scholarly journals Left ventricular hypertrophy and renin-angiotensin-aldosterone system: AT1-receptor blockers are in the focus

2013 ◽  
Vol 10 (1) ◽  
pp. 88-96
Author(s):  
A V Barsukov ◽  
D V Glukhovskoy ◽  
M S Talantseva ◽  
Z V Bagaeva ◽  
E V Pronina ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Left Ventricle ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Renin Angiotensin ◽  
Reasonable Approach ◽  
Receptor Blockers ◽  
Cardio Vascular ◽  
At1 Receptor Blockers

Left ventricular hypertrophy (LVH) is one of the cardio-vascular continuum components, determining the prognosis of patient with essential hypertension (EH). Pathogenesis of LVH has a multifactor character. Important role in development of cardiomyocites hypertrophy, Intracardiac fibrosis, left ventricle cavity dilation belongs to renin-angiotensin-aldosteron system (RAAS). Pharmacologic blockade of RAAS composes the basis of therapy, directed to LVH regress. Application of Telmisartan is considered high-reasonable approach to treatment of EH-patient with LVH.

Reversal of Left Ventricular Hypertrophy after Treatment of Hypertension by Atenolol for One Year

1982 ◽  
Vol 63 (s8) ◽  
pp. 367s-369s ◽  
Author(s):  
F. Sau ◽  
A. Cherchi ◽  
C. Seguro
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Essential Hypertension ◽  
Left Ventricle ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Wall Stress ◽  
Left Ventricular ◽  
R Ratio ◽  
Blood Pressures

1. Fifteen patients with essential hypertension, class I, II WHO, nine males and six females, whose mean age was 46 years, were given atenolol, 100 mg a day, for 1 year. 2. After 1 month, compared with control, systolic and diastolic blood pressures, heart rate and cardiac output were reduced, whereas left ventricular end-diastolic dimension and stroke volume were increased and total vascular resistances, wall stress, left ventricular mass and h/diastolic radius (R) ratio were unchanged. 3. After 1 year, compared with control, systolic and diastolic blood pressures, heart rate and cardiac output were still reduced, total vascular resistance and wall stress were unchanged. End-diastolic dimension and stroke volume reverted to previous values; left ventricular mass and h/R ratio were significantly decreased. 4. These results show that left ventricular hypertrophy in essential hypertension can revert after 1 year of treatment with atenolol, at least in relatively young people. Since the left ventricle wall stress was not changed after atenolol, the regression of left ventricle hypertrophy seems prevalently to be related to the decrease of adrenergic activity of the heart.

scholarly journals Cardiac Arrhythmias and Left Ventricular Hypertrophy in Dipper and Nondipper Patients With Essential Hypertension

2000 ◽  
Vol 64 (7) ◽  
pp. 499-504 ◽  
Author(s):  
Hiroshi Ijiri ◽  
Isao Kohno ◽  
DongFeng Yin ◽  
Hiroshi Iwasaki ◽  
Masahiro Takusagawa ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Left Ventricular Hypertrophy ◽  
Cardiac Arrhythmias ◽  
Ventricular Hypertrophy ◽  
Left Ventricular

scholarly journals Serum Zinc and Selenium Concentrations in Patients with Hypertrophy and Remodelling of the Left Ventricle Secondary to Arterial Hypertension

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1803
Author(s):  
Paweł Gać ◽  
Karolina Czerwińska ◽  
Małgorzata Poręba ◽  
Adam Prokopowicz ◽  
Helena Martynowicz ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Left Ventricular Hypertrophy ◽  
Arterial Hypertension ◽  
Ventricular Hypertrophy ◽  
Serum Zinc ◽  
Left Ventricular ◽  
Left Ventricular Geometry ◽  
Serum Selenium ◽  
Hypertensive Patients ◽  
Concentric Hypertrophy

The aim of the study was to assess the relationship between serum selenium and zinc concentrations (Se-S and Zn-S) and the left ventricle geometry in patients suffering from arterial hypertension. A total of 78 people with arterial hypertension (mean age: 53.72 ± 12.74 years) participated in the study. Se-S and Zn-S were determined in all patients. The type of left ventricular remodelling and hypertrophy was determined by the left ventricular mass index (LVMI) and relative wall thickness (RWT) measured by echocardiography. Se-S and Zn-S in the whole group were 89.84 ± 18.75 µg/L and 0.86 ± 0.13 mg/L. Normal left ventricular geometry was found in 28.2% of patients; left ventricular hypertrophy (LVH) in 71.8%, including concentric remodelling in 28.2%, concentric hypertrophy in 29.5%, and eccentric hypertrophy in 14.1%. LVH was statistically significantly more frequent in patients with Se-S < median compared to patients with Se-S ≥ median (87.2% vs. 56.4%, p < 0.05), as well as in patients with Zn-S < median compared to patients with Zn-S ≥ median (83.8% vs. 60.9%, p < 0.05). In hypertensive patients, older age, higher LDL cholesterol, higher fasting glucose, lower Se-S, and lower Zn-S were independently associated with LVH. In conclusion, in hypertensive patients, left ventricular hypertrophy may be associated with low levels of selenium and zinc in the serum.

scholarly journals Left ventricular hypertrophy in patients treated with regular hemodialyses

2008 ◽  
Vol 61 (7-8) ◽  
pp. 369-374 ◽  
Author(s):  
Dejan Petrovic ◽  
Biljana Stojimirovic
Keyword(s):  
Risk Factors ◽  
Left Ventricle ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Cardiovascular Morbidity ◽  
Morbidity And Mortality ◽  
Concentric Hypertrophy ◽  
Cardiovascular Morbidity And Mortality

Left ventricular hypertrophy is the main risk factor for development of cardiovascular morbidity and mortality in patients on hemodialysis. Left ventricular hypertrophy is found in 75% of the patients treated with hemodialysis. Risk factors for left ventricular hypertrophy in patients on hemodialysis include: blood flow through arterial-venous fistula, anemia, hypertension, increased extracellular fluid volume, oxidative stress, microinflammation, hyperhomocysteinemia, secondary hyperpara- thyroidism, and disturbed calcium and phosphate homeostasis. Left ventricular pressure overload leads to parallel placement of new sarcomeres and development of concentric hypertrophy of left ventricle. Left ventricular hypertrophy advances in two stages. In the stage of adaptation, left ventricular hypertrophy occurs as a response to increased tension stress of the left ventricular wall and its action is protective. When volume and pressure overload the left ventricle chronically and without control, adaptive hypertrophy becomes maladaptive hypertrophy of the left ventricle, where myocytes are lost, systolic function is deranged and heart insufficiency is developed. Left ventricular mass index-LVMi greater than 131 g/m2 in men and greater than 100 g/m2 in women, and relative wall thickness of the left ventricle above 0.45 indicate concentric hypertrophy of the left ventricle. Eccentric hypertrophy of the left ventricle is defined echocardiographically as LVMi above 131 g/m2 in men and greater than 100 g/m2 in women, with RWT ?0.45. Identification of patients with increased risk for development of left ventricular hypertrophy and application of appropriate therapy to attain target values of risk factors lead to regression of left ventricular hypertrophy, reduced cardiovascular morbidity and mortality rates and improved quality of life in patients treated with regular hemodialyses.

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