Echocardiographic assessment of global left ventricular function in mice

Stypmann, Jörg; Engelen, Markus A.; Troatz, Clemens; Rothenburger, Markus; Eckardt, Lars; Tiemann, Klaus

doi:10.1258/la.2007.06001e

Cited by 102 publications

(78 citation statements)

References 60 publications

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“…In Münster, another cohort was assessed: 26-month-old mice in which rapamycin or vehicle treatment had been initiated at 13 months of age, and 3-to 4-month-old young controls. Examinations were performed as previously described (52). In brief, following induction of anesthesia with isoflurane (2.0% isoflurane, 98% O2), examinations were performed with the system's 30-MHz linear probe.…”

Section: Methodsmentioning

confidence: 99%

Rapamycin extends murine lifespan but has limited effects on aging

Neff

Flores-Dominguez²,

Ryan³

et al. 2013

J. Clin. Invest.

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332

408

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Aging is a major risk factor for a large number of disorders and functional impairments. Therapeutic targeting of the aging process may therefore represent an innovative strategy in the quest for novel and broadly effective treatments against age-related diseases. The recent report of lifespan extension in mice treated with the FDA-approved mTOR inhibitor rapamycin represented the first demonstration of pharmacological extension of maximal lifespan in mammals. Longevity effects of rapamycin may, however, be due to rapamycin's effects on specific life-limiting pathologies, such as cancers, and it remains unclear if this compound actually slows the rate of aging in mammals. Here, we present results from a comprehensive, large-scale assessment of a wide range of structural and functional aging phenotypes, which we performed to determine whether rapamycin slows the rate of aging in male C57BL/6J mice. While rapamycin did extend lifespan, it ameliorated few studied aging phenotypes. A subset of aging traits appeared to be rescued by rapamycin. Rapamycin, however, had similar effects on many of these traits in young animals, indicating that these effects were not due to a modulation of aging, but rather related to aging-independent drug effects. Therefore, our data largely dissociate rapamycin's longevity effects from effects on aging itself.

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Section: Methodsmentioning

confidence: 99%

Rapamycin extends murine lifespan but has limited effects on aging

Neff

Flores-Dominguez²,

Ryan³

et al. 2013

J. Clin. Invest.

Self Cite

332

408

View full text Add to dashboard Cite

show abstract

“…Peak E and A heights were determined on mitral valve sequential waveforms in at least 5 waveforms. The mean performance index was calculated as the isovolumetric contraction time (ICT) plus the isovolumetric relaxation time (IRT) divided by the ejection time ([ICT+IRT]/ET) to determine if either systolic or diastolic dysfunction was present 21, 22, 23, 24, 25. Doppler measurement data represent 3 to 6 averaged cardiac cycles from at least 2 scans per mouse.…”

Section: Methodsmentioning

confidence: 99%

Modeling the Transition From Decompensated to Pathological Hypertrophy

Pascual

Schisler

Grevengoed

et al. 2018

JAHA

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BackgroundLong‐chain acyl‐CoA synthetases (ACSL) catalyze the conversion of long‐chain fatty acids to fatty acyl‐CoAs. Cardiac‐specific ACSL1 temporal knockout at 2 months results in a shift from FA oxidation toward glycolysis that promotes mTORC1‐mediated ventricular hypertrophy. We used unbiased metabolomics and gene expression analyses to examine the early effects of genetic inactivation of fatty acid oxidation on cardiac metabolism, hypertrophy development, and function.Methods and ResultsGlobal cardiac transcriptional analysis revealed differential expression of genes involved in cardiac metabolism, fibrosis, and hypertrophy development in Acsl1 H−/− hearts 2 weeks after Acsl1 ablation. Comparison of the 2‐ and 10‐week transcriptional responses uncovered 137 genes whose expression was uniquely changed upon knockdown of cardiac ACSL1, including the distinct upregulation of fibrosis genes, a phenomenon not observed after complete ACSL1 knockout. Metabolomic analysis identified metabolites altered in hearts displaying partially reduced ACSL activity, and rapamycin treatment normalized the cardiac metabolomic fingerprint.ConclusionsShort‐term cardiac‐specific ACSL1 inactivation resulted in metabolic and transcriptional derangements distinct from those observed upon complete ACSL1 knockout, suggesting heart‐specific mTOR (mechanistic target of rapamycin) signaling that occurs during the early stages of substrate switching. The hypertrophy observed with partial Acsl1 ablation occurs in the context of normal cardiac function and is reminiscent of a physiological process, making this a useful model to study the transition from physiological to pathological hypertrophy.

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“…All M-mode measurements should follow the guidelines of the American Society of Echocardiography. Fractional shortening (FS), which is considered as an important parameter for the evaluation of systolic function, can be easily obtained from the following equation (Stypmann, Engelen et al 2009):…”

Section: Relevant Equations Used In Echocardiographymentioning

confidence: 99%

“…The limitation of M-mode functional measurements is that these parameters are estimated by assuming symmetry of the LV; besides cardiac function is only assessed at the one dimensional level, unlike measurements in B-mode view which are assessed based on the area of LV at two dimensional levels (Stypmann, Engelen et al 2009). …”

Section: Relevant Equations Used In Echocardiographymentioning

confidence: 99%

See 1 more Smart Citation

In Vivo Measurements of Biophysical Properties of a Heart and Aorta in a Mouse Model of Marfan Syndrome

Lee

Esfandiarei

Sheng

et al. 2014

Canadian Journal of Cardiology

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In Marfan Syndrome (MFS) patients cardiovascular complications are the most life-threatening manifestations and death is often sudden due to aortic dissection and rupture. Echocardiography is critical in the diagnosis and follow-up of MFS patients to detect and evaluate their cardiovascular phenotype. High frequency echocardiography was used to investigate the structural and functional properties on 6-and 12-mo WT and MFS [Fbn1 (C1039G/+)] mice (n = 8). The data show that Pulse Wave Velocity (PWV) was significantly increased in 6-mo MFS vs. WT (366.6 ± 19.9 vs. 205.2 ± 18.1 cm/s; p < 0.001) and 12-mo MFS vs. WT (459.5 ± 42.3 vs. 205.3 ± 30.3 m/s; p = 0.001) and the PWV increased directly in proportion to age in MFS mice but not in WT mice. LV mass (3.06 ± 0.16 vs. 2.46 ± 0.09 μm/g; p = 0.007) was significantly increased in 6-mo MFS mice compared with WT. We also found a significantly enlarged aortic root, decreased E/A ratio, prolonged isovolumic relaxation time and increased myocardial performance index in MFS mice compared with WT for both age groups. This study shows significant aortic dilation and central aortic stiffness in the MFS mice which are associated with LV hypertrophy, systolic and diastolic dysfunction. Moreover, the symptoms progressed with increasing age from six months to twelve months.

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Echocardiographic assessment of global left ventricular function in mice

Cited by 102 publications

References 60 publications

Rapamycin extends murine lifespan but has limited effects on aging

Rapamycin extends murine lifespan but has limited effects on aging

Modeling the Transition From Decompensated to Pathological Hypertrophy

In Vivo Measurements of Biophysical Properties of a Heart and Aorta in a Mouse Model of Marfan Syndrome

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