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.