The review is focused on clinical significance of the left ventricle hypertrophy (LVH) — presentation of heart lesion as a target organ for systemic hypertension (SH). Various LVH development mechanisms are presented, and special attention is paid to sympathic nervous system and β-adrenoreceptors in pathogenesis. Fundamental methods of diagnostics are described for LVH, in comparison. The pathology is classified from the perspective of recent guidelines on echocardiographic diagnostics. Epidemiology provided. Taken current evidence, the prognostic role of LVH is described as a factor increasing the risk of fatal and non-fatal cardiovascular, cerebrovascular and renal complications in SH patients. Trials data presented that points on LVH regression with highly selective β1-blocker bisoprolol treatment. Pathophysiology of LVH regression is discussed for β1-blocker treatment.
Aim. To investigate the impact of amlodipine/valsartan single-pill combination (A/V SPC) on left ventricular hypertrophy (LVH) and left ventricular (LV) myocardial strain and stiffness parameters in naїve middle-aged patients with stage II grade 1-2 essential arterial hypertension (EAH).Material and methods. A group of patients with stage II grade 1-2 EAH who had not previously received regular antihypertensive treatment (AHT) [n=38; mean age 49.7±7.0 years] was retrospectively formed. All the patients were treated with A/V SPC and all of them achieved target office blood pressure (BP) (less than 140/90 mm Hg). And after 12 weeks follow-up (since the time of reaching the target BP) the AHT effectiveness assessment, its impact on LVH and LV myocardial strain and stiffness parameters (general clinical data, ambulatory blood pressure monitoring, conventional and 2D-speckle tracking echocardiography) were performed in all included patients.Results. The number of patients with LVH significantly (p=0.039) decreased from 25 individuals (65.8%) at baseline to 15 patients (39.5%) at the end of follow-up. Among patients with LVH at baseline after the treatment with A/V SPC significantly decreased (p<0.001 for all) interventricular septum thickness (from 1.36±0.19 to 1.28±0.18 cm), LV posterior wall thickness (from 1.08±0.09 to 0.97±0.11 cm) and the LV myocardial mass index (from 123.3±19.3 to 110.8±20.8 g/m2). At the end of follow-up end-systolic elastance significantly (p<0.001) decreased from 4.01±1.12 to 3.46±0.88 mm Hg/ml. In the subgroup of patients with reduced (in absolute value) LV longitudinal 2D-strain (n=27) at baseline, there was a significantly (p=0.005) increasing in this parameter at the end of the study (from -16.14±2.21% to -17.30±2.13%, Δ%=8.45±13.35).Conclusion. In naive patients 40-65 years old with stage II grade 1-2 EAH AHT with A/V SPC provides effective 24 hours BP control, significantly reduced LVH and improves LV strain parameters, which indicates decreasing of LV myocardial stiffness.
Arterial hypertension (AH) is one of the most significant modifiable risk factors that increase cardiovascular morbidity and mortality worldwide, including Russia. The complex of structural and functional changes in the heart that occurs during AH consists not only in the formation of left ventricular (LV) myocardial hypertrophy, but also in the myocardial stiffness increasing due to collagen formation and cardiomyocytes apoptosis. These abnormalities are substrate for diastolic function disturbances, electrical myocardial instability and ischemia. The article provides a clinical case of amlodipine/lisinopril single-pill combination (A/L SPC) use in real clinical practice in a patient with stage II grade 2 newly diagnosed AH and its effect on blood pressure and echocardiographic myocardial fibrosis markers, including speckle tracking parameters The high antihypertensive efficacy of A/L SPC, a favorable effect on blood pressure circadian rhythm, as well as pronounced target-organ protective properties, in particular the ability to reduce LV and left atrial stiffness, were demonstrated. So, we conclude that A/L SPC improve the elastic properties of the left heart.
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