Echocardiographic assessment of left ventricular midwall mechanics in spontaneously hypertensive rats

ESCUDERO, E

doi:10.1016/s1525-2167(03)00124-0

Cited by 2 publications

(3 citation statements)

References 18 publications

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“…2) properties indicative of an early increase in LV function due to compensated hypertrophy followed by intermediate and late stages of remodeling associated with onset of mechanical dysfunction ( Table 1). Specifically, our measurements of fractional shortening, which in the sham-treatment group were comparable to those reported by others (6,12), indicated a significant increase in fractional shortening at the early stage (2 wk) of PoH compared with sham-operated animals and more advanced stages of PoH (Supplemental Fig. 1), also consistent with earlier reports (13).…”

Section: Structural and Mechanical Remodeling During Progression Of Hsupporting

confidence: 92%

Mechanoelectrical remodeling and arrhythmias during progression of hypertrophy

et al. 2009

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Despite a clear association between left ventricular (LV) mechanical dysfunction in end-stage heart failure and the incidence of arrhythmias, the majority of sudden cardiac deaths occur at earlier stages of disease development. The mechanisms by which structural, mechanical, and molecular alterations predispose to arrhythmias at the tissue level before the onset of LV dysfunction remain unclear. In a rat model of pressure overload hypertrophy (PoH) produced by ascending aortic banding, we correlated mechanical and structural changes measured in vivo with key electrophysiological changes measured ex vivo in the same animals. We found that action potential prolongation, a hallmark of electrical remodeling at the tissue level, is highly correlated with changes in LV wall thickness but not mechanical function. In contrast, conduction delays are not predicted by either mechanical or structural changes during disease development. Moreover, disrupted Cx43 phosphorylation at intermediate (increased) and late (decreased) stages of PoH are associated with moderate and severe conduction delays, respectively. Interestingly, the level of interaction between Cx43 and the cytoskeletal protein ZO-1 is exclusively decreased at the late stage of PoH. Closely coupled action potentials consistent with afterdepolarization-mediated triggered beats were readily observed in 6 of 15 PoH hearts but never in controls. Similarly, PoH (8/15) but not control hearts exhibited sustained episodes of ventricular tachycardia after rapid stimulation. The initiation and early maintenance of arrhythmias in PoH were formed by rapid and highly uniform activation wavefronts emanating from sites distal to the former site of stimulation. In conclusion, repolarization but not conduction delays are predicted by structural remodeling in PoH. Cx43 phosphorylation is disrupted at intermediate (increased) and late (decreased) stages, which are associated with conduction delays. Dephosphorylation of Cx43 is associated with loss of interaction with ZO-1 and severe conduction delays. Remodeling at all stages of PoH predisposes to triggers and focal arrhythmias.

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Section: Structural and Mechanical Remodeling During Progression Of Hsupporting

confidence: 92%

Mechanoelectrical remodeling and arrhythmias during progression of hypertrophy

et al. 2009

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“…Chests were shaven and echocardiographic measurements were performed in lateral decubitus position. Mitral flow and aortic flows were recorded at the tip of the mitral valve and aortic valve from an apical view using Doppler imaging 32‐34 . Isovolumetric relaxation time (IVRT) was measured as the interval between the aortic closure click and the start of mitral flow.…”

Section: Methodsmentioning

confidence: 99%

“…Mitral flow and aortic flows were recorded at the tip of the mitral valve and aortic valve from an apical view using Doppler imaging. [32][33][34] Isovolumetric relaxation time (IVRT) was measured as the interval between the aortic closure click and the start of mitral flow. Tei index or myocardial performance index (MPI) is calculated by the given formula: 35…”

Section: Transverse Aortic Constriction and Transthoracic Echocardimentioning

confidence: 99%

Beta 1 adrenoceptor blockade promotes angiogenesis in hypertrophied myocardium of transverse aortic constricted mice

Kakaraparthi

Potnuri

Allakonda

2020

Clin Exp Pharma Physio

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Left ventricular hypertrophy (LVH) is an adaptive structural remodelling consequent to uncontrolled blood pressure. Impaired angiogenesis plays a vital role in transiting LVH into cardiac failure. Catecholamines modulate myocardial function through beta adrenoceptors, and their blockers (β-AR) reduce cardiovascular morbidity and mortality by decelerating the LVH progression. Nonetheless, the effect of β-AR blockers on myocardial vascular bed remains largely obscure. Hence, this study is focussed on analysing the possible outcomes of β-AR blockers on myocardial vascular remodelling using a surgically induced LVH mice model. Transverse aortic constricted mice and sham-operated mice were administered with metoprolol at a dose of 30 mg/ kg/d for 60 days and myocardial vascular endothelial growth factor (VEGF) alpha levels, GSH/GSSG ratio, myocardial protein carbonyl content, hypertrophy index and global myocardial function, trans-aortic fluid dynamics and expression pattern of angiopoietin-1 and VEGF alpha were assessed. These findings were further confirmed by histochemical analysis for myocardial capillary density, perivascular fibrosis ratio and intimal thickening. Sub-chronic β-AR blockade reduced the oxidative stress, hypertrophic index, intimal thickening and perivascular fibrosis ratio. A marked increase in myocardial VEGF, angiopoietin 1, global myocardial function and myocardial capillary density was also observed. There was a reduction in the LVH and upregulation of myocardial angiogenesis concluding that β-AR blockers prevent adverse vascular remodelling which might underlie its concealed mechanism of action.

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Echocardiographic assessment of left ventricular midwall mechanics in spontaneously hypertensive rats

Cited by 2 publications

References 18 publications

Mechanoelectrical remodeling and arrhythmias during progression of hypertrophy

Mechanoelectrical remodeling and arrhythmias during progression of hypertrophy

Beta 1 adrenoceptor blockade promotes angiogenesis in hypertrophied myocardium of transverse aortic constricted mice

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