To the best of our knowledge, this is the first study to perform echocardiographic assessment of myocardial work to predict adverse events in patients with RH. In our study, all of the 283 enrolled patients underwent a complete echocardiographic examination and global MW analysis. We found the following results. (i) Echocardiography is still a safe and effective method to evaluate myocardial damage and cardiac contractile function, and can also be used to predict adverse events in patients with RH. (ii) Related indicators of MW were significantly different between patients with RH and adverse events and those without adverse events. Among these indicators, GLS, GWI, GCW, GWE in patients with adverse events were significantly reduced, and GWW was increased. (iii) Patients with a family history of hypertension developed high blood pressure (HBP) earlier, and LV remodeling occurred earlier and was more significant. If patients consumed alcohol, and had high blood glucose and high-density lipoprotein concentrations, adverse events were more likely to occur. The effect of hypertension on the heart is mainly achieved through the following three factors. (i) At the early stage of hypertension, the main damage is cardiac diastolic dysfunction, which increases LV filling pressure and heart cavity preload. High afterload caused by high BP then leads to LV eccentric or centripetal hypertrophy, and oxygen consumption to the subendocardial myocardium increases. Regardless of eccentric hypertrophy or centripetal hypertrophy, the myocardial alignment changes to some extent, and the interaction between cardiomyocytes also changes. This in turn affects effective myocardial contraction, and wasted work is increased. In addition, because of the heart resisting the high BP, myocardial contraction force is enhanced, and the lumen of the coronary arteries in the subendocardial myocardium is compressed and narrowed, eventually leading to myocardial ischemia. (ii) An increase in arterial BP leads to an increase in cardiac afterload to resist the increased BP and ensure cardiac output. Cardiomyocytes then increase in thickness, the coronary lumen collapses, and extravascular resistance increases, further leading to an increase in myocardial oxygen consumption. In addition, the thickened myocardium decreases the coronary blood flow reserve, leading to myocardial ischemia and hypoxia. (iii) Hypertension itself can lead to coronary artery stiffness, thereby causing myocardial ischemia and hypoxia. The result of the combination of myocardial ischemia and hypoxia causes myocardial fibrosis, myocardial uncoordinated contraction, and increased myocardial inactivity, which in turn acts on the heart, leading to cardiac hypertrophy and then heart failure.

Myocardial strain has been used to identify subclinical myocardial dysfunction in patients with hypertension for more than a decade. Among the different deformation (strain) components, longitudinal strain is important for predicting adverse events in patients with RH. Longitudinal strain corresponds to the function of the subendocardial layer of the myocardium in which longitudinal fibers are subjected to the negative effect of early development of fibrosis in hypertensive heart disease [23]. A histological analysis showed that the amount of subendocardial fibrosis was an independent determinant of longitudinal strain after adjusting for systolic wall stress [24]. Therefore, as subendocardial myocardial fibrosis increases, the effect on the longitudinal strain capacity of the myocardium increases. The longitudinal fibers located in the subendocardium are more susceptible to ischemia and are thus affected earlier in the ischemic cascade [25]. Myocardial contraction is closely associated with not only the ability of myocardial strain, but also with coronary flow and oxygen delivery. The balance between oxygen supply and demand is a critical determinant of the normal beat-to-beat function of the heart [26]. In patients with RH and long-term myocardial ischemia, the myocardium is gradually damaged, especially in the subendocardium, and the myocardial contractile stress is weakened. Based on these theories, when the myocardium is damaged, the strain generated by the subendocardial myocardium occurs first and most directly, which is manifested as a decrease in GLS. As we know, GLS is a semi-automated tool used to assess multidimensional myocardial mechanics, and it is more reproducible, and non-reliant on geometric assumptions [27], and is a strong predictor of outcome, particularly in individuals with a preserved ejection fraction [28]. In a study of 388 asymptomatic patients with hypertensive heart disease [29], the baseline GLS provided prognostic information that was independent and incremental over clinical parameters (age sex, heart rate, systolic BP, and atrial fibrillation) and concentric hypertrophy, and the optimal cutoff was − 16%. In our study, GLS also showed a good predictive performance for the occurrence of adverse events in 3 years in patients with RH, and − 16% was the cut-off value.

From the results of our study, GWW is another useful predictive index, it was higher in adverse events’ group. This finding may be related to long-term hypertension, leading to myocardial ischemia, especially the subendocardial myocardium, plays the main contractile role during the contraction process, leading to the wasted work increased. Slimani et al. assessed intraoperative myocardial histology and the stress–strain relationship in 101 patients with aortic stenosis (AS) who underwent aortic valve replacement [30], they found that, predictably, higher end-systolic stress led to lower LV GLS and circumferential strain, even after correcting for afterload, LV GLS, and LV GCW remained at or below the lower limit of normal. These results indicate that myocardial damage caused by myocardial ischemia is basically irreversible. From the level of MW, GLS-based myocardial work index, due to the irreversibility of GLS, leads to the decrease of myocardial GCW, while GWW has the opposite change. Our study also showed the increased GWW, RH patients with GWW > 127 mmHg% were more likely to have adverse events in 3 years.

Diabetes mellitus is an independent risk factor for coronary heart disease, and the proportion of patients with coronary heart disease can be as high as that in the diabetic population (55%) [31]. Coronary artery lesions in patients with diabetic coronary heart disease are complex and diffuse, and the degree of atherosclerosis is more serious than that without diabetes, which easily causes large-scale myocardial infarction, leading to hemodynamic instability and a poor prognosis. In our study, patients with RH and hyperglycemia were more likely to have adverse events. Previous reports have shown that alcohol consumption is associated with the development of hypertension [32,33,34,35,36]. In our study, alcohol consumption increased the risk of adverse events in patients with RH.

In conclusion, a family history of hypertension, hyperglycemia, hypertension itself, and LV hypertrophy eventually lead to abnormal coronary blood perfusion, and myocardial coronary artery perfusion is reduced. These series of events result in myocardial damage, decreased GLS, and increased GWW, which play an important role in adverse events in patients with RH.

This was a single-center study, and the enrolled subjects were limited to those who visited our hospital. Additionally, the number of RH patients included was not large and not sufficiently representative. Therefore, the results may only represent the population in the region where our hospital is located. There was also no group comparison by sex, and this remains to be further studied. The observation time was only 3 years, the data may be more meaningful if the follow-up period is extended. In addition, our criteria for the diagnosis of hypertension were SBP ≥140 mmHg and/or DBP ≥90 mmHg according to the American College of Cardiology/American Heart Association Guideline for the Prevention, Detection, Evaluation and Management of High Blood Pressure in Adults [37]. This guideline defines hypertension as SBP ≥130 mmHg and/or DBP ≥80 mmHg. We classified SBP between 130 and 140 mmHg, and DBP between 80 and 90 mmHg as normal. Therefore, whether our results are still appropriate according to the new standards of hypertension recommended by the American College of Cardiology/American Heart Association remains to be determined. As we know, MW is based on strain and BP, and strain is evaluated by the technique of 2D-STE. 2D-STE has its own limitation, for example, it depends on the temporal stability of tracking patterns and needs high quality grey-scale images for reducing inter- and intra-observer variability of tracking data. Another major limitation of 2D-STE methodology is the lack of standardisation, due to a relevant intervendor variability [38]. In addition, recent evidences have highlighted the possible influence of the chest wall conformation on the cardiac kinetics and deformation indices [39].