Wall stress in the normal and hypertrophied human left ventricle

Hood, William P.; Rackley, Charles E.; Rolett, Ellis L.

doi:10.1016/0002-9149(68)90343-3

Cited by 14 publications

(17 citation statements)

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“…In earlier clinical trials (Hood et al, 1968, Grossman et al, 1975, it was observed that pressure overload of the left heart was exactly counterbalanced by increased wall thickness in the left ventricle. Subsequent studies have shown that this left ventricular hypertrophy is associated with a significantly increased risk of clinical events, such as an enhanced incidence of coronary heart disease as well as increased mortality from cardiovascular disease (Levy et al, 1990, Koren et al, 1991.…”

Section: A Brief Macroscopic View Of the Process Of Cardiac Hypertrophymentioning

confidence: 98%

Endothelial cell modulation of cardiomyocyte gene expression

Jiang

Mohr

Ullrich

et al. 2019

Experimental Cell Research

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WB Western blot WGA Wheat germ agglutinin β-MHC -Myosin heavy chain 2013, Fredriksen et al., 2001). Kidney disease is commonly found in heart failure (HF) patients (Grande et al., 2017). It was found that GFR is associated with the degree of cardiac diastolic dysfunction and adverse clinical outcomes (Jain et al., 2017). A recent nationwide population-based cohort study showed that heart failure patients have a higher risk of developing dementia (Adelborg et al., 2017). Studies also revealed post-mortem that 73.6% ± 7.0% of all cardiomyocytes were mono-nucleated, 25.5% ± 7.4% were bi-nucleated, and 1.0% ± 1.2% were tri-nucleated in the heart of individuals aged one month to 73 years. In agreement with previous studies (Mollova et al., 2013, Olivetti et al., 1996), they established that already 1 month after birth; the final number of cardiomyocytes was reached (3.2 ± 0.75 × 10 9 cells) and remained constant throughout life. By stereological measuring the average volume of cardiomyocytes at different ages, it was found that the adaptive about 3-fold greater (endothelium-derived contracting factors) (Flammer et al., 2012). Furchgott and Zawadzki (Furchgott and Zawadzki, 1980) first described the phenomenon of endothelium-dependent relaxation in 1980. Subsequently, the identification of nitric oxide (NO) as the crucial endothelium-derived mediator of vascular relaxation led to substantial progress in cardiovascular research (Flammer et al., 2012). In addition to with arterial hypertension and echocardiographically documented left ventricular hypertrophy, who received either the AT 1 receptor blocker losartan or the β 1 receptor blocker atenolol, were much less likely to experience such a major cardiovascular event (Kjeldsen et al., 2002). Also whereby NT-proBNP levels are more sensitive and specific to distinguish HF from non-HF subjects (Fonseca et al., 2004). NT-proBNP levels were also suggested to be highly predictive of incident atrial fibrillation, the most common cardiac rhythm abnormality, after adjustment for an extensive number of covariates (Patton et al., 2009). Although ANP and BNP have been recommended to provide prognostic information

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Section: A Brief Macroscopic View Of the Process Of Cardiac Hypertrophymentioning

confidence: 98%

Endothelial cell modulation of cardiomyocyte gene expression

Jiang

Mohr

Ullrich

et al. 2019

Experimental Cell Research

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“…В связи с тангенциальным расположением в стенке желудочков КМЦ, форма которых близка к цилиндрической, сформулирована гипотеза, согласно которой увеличение диаметра КМЦ может приводить к утолщению стенки желудочка, а удлинение КМЦ -к расширению полости желудочка [2,3]. Если данная гипотеза верна, то информация об изменении диаметра и длины КМЦ может быть полезной для анализа анатомии гипертрофированного сердца, поскольку именно соотношение между толщиной стенки и радиусом полости (относительная толщина стенки) [1] вместе с кровяным давлением по закону Лапласа определяют систолическое напряжение стенки, влияя на состояние компенсации или декомпенсации гипертрофированного сердца [2,12].…”

Section: результаты и обсуждениеunclassified

Morphometric features of cardiomyocytes in the ventricular septum of patients with hypertrophic cardiomyopathy

Егорова¹,

Серов²,

Bockeriа³

2017

Arkh. patol.

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The findings could suggest that the factor raising VS thickness in HCM may be an increase in not only diameter of CMCs, but also in length of CMCs, which had impaired orientation in the VS - which are oriented perpendicular to their normal tangential position. The presence of such CMCs in the VS myocardium in patients with HCM can be discussed due to the typical large number of myocardial areas with the impaired parallel arrangement of CMCs.

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“…Утолщение стенки желудочка нормализует систолический стресс его стенки, компенсируя увеличение давления крови или объема полости [2] в соответствии с законом Лапласа, согласно которому систолический стресс стенки желудочка прямо пропорционален давлению крови, радиусу полости и обратно пропорционален толщине стенки желудочка. Переход гипертрофии миокарда в стадию декомпенсации при концентрической и эксцентрической гипертрофии происходит при несбалансированном расширении полости желудочка -отношение радиуса полости желудочка к толщине стенки увеличивается [11] и систолический стресс желудочковой стенки возрастает [12].…”

Section: кардиомиоциты дилатированного левого желудочка у больныхunclassified

Changes in the diameter and length of hypertrophic cardiomyocytes in the dilated left ventricle of cardiac surgical patients

et al. 2017

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The findings suggest that after completion of their transverse growth, hypertrophic CMCs are involved in a restructuring process with PML. The findings are consistent with the hypothesis that dilatation of the hypertrophied LV cavity is related to the preferential elongation of CMCs with an inadequate increase in their diameter. The results of the investigation may assume that the higher CMC diameter that brings to completion before the entry of the cells into the restructuring process with PML, resumes in the cells, the ploidy of which increases in the course of restructuring with PML, triggering an additional mechanism for raising the CMC diameter at this stage of myocardial hypertrophy. The results are indicative of different mechanisms for increasing the diameter and length of hypertrophic CMCs, since the diameter of CMCs directly correlates with that of their nuclei, and the length increases as the zones of PML extend in the CMCs.

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Wall stress in the normal and hypertrophied human left ventricle

Cited by 14 publications

References 0 publications

Endothelial cell modulation of cardiomyocyte gene expression

Endothelial cell modulation of cardiomyocyte gene expression

Morphometric features of cardiomyocytes in the ventricular septum of patients with hypertrophic cardiomyopathy

Changes in the diameter and length of hypertrophic cardiomyocytes in the dilated left ventricle of cardiac surgical patients

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