Validation of the wall motion score and myocardial performance indexes as novel techniques to assess cardiac function in mice after myocardial infarction

Zhang, Yan; Takagawa, Junya; Sievers, Richard E.; Khan, Muhammad Fahad; Viswanathan, Mohan; Springer, Matthew L.; Foster, Elyse; Yeghiazarians, Yerem

doi:10.1152/ajpheart.00895.2006

Cited by 82 publications

(60 citation statements)

References 21 publications

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“…[27], [28], [29], [30] The calculation of ejection fraction is also consistent with a recent study. [31] The additional capability of directly measuring percent ejection fraction in the 2D parasternal long axis allows high frequency echocardiography to be used alongside other newer imaging modalities such as 3D echo and MRI. [32], [33], [34] Our histological results are in agreement with previous studies demonstrating patchy fibrosis in the ventricles of mdx mice.…”

Section: Discussionmentioning

confidence: 99%

Dystrophin-deficient cardiomyopathy in mouse: Expression of Nox4 and Lox are associated with fibrosis and altered functional parameters in the heart

Spurney

Knoblach

Pistilli

et al. 2008

Neuromuscular Disorders

136

133

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Duchenne muscular dystrophy (DMD; dystrophin-deficiency) causes dilated cardiomyopathy in the second decade of life in affected males. We studied the dystrophin-deficient mouse heart (mdx) using high frequency echocardiography, histomorphometry, and gene expression profiling. Heart dysfunction was prominent at 9-10 months of age and showed significantly increased LV internal diameter (end systole) and decreased posterior wall thickness. This cardiomyopathy was associated with a 30% decrease in shortening fraction. Histologically, there was a 10-fold increase in connective tissue volume (fibrosis). mRNA profiling with RT-PCR validation showed activation of key profibrotic genes, including Nox4 and Lox. The Nox gene family expression differed in mdx heart and skeletal muscle, where Nox2 was specifically induced in skeletal muscle while Nox4 was specifically induced in heart. This is the first report of an altered profibrotic gene expression profile in cardiac tissue of dystrophic mice showing echocardiographic evidence of cardiomyopathy.

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Section: Discussionmentioning

confidence: 99%

Dystrophin-deficient cardiomyopathy in mouse: Expression of Nox4 and Lox are associated with fibrosis and altered functional parameters in the heart

Spurney

Knoblach

Pistilli

et al. 2008

Neuromuscular Disorders

136

133

View full text Add to dashboard Cite

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“…Measurements were standardized at a lower and comparable heart rate in all of the groups to control for loading. 19,20 The normal physiological heart rate in mice is rapid (Ͼ600 bpm) and results in the loss of the A velocity. 19,20 Aldosterone increased the mitral E velocity (early diastolic filling velocity) with minimal change in late diastolic filling (mitral A wave).…”

Section: Hisdn Improved Diastolic Dysfunctionmentioning

confidence: 99%

“…19,20 The normal physiological heart rate in mice is rapid (Ͼ600 bpm) and results in the loss of the A velocity. 19,20 Aldosterone increased the mitral E velocity (early diastolic filling velocity) with minimal change in late diastolic filling (mitral A wave). The resultant E/A ratio (diastolic dysfunction) was, therefore, increased, indicating reduced LV compliance (increased stiffness).…”

Section: Hisdn Improved Diastolic Dysfunctionmentioning

confidence: 99%

Effects of Fixed-Dose Isosorbide Dinitrate/Hydralazine on Diastolic Function and Exercise Capacity in Hypertension-Induced Diastolic Heart Failure

et al. 2009

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Abstract-Hypertension-induced diastolic heart failure accounts for a large proportion of all heart failure presentations.Hypertension also induces left ventricular (LV) hypertrophy. Fixed-dose isosorbide dinitrate/hydralazine (HISDN) decreased mortality in human systolic heart failure but it is unknown whether it improves maladaptive myocardial remodeling. We sought to test the hypothesis that chronic HISDN modulates LV hypertrophy and myocardial remodeling in hypertension-induced diastolic heart failure. FVB mice underwent either saline (nϭ18) or aldosterone (nϭ28) infusion. All underwent uninephrectomy and drank 1% salt water for 4 weeks. Mice were randomized after surgery to regular chow or chow containing HISDN (isosorbide dinitrate: 26 mg/kg per day; hydralazine: 50 mg/kg per day) for 4 weeks. Aldosterone infusion increased tail-cuff blood pressure (161Ϯ3 mm Hg) versus saline-infused mice (129Ϯ2 mm Hg). Aldosterone induced LV hypertrophy versus saline-infused mice (LV:body weight ratio: 4.2Ϯ0.1 versus 3.6Ϯ0.1 mg/g). HISDN attenuated the aldosterone-induced increased in systolic blood pressure (137Ϯ5 mm Hg) and also lowered blood pressure in saline-infused mice (114Ϯ2 mm Hg). However, HISDN did not cause LV hypertrophy regression in aldosterone-infused mice. Aldosterone increased LV end-diastolic dimensions that were not attenuated by HISDN. Similarly, neither aldosterone infusion nor HISDN affected LV end-systolic dimensions. LV ejection fraction and wet:dry lung ratio were not different between aldosterone-untreated and aldosterone-HISDN mice. However, mitral Doppler E/A ratio (a measure of diastolic function), exercise capacity, and plasma soluble vascular cell adhesion molecule 1 levels were improved in aldosterone-HISDN hearts. In conclusion, fixed-dose HISDN improved hypertension, diastolic function, and exercise capacity and reduced soluble vascular cell adhesion molecule 1 levels. There were no reductions in LV hypertrophy, cardiac fibrosis, or pulmonary congestion. These functional improvements are likely related to extracardiac effects, such as effects on the vasculature. Key Words: diastolic heart failure Ⅲ hydralazine Ⅲ nitrates Ⅲ hypertension Ⅲ exercise capacity H ypertension induces left ventricular (LV) hypertrophy (LVH) and is a major cause of both diastolic and systolic heart failures (HF). 1 Diastolic HF accounts for up to Յ50% of all HF presentations 2 and is associated with increasing morbidity and mortality. 3 Diastolic HF refers to the clinical syndrome of pulmonary congestion in the presence of a normal LV ejection fraction, whereas diastolic dysfunction denotes an abnormality of mechanical properties that exist during LV relaxation and filling. 4,5 Diastolic dysfunction may be an intermediary between hypertension and HF. 6 In the setting of hypertension, diastolic HF represents a diverse clinical syndrome with various associated comorbidities (eg, age and sex) and manifests a spectrum of symptoms ranging from exercise intolerance to acute pulmonary edema. In addition to LVH, cardiac...

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“…The echocardiographic measurements were recorded according to standard methods from previously published reports 7,11,16,17 . A parasternal long-axis B-mode image was acquired with appropriate positioning of the scan head so that the maximum LV length could be identified, then a clockwise 90° rotation at the papillary muscle level was performed to obtain the parasternal short-axis view.…”

Section: Echocardiographic Measurementsmentioning

confidence: 99%

Effect of anesthesia level on murine cardiac function

et al. 2014

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Echocardiography allows for sensitive and non-invasive Background: assessment of cardiac function in mice, but requires sedation and immobility, which influences cardiac performance. Minimizing the hemodynamic effects of anesthesia is extremely important for improving the applicability of animal models to the clinical setting. We sought to evaluate the effects of isoflurane dose on myocardial function in a murine model.Twelve healthy C57BL/6 mice were studied with three different Methods: isoflurane anesthesia regimens: deep anesthesia with an objective of heart rate (HR) between 350 and 400 beats per minute (bpm), light anesthesia with an objective of HR between 475 and 525 bpm and just before the mice woke up (>575 bpm). Using a high-resolution ultrasound system, stroke volume, cardiac output, left ventricle dimension and fractional shortening were recorded.Fractional shortening was not statistically different in the awake group Results: and the light anesthesia group (49±5% in awake mice vs. 48±5%; p=0.62), whereas it was different compared to the deep anesthesia group (31±5%, p<0.0001 compared to both groups). Similar results were found for stroke volume (41.4±5.8 ml vs. 41.6±6.9 ml; p=0.81 and 35±8.3 ml; p<0.05 compared to both groups). Cardiac output was slightly lower in the light anesthesia group compared to the awake group (21.9±3.6 ml/min vs. 25.6±3.3; p=0.02) due to HR significant difference (522±17 bpm vs. 608±23 bpm; p<0.0001).Doppler echocardiography can be performed under very light Conclusions: anesthesia using small doses of isoflurane without influencing cardiac inotropic function. This technique allows for accurate and reproducible assessment of cardiac function while minimizing hemodynamic perturbations.

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Validation of the wall motion score and myocardial performance indexes as novel techniques to assess cardiac function in mice after myocardial infarction

Cited by 82 publications

References 21 publications

Dystrophin-deficient cardiomyopathy in mouse: Expression of Nox4 and Lox are associated with fibrosis and altered functional parameters in the heart

Dystrophin-deficient cardiomyopathy in mouse: Expression of Nox4 and Lox are associated with fibrosis and altered functional parameters in the heart

Effects of Fixed-Dose Isosorbide Dinitrate/Hydralazine on Diastolic Function and Exercise Capacity in Hypertension-Induced Diastolic Heart Failure

Effect of anesthesia level on murine cardiac function

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