Apical Sparing of Longitudinal Strain and Myocardial Fibrosis in Hypertensive Patients and Spontaneously Hypertensive Rats: Based on Speckle Tracking and Histological Analysis

ABSTRACT Background This study aimed to investigate regional myocardial strain and fibrosis distribution to analyze the apical sparing pattern and the relation with hypertrophy in hypertension. Methods This study included clinical and experimental animal investigations. Seventy‐three hypertensive patients were divided into two groups: hypertension without left ventricular hypertrophy (HT‐NLVH) and hypertension with LVH (HT‐LVH). Six 16‐week‐old male spontaneously hypertensive rats (SHR) and six age‐matched male Wistar‐Kyoto (WKY) rats were included in this experiment. Echocardiographic measurements were obtained. Myocardial strain indexes, including global longitudinal strain (GLS), the basal, middle, and apical segmental LS (LS‐bas, LS‐mid, LS‐ap), and the proportion of LS‐ap/(LS‐bas + LS‐mid + LS‐ap) (P‐ap) were measured. The histological collagen volume fraction (CVF) and perivascular collagen area (PVCA) of basal and apical segments (CVF‐bas, CVF‐ap, PVCA‐bas, PVCA‐ap) were observed in all rats. Results Despite preserved systolic function (FS, LVEF), the HT‐NLVH and HT‐LVH groups exhibited diastolic impairment (elevated LAVI, E/e’) (all p < 0.05). LS‐ap declined only in HT‐LVH, while LS‐mid and LS‐bas worsened from HT‐NLVH to HT‐LVH, and the HT‐LVH group exhibited a significantly elevated P‐ap (all p < 0.05). P‐ap was associated with LV remodeling indexes and E/e’ (all p < 0.05). Compared with WKY, LS‐bas decreased in SHR ( p < 0.05). The SHR group demonstrated significantly elevated PVCA‐bas, PVCA‐ap, and CVF‐bas ( p < 0.05), while the CVF‐ap had no significant difference. Conclusion Myocardial dysfunction and fibrosis exhibited regional heterogeneity with predominant basal damage and apical sparing in hypertensive cardiac hypertrophy. This apical‐sparing pattern correlated significantly with both diastolic dysfunction and hypertrophic progression, suggesting its potential as a clinically observable hallmark.