood pressure management and hypertension screening should be conducted in patients with BSH. A previously published cohort study showed that hypertensive subjects with BSH were older than non-BSH subjects and had a higher BMI and systolic blood pressure [13]. In our study, age and systolic blood pressure tended to be higher in patients with BSH than in those without, although the difference was not significant. There was no difference in the prevalence of hypertension between the BSH group and the non-BSH group, which may be because the overall population was older and the prevalence of hypertension was higher in our study.
A previous cohort study showed that hypertensive patients with BSH had a higher LV ejection fraction and lower LV end-diastolic and end-systolic volumes, while no significant differences were observed in left atrial size between the two groups [13]. In the present study, we found that LVEDD was lower in patients with BSH, while left atrial diameter was not significantly different. Unlike previous studies, the LVMI in the BSH group was lower than in the non-BSH group in our study, which may be related to the baseline level of the included populations. Early clinical studies suggested that BSH is related to LV diastolic function [2]. Another study showed that BSH is less likely to cause increased LV stiffness without LV hypertrophy [14], but that it can affect LV diastolic function during stress [15]. BSH is related to cardiac function in patients with hypertension with well-controlled blood pressure. Basal and mid-posterior wall systolic deformation, LV diastolic function, and left atrial function are decreased in these patients [13]. Thus, such patients are prone to heart failure with preserved ejection fraction.
BSH is also common in patients with severe aortic stenosis. This result suggests that an increase in afterload can cause BSH in patients with aortic stenosis, which is similar to patients with hypertension. A retrospective study using comprehensive echocardiography analyzed patients undergoing surgical aortic valve replacement (SAVR) or transcatheter aortic valve replacement (TAVR). The study showed that SAVR improved BSH, while TAVR did not. One of the mechanisms of BSH might be augmented compression of the basal IVS by a longitudinally elongated ascending aorta. SAVR involves incision and suture of the anterior wall of the ascending aorta; thus, the elongated aorta is shortened during SAVR. Aortic wall shortening may exert a superiorly directed force on the basal IVS, causing the myocardium to be less compressed and therefore less thick, improving basal IVS contraction. The effects of SAVR on BSH may not be expected from TAVR, given that TAVR does not involve wall shortening [16]. Patients with BSH are more likely to undergo postdilation during the TAVR procedure, and BSH is not associated with conduction outcomes after TAVR in patients without preexisting pacemakers [17]. This may contribute to LV outflow tract obstruction [18]. Thus, when TAVR is performed in patients with severe aortic stenosis, attention should be given to BSH to reduce the chance of missing a diagnosis of LV outflow tract.
In the present study, concentric remodeling was the most frequent LV geometry in patients with BSH. A retrospective analysis of a large clinical population (n = 35,602) showed an abnormal LV geometry in 46% of patients, with concentric remodeling present in 35% of patients (n = 12,362) and LV hypertrophy present in 11% of patients (n = 3,958) [5]. Patients with hypertension had race-related differences in LV geometry and RWT. A descriptive study previously reported that Africans exhibited a greater IVS thickness and RWT than Caucasians [19]. A study with a mean follow-up period of 2.5 years assessed the effect of potential changes in cardiac structure and found that 1,610 patients (45%) demonstrated no change in LV geometry and maintained a pattern of concentric remodeling, 439 patients (12%) progressed to LV hypertrophy, and 1,567 patients (43%) converted to a normal LV geometry. There was a strong relationship between an abnormal LV geometry and all-cause mortality. Patients with concentric remodeling and LV hypertrophy (eccentric and concentric LV hypertrophy) exhibited considerably higher mortality than patients with a normal LV geometry (8.7%, 8.4%, and 10.4% vs. 4.4%, respectively, p < 0.0001) [5]. An American population-based case–control study showed that concentric remodeling is associated with stroke risk [20]. A prospective study showed that all-cause mortality was significantly more likely in patients with concentric remodeling (hazard ratio 1.417, 95% CI 1.045–1.920) [21]. Therefore, follow-up and risk factor control of patients with concentric remodeling should be strengthened to reduce the occurrence of cardiovascular events, but we did not pay sufficient attention to LV geometry.
In this study, BSH independently correlated with RWT. A previous study showed that an increase in RWT is a strong independent predictor of mortality [5]. RWT significantly increases stroke risk, but no interactions have been detected between RWT and LVM [20]. A prospective study showed that RWT is an independent predictor of all-cause and cardiovascular mortality in patients who experience ischemic stroke, whereas the association between LVMI and all-cause death is not significant [21]. In the present study, hypertensive patients with BSH demonstrated a greater RWT and accounted for the highest proportion of patients with concentric remodeling. Therefore, if LV geometry is routinely measured in clinical practice, cardiovascular risk in patients with BSH may be increased.
Our study has several limitations that should be noted. First, because of the cross-sectional study design, a causal relationship between BSH and LV geometry could not be determined. Prospective studies examining whether BSH is predictive of LV geometry and cardiovascular disease are required. Second, the majority of patients were aged >40 years; thus, our findings may not reflect the characteristics of BSH in a younger population.