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.