INTRODUCTION
Although many long-term benefits for the treatment and control of
hypertension such as reduced risk of stroke, renal failure or myocardial
infarction have been well documented, an important part of the need for
hypertension control is related to prevent left ventricular hypertrophy
and thus to reduce its adverse consequences. Left ventricular
hypertrophy and its associated ventricular wall abnormalities are mainly
the result of an excessive overload and chronic response to ventricular
wall injury and are thus considered as an important risk factor in
hypertensive patients. In the Framingham Heart Study, even the presence
of borderline hypertension in the elderly has been associated with
increased left ventricular wall thickness and subsequent ventricular
diastolic filling defect (1). Patients with moderate arterial
hypertension may also experience a wide range of changes in ventricular
mass, from normal ventricular mass to severe hypertrophy. In addition,
left ventricular remodeling may have an eccentric or concentric form,
independent of the hypertension intensity. Since hypertension does not
always lead to left ventricular hypertrophy, simultaneous evaluation of
both cardiac indices such as hypertension and assessment of left
ventricular wall stress condition is essential. Diagnosis and detection
of left ventricular hypertrophy is very important because the risk of
cardiac mortality and morbidity in these patients will be approximately
two to four times higher than patients with normal left ventricular mass
(2,3).
Another important issue about the incidence and detection of left
ventricular hypertrophy in the context of hypertension is to evaluate
this event through various imaging modalities, especially focusing on
changes in left ventricular wall function which can be detected by
ventricular strain analysis . First, it should be remembered that
secondary left ventricular hypertrophy is a major pathological finding
of hypertension coupled with histological changes in the ventricular
wall, such as stimulation of fibroblast growth, incidence of
interstitial fibrosis, and ultimately structural remodeling in the left
ventricular wall (4,5). Therefore, strong evidence suggests that in
secondary left ventricular hypertrophy due to essential hypertension,
shrinkage of the left ventricle volume is associated with increased
diastolic filling and decreased coronary blood flow reserve and
ultimately ventricular wall hypertrophy. In particular, evaluation of
diastolic filling by Doppler echocardiography would be very valuable
(6).
Another important point regarding the effect of hypertension on the left
ventricle is the induction of reverse remodeling to the incidence of
heart failure (7,8). This change increase both the size of the
cardiomyocytes and the accumulation of fibrosis in the extracellular
matrix. These pathological changes will eventually have heterogeneous
effects on the left ventricular wall (9,10). The left ventricular
myocardial layers contain myocardial fibers with distinctive features
such that the longitudinal fibers in the subendocardial layer gradually
switch to the circumferential format in the middle layer and eventually
recapitulate in the subepicardial layer (11). Two-dimensional speckle
tracking echocardiography allows the quantitative evaluation of local
strain deformities (12,13). The change in left ventricular strain in a
cardiac cycle has a close relationship with the structural status of
ventricular myofibers (12). Among these features, longitudinal strain is
of particular interest because its clinical significance is extremely
high in patients with heart failure as well as in hypertensive patients
(14,15). Some studies have shown that the status of longitudinal left
ventricular strain changes has a strong relationship with the physical
and functional capacity of patients as well as the prognosis of patients
(15-17). However, what still remains to be a fundamental question is how
in the context of hypertension, changes in the left ventricular wall
strain will be particularly relevant to varying degrees of left
ventricular hypertrophy.