DISCUSSION
Left ventricular remodeling caused by hypertension is a well-known phenomenon that can be evaluated by echocardiographic techniques. In recent decades, new echocardiographic techniques such as Speckle Tracking Echocardiography have made it possible to evaluate mechanical changes of the left ventricle in the context of hypertension. The evaluation of the strain index as an important part of the evaluation of the ventricular wall in various layers of the ventricle in these patients has received much attention. In this regard, evaluation of the left ventricular strain, especially the longitudinal strain in the triple layers of the ventricular wall, was a stronger predictor of cardiovascular morbidity and morbidity than the LVEF index. Given that hypertensive heart disease is one of the important risk factors for the development of heart failure and impaired cardiac systolic and diastolic function even in cases with normal LVEF, careful determination of ventricular strain changes in various layers in the presence of hypertension is essential. In particular, the impact of hypertension in the background of ventricular diastolic dysfunction on ventricular wall dimensionality remains to be elucidated.  What we focused on in the present study was to evaluate and compare strain changes in the triple layers of the ventricular wall in hypertensive and normotensive patients in the presence or absence of left ventricular diastolic dysfunction.
In this study, patients were classified into hypertensive and normotensive groups; then both GLS and GCS indices were evaluated in three layers of endocardial,mid myocardial and epicardial ventricular walls. The presence of ventricular diastolic dysfunction as a confounding factor in the effect of hypertension on ventricular strain was considered important. The important finding of this study was the significant effect of hypertension on the reduction of GLS and GCS in mid myocardial and epicardial layers in the presence of left ventricular diastolic dysfunction. In other words, first, the presence of diastolic dysfunction in the reduction of left ventricular wall strain in the context of hypertension seems to be essential as a trigger factor; therefore, in cases of preserved diastolic function, left ventricular wall strain involvement may not be very noticeable. Second, there was no evidence of any decrease in endocardial layer strain and therefore no endocardial layer involvement; it is possible that our sample cases were mostly in the early stages of hypertention with lesser chronicity and better medically controlled disease and if this study was performed in different patient group with poorly controlled hypertention , or patients with longer history and advanced stages of disease ,would have shown that uncontrolled hypertension may eventually lead to endocardial layer strain reduction later in the disease course. Overall, it can be concluded that proper control of hypertension in patients with a history of hypertension, especially in the context of left ventricular diastolic dysfunction, will lead to improved left ventricular wall function and thus improved prognosis.
Impaired strain in various layers of the left ventricular wall in the background of hypertension has been studied and confirmed in various studies, although the stimulatory effect of diastolic dysfunction in such disorder has been indicated in few studies. In Tadic et al study (18), GLS was significantly lower in hypertensive men than in normotensive patients. The major factor in the development of left ventricular remodeling following hypertension was the effect of sex hormones and its associated biohormonal systems. The results of the above study were similar to ours, but these changes were not limited to a specific gender. Diastolic dysfunction was also a triggering factor in our study. In Navarini et al study (19), there was no difference between the hypertensive and the normotensive groups in terms of left ventricular volume and LVEF. GLS values in the two groups were -15.1 and -18.5, GCS values were -15.2 and -19.9, and GRS values were + 44.0 and + 63.4, respectively indicating a difference between the two groups that was consistent with our study. In Tadic et al study (20), and quite unlike our study, a decrease in left ventricular strain in hypertensive patients was restricted to the endocardial layer, although in our study, the presence of diabetes was also considered as an exclusion indicator while this has not been the case in their study. In a study by Craciunescu et al (21) and similar to our study, both GLS and GCS were significantly lower in the group with uncontrolled hypertension than in patients with controlled hypertension. In a study by Nagata et al (22), the GLS and GLS values in the endocardial layer were higher than in the other layers, and this may justify strain retention in the context of hypertension in the endocardial layer. In Kim et al study (23), the evaluation of strain in each layer showed a decreasing endocardial gradient toward the epicardium in both groups with and without hypertension, but there was a significant difference between the two groups in all three layers. In a study by Sharif et al (24), patients with diastolic dysfunction experienced a relative decrease in GLS in all three myocardial layers compared to patients without diastolic dysfunction, which was consistent with the findings of our study. Toufan M et al study(25) demonstrated that in HFNEF patients with diastolic dysfunction; the global, basal, mid and apical PSLSs(The global peak systolic longitudinal strain) were significantly lower compared to control group. They observed a significant positive correlation between the global PSLS and the septal e’ ,as well as a negative correlation between the global PSLS and the E/e’ratio. Results also revealed negative correlations between the IVRT and the global PSLS .Similar results were observed in our study in which diastolic dysfunction was substantial factor in the left ventricular wall strain decrement in hypertensive patients . all these studies demonstrate that strain imaging can uncover some degree of systolic dysfunction despite a preserved LVEF indicated by conventional echocardiography.What can be emphasized as a final result is that prolonged and uncontrolled hypertension with intensification of cardiomyocyte growth as well as cardiomyocyte fibrosis secondary to inflammatory and growth factors secretion can induce left ventricular hypertrophy and thereby reduction of strain indices in the layers, especially mid myocardial and epicardial layers. Of course, the role of ventricular diastolic dysfunction is very important in determining these changes.