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

## TL;DR

This study finds that in hypertension, heart muscle damage and fibrosis mainly occur in the base of the heart, while the tip remains relatively unaffected, linking this pattern to worsening heart function.

## Contribution

The study identifies a novel 'basal-damage, apical-sparing' pattern in myocardial strain and fibrosis in hypertensive patients and rats, linking it to diastolic dysfunction and hypertrophy progression.

## Key findings

- Myocardial dysfunction and fibrosis show regional heterogeneity with more damage at the base and sparing at the apex in hypertensive cardiac hypertrophy.
- Apical sparing pattern correlates with diastolic dysfunction and hypertrophic progression in hypertension.
- Spontaneously hypertensive rats show increased fibrosis in basal segments but not in apical segments compared to controls.

## Abstract

This study aimed to investigate regional myocardial strain and fibrosis distribution to analyze the apical sparing pattern and the relation with hypertrophy in hypertension.

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.

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.

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.

Hypertensive cardiac hypertrophy shows a “basal‐damage, apical‐sparing” pattern in strain and fibrosis. This apical sparing correlates with diastolic dysfunction and hypertrophy progression, highlighting its value as an observable clinical hallmark of adverse remodeling.