Leptin induces elongation of cardiac myocytes and causes eccentric left ventricular dilatation with compensation

2007 ◽  
Vol 292 (5) ◽  
pp. H2387-H2396 ◽  
Author(s):  
Yukiko Abe ◽  
Koh Ono ◽  
Teruhisa Kawamura ◽  
Hiromichi Wada ◽  
Toru Kita ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Myocytes ◽  
Systolic Function ◽  
Left Ventricular ◽  
Leptin Receptors ◽  
Jak2 Inhibitor ◽  
Axis Length ◽  
And Function ◽  
Plasma Leptin ◽  
Fractional Shortening

One of the major manifestations of obesity is an increased production of the adipocyte-derived 16-kDa peptide leptin, which acts mainly on hypothalamic leptin receptors. Leptin receptors are widely distributed in various tissues, including the heart. Whereas increased plasma leptin levels have been reported in patients with congestive heart failure, systemic alterations induced by obesity can affect cardiac hypertrophy, and the direct effects of leptin on cardiac structure and function still remain to be determined. We first exposed primary cardiac myocytes from neonatal rats to leptin for 48 h. This resulted in a significant increase in myocyte long-axis length ( P < 0.05 at 50 ng/ml) but not in the short-axis width. Leptin induced the rapid phosphorylation of STAT3 and its DNA binding in cardiac myocytes. Administration of a JAK2 inhibitor, AG-490, completely inhibited all of these effects by leptin. Furthermore, we examined the effect of continuous infusion of leptin for 4 wk following myocardial infarction in mice. Echocardiography demonstrated that left ventricular fractional shortening in the leptin-infused group (28.4 ± 2.8%) was significantly higher than that in the PBS-infused group (18.4 ± 2.2%) following myocardial infarction. Interestingly, left ventricular diastolic dimension in the leptin-infused group (4.56 ± 0.12 mm) was also higher than that in the PBS-infused group (4.13 ± 0.09 mm). These results demonstrate that leptin induces the elongation of cardiac myocytes via a JAK/STAT pathway and chronic leptin infusion causes eccentric dilatation with augmented systolic function after myocardial infarction.

scholarly journals Subtle Right Ventricular Affection in Patients with Acute Myocardial Infarction, Echocardiographic Assessment

2020 ◽  
Vol 8 (B) ◽  
pp. 1212-1218
Author(s):  
Abdallah Mohamed ◽  
Shaaban Alramlawy ◽  
Samir El-Hadidy ◽  
Mohamed Ibrahiem Affify ◽  
Waheed Radwan
Keyword(s):  
Myocardial Infarction ◽  
Right Ventricular ◽  
Significant Relationship ◽  
Longitudinal Strain ◽  
Systolic Function ◽  
Coronary Intervention ◽  
Left Ventricular ◽  
Adverse Outcomes ◽  
The Right ◽  
And Function

BACKGROUND: The right ventricle (RV) has historically received less attention than its counterpart of the left side of the heart, yet there is a substantial body of evidence showing that RV size and function are perhaps equally important in predicting adverse outcomes in cardiovascular diseases. AIM: The aim of our work was to evaluate incidence and impact of right ventricular (RV) affection in patients with acute left ventricular myocardial infarction subjected to primary percutaneous coronary intervention (1ry PCI). METHODS: The study was conducted on 80 patients who had acute left ventricle ST elevated myocardial infarction (LV STEMI) and subjected to 1ry PCI. The study was done in Cairo University, critical care department. All patients were studied within 2 days after 1ry PCI, RV function was assessed by echocardiography through tricuspid annular plane systolic excursion (TAPSE) and speckle tracking echocardiography. We excluded patients with RV infarction, moderate to severe tricuspid regurgitation, pulmonary hypertension, dilated cardiomyopathy, atrial or ventricular septal defect, and patients who had cardiac dysrhythmias. RESULTS: Out of 80 patients (64 men and 16 women) included in the study, 38 patients (47.5%) had TAPSE <1.7 cm, and 48 patients (60%) had RV longitudinal strain less negative than −19%.There was a statistically significant relationship between RV affection and anterior STEMI, left anterior descending artery as an infarct-related artery, duration of intensive care unit stay, impairment of LV global and regional systolic function, in-hospital complications, and 1-year mortality. CONCLUSION: RV dysfunction is not uncommon in acute LV STEMI when using the definition of TAPSE <17 cm and RV longitudinal strain less negative than −19%.There was a significant relationship between RV dysfunction and poor outcome in patients with acute LV STEMI.

Abstract 99: Ac-SDKP Protects the Heart From Post-myocardial Infarction Remodeling and Dysfunction in Mice

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Hongmei Peng ◽  
Jiang Xu ◽  
Xiao-Ping Yang ◽  
Xiangguo Dai ◽  
Edward Petersion ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Posterior Wall ◽  
Capillary Density ◽  
Left Ventricular ◽  
Posterior Wall Thickness ◽  
Lv Remodeling ◽  
Anti Inflammatory ◽  
And Function ◽  
Fractional Shortening

N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) has anti-inflammatory, anti-fibrotic and pro-angiogenic effects. We previously observed that Ac-SDKP reduces incidence of cardiac rupture in mice with acute myocardial infarction (MI), which is associated with its anti-inflammatory and pro-angiogenic properties. We hypothesized that Ac-SDKP, via its anti-fibrotic and pro-angiogenic actions, ameliorates left ventricular (LV) dilatation and fibrosis, thus improving cardiac function post-MI. C57BL/6J mice were divided into three groups: 1) sham MI, 2) MI + vehicle (VEH), and 3) MI + Ac-SDKP. Ac-SDKP (1.6 mg/kg/day) was given immediately after MI induction ( i.p. via osmotic pump) for 5 weeks. Cardiac remodeling and function were assessed by echocardiography, and interstitial collagen fraction (ICF) and capillary density was determined histologically. We found that Ac-SDKP 1) reduced LV remodeling, evidenced by decreased LV chamber dimensions and areas, and reduced ICF and increased capillary density, with no changes in posterior wall thickness and LV weight (LVW), and 2) improved cardiac function, demonstrated by increased fractional shortening (FS) and ejection fraction (EF) (Table). We conclude that in murine models of MI, Ac-SDKP protects the heart from more severe remodeling and dysfunction, possibly via its anti-fibrotic and pro-angiogenic actions. Thus, the use of Ac-SDKP or its analogues could be a new and effective alternative in restoring cardiac function in patients after MI.

P3441Impact of maternal preeclampsia on left ventricular structure and function in the newborn heart

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
R O B Voegg ◽  
J Ghouse ◽  
A S Sillesen ◽  
C A Pihl ◽  
A Axelsson Raja ◽  
...  
Keyword(s):  
Systolic Function ◽  
Interventricular Septum ◽  
Posterior Wall ◽  
Population Based ◽  
Left Ventricular ◽  
P Value ◽  
Internal Diameter ◽  
Increased Risk ◽  
And Function ◽  
Fractional Shortening

Abstract Background Maternal preeclampsia (PE) has been associated with an increased risk of a variety of congenital heart defects in the infant. Whether PE also confers an increased risk of subtle structural and functional cardiac deficits is unknown. Purpose We investigated whether left ventricular dimensions and systolic function differed among infants of mothers with PE, compared to infants born after uncomplicated pregnancies. Method Systematic transthoracic echocardiography (TTE) was performed in neonates included in a population-based study in the period 2016–2018 (n=25,000). TTE was preferably performed within 14 days of birth. Left ventricular (LV) posterior wall end-diastolic thickness (LVPWd), interventricular septum end-diastole thickness (IVSd), LV internal diameter in end-diastole and end-systole (LVIDd and LVIDs), LV ejection fraction (LVEF) and fractional shortening (FS) were assessed. Information on maternal PE (ICD-10 codes DO140–142 and DO159) was retrieved from an obstetric database. Using linear regression in a sample of echocardiograms, we compared the LV structure and function adjusted for maternal age; gestational age; sex; weight and length. Results In total, 447 infants were exposed to PE, and 7,178 were born to uncomplicated pregnancies (Table). In infants of PE mothers, we found significantly larger LVPWd and IVSd (0.18 mm, 95% CI [0.14; 0.22], p<0.001 and 0.06 mm, 95% CI [0.02; 0.10], p=0.001, resp.) and LVIDd as LVIDs were significantly smaller (−0.15 mm, 95% CI [−0.29; −0.01], p=0.032 and −0.16 mm 95% CI [−0.28; −0.04], p=0.009, resp.) compared to infants of non-PE mothers. We found no differences in systolic function. LV measures in PE and non-PE infants Parameter Infants of PE mothers, Infants of non-PE mothers, p-value Estimate* [95% CI] p-value mean [± SD] (n=447) mean [± SD] (n=7,178) Left Ventricular Posterior Wall in end-Diastole, LVPWd (mm) 2.20 [±0.58] 2.07 [±0.40] <0.001 0.18 [0.14; 0.22] <0.001 Interventricular Septum in end-Diastole, IVSd (mm) 2.53 [±0.52] 2.55 [±0.41] 0.562 0.06 [0.02; 0.10] 0.001 Left Ventricular Internal Diameter in end-Diastole, LVIDd (mm) 19.35 [±2.00] 20.10 [±1.41] <0.001 −0.15 [−0.29; −0.01] 0.032 Left Ventricular Internal Diameter in end-Diastole, LVIDs (mm) 13.13 [±1.43] 13.65 [±1.79] <0.001 −0.16 [−0.28; −0.04] 0.009 Fractional Shortening, FS (%) 32.10 [±4.07] 32.11 [±3.86] 0.937 0.26 [−0.11; 0.63] 0.168 Left Ventricular Ejection Fraction, LVEF (%) 63.19 [±5.61] 63.09 [±5.30] 0.690 0.34 [−0.17; 0.85] 0.192 *Adjusted for maternal age; gestational age; sex; weight and length. Conclusion In the largest population-based group of neonates to date, we showed that infants born to PE mothers compared to infants of non-PE mothers had significantly thicker left ventricular myocardium, and reduced left ventricular volumes. However, PE was not associated with altered systolic function. Our results might reflect an adaption of the fetal heart to the increased resistance in the placental arteries in PE mothers, and a secondary increased left ventricular afterload. Acknowledgement/Funding Danish Heart Association, Danish Children's Heart Foundation, Candy's Found., Toyota Found., Herlev-Gentofte Hospital Research Found., Lundbeck Found.

scholarly journals Effects of Isoflurane Concentration on Basic Echocardiographic Parameters of the Left Ventricle in Rats

2012 ◽  
pp. 419-423 ◽  
Author(s):  
H. ŘÍHA ◽  
F. PAPOUŠEK ◽  
J. NECKÁŘ ◽  
J. PIRK ◽  
B. OŠŤÁDAL
Keyword(s):  
Systolic Function ◽  
Animal Experiments ◽  
Left Ventricular ◽  
Isoflurane Concentration ◽  
Anesthetic Agents ◽  
Male Wistar Rats ◽  
Echocardiographic Parameters ◽  
Echocardiographic Images ◽  
And Function ◽  
Fractional Shortening

Transthoracic echocardiography (TTE) has become an important modality for the assessment of cardiac structure and function in animal experiments. The acquisition of echocardiographic images in rats requires sedation/anesthesia to keep the rats immobile. Commonly used anesthetic regimens include intraperitoneal or inhalational application of various anesthetics. Several studies have compared the effects of anesthetic agents on echocardiographic parameters in rats; however, none of them examined the effects of different concentrations of inhalational anesthetics on echocardiographic parameters. Accordingly, the aim of this study was to examine the effects of different concentrations of isoflurane used for anesthesia during TTE examination in rats on basic echocardiographic parameters of left ventricular (LV) anatomy and systolic function. TTE examinations were performed in adult male Wistar rats (n=10) anesthetized with isoflurane at concentrations of 1.5-3 %. Standard echocardiograms were recorded for off-line analysis. An absence of changes in basic echocardiographic parameters of LV anatomy and systolic function was found under isoflurane anesthesia using concentrations between 1.5-2.5 %. An isoflurane concentration of 3 % caused a small, but statistically significant, increase in LV chamber dimensions without a concomitant change in heart rate or fractional shortening. For the purpose of TTE examination in the rat, our results suggest that isoflurane concentrations ≤ 2.5 % can be safely recommended.

Exercise attenuates inflammation and limits scar thinning after myocardial infarction in mice

2015 ◽  
Vol 309 (2) ◽  
pp. H345-H359 ◽  
Author(s):  
Sarah-Lena Puhl ◽  
Andreas Müller ◽  
Michael Wagner ◽  
Yvan Devaux ◽  
Michael Böhm ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Systolic Function ◽  
Left Ventricular ◽  
Heart Weight ◽  
Lv Function ◽  
Sham Operation ◽  
Beneficial Effects ◽  
End Diastolic Volume ◽  
Underlying Mechanisms ◽  
And Function

Although exercise mediates beneficial effects in patients after myocardial infarction (MI), the underlying mechanisms as well as the question of whether an early start of exercise after MI is safe or even beneficial are incompletely resolved. The present study analyzed the effects of exercise before and reinitiated early after MI on cardiac remodeling and function. Male C57BL/6N mice were housed sedentary or with the opportunity to voluntarily exercise for 6 wk before MI induction (ligation of the left anterior descending coronary artery) or sham operation. After a 5-day exercise-free phase after MI, mice were allowed to reexercise for another 4 wk. Exercise before MI induced adaptive hypertrophy with moderate increases in heart weight, cardiomyocyte diameter, and left ventricular (LV) end-diastolic volume, but without fibrosis. In sedentary mice, MI induced eccentric LV hypertrophy with massive fibrosis but maintained systolic LV function. While in exercised mice gross LV end-diastolic volumes and systolic function did not differ from sedentary mice after MI, LV collagen content and thinning of the infarcted area were reduced. This was associated with ameliorated activation of inflammation, mediated by TNF-α, IL-1β, and IL-6, as well as reduced activation of matrix metalloproteinase 9. In contrast, no differences in the activation patterns of various MAPKs or adenosine receptor expressions were observed 5 wk after MI in sedentary or exercised mice. In conclusion, continuous exercise training before and with an early reonset after MI ameliorates adverse LV remodeling by attenuating inflammation, fibrosis, and scar thinning. Therefore, an early reonset of exercise after MI can be encouraged.

Effect of overweight and obesity on the left ventricular systolic and diastolic functions in patients with acute myocardial infarction

2012 ◽  
Vol 35 (4) ◽  
pp. 229 ◽  
Author(s):  
Fatih Poyraz ◽  
Murat Turfan ◽  
Sinan A. Kocaman ◽  
Huseyin U. Yazici ◽  
Nihat Sen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Diastolic Function ◽  
Systolic Function ◽  
Study Groups ◽  
Left Ventricular ◽  
Normal Weight ◽  
Overweight And Obesity ◽  
Weight Group ◽  
Normal Weight Group ◽  
Diastolic Functions

Purpose: The purpose of this study was to evaluate whether a association exits among overweight and obesity and left ventricular systolic and diastolic functions in patients admitted with first ST-elevation myocardial infarction (STEMI). Methods: The present study was performed on 451 consecutive patients diagnosed with first STEMI (376 men, 75 women; mean age 56.1±10.8 years). The patients were classified into three groups based on their body mass index (BMI) as normal weight (BMI < 25 kg/m2), overweight (BMI: 25-29.9 kg/m2) and obese (BMI > 30 kg/m2). Echocardiographic features were evaluated and compared among the three groups. Results: Mitral annulus E velocities were higher in obese individuals than normal weight group (p < 0.01). In contrast, mitral A velocities were lower (p =0.03); consequently, E\A and E'\A' ratios were lower (both p =0.01) in the obese group with respect to normal weight group. When the correction of entire variations existing among the groups were performed using multivariate linear regressions analyses, it turned out that BMI was independently associated with E/A (β= -0.19, p =0.044) and with E'/A' (β= -0.016, p=0.021). Ejection fraction, wall motion score index and myocardial S velocities were comparable among the study groups (p > 0.05). Conclusion: These results suggest that while obesity has no adverse effect on the left ventricular systolic function, it has unfavorable consequences on the left ventricular diastolic function in the patients with first STEMI. In contrast, no unfavorable effects of overweight on the left ventricular systolic and diastolic function were detected.

Implication of anti-angiogenic VEGF-A165b in angiogenesis and systolic function after reperfused myocardial infarction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
V Marcos Garces ◽  
C Rios-Navarro ◽  
L Hueso ◽  
A Diaz ◽  
C Bonanad ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Adjuvant Therapy ◽  
Ejection Fraction ◽  
Infarct Size ◽  
Systolic Function ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Funding Source ◽  
Coronary Reperfusion ◽  
Ventricular Ejection Fraction

Abstract Background Angiogenesis participates in re-establishing microcirculation after myocardial infarction (MI). Purpose In this study, we aim to further understand the role of the anti-angiogenic isoform vascular endothelial growth factor (VEGF)-A165b after MI and explore its potential as a co-adjuvant therapy to coronary reperfusion. Methods Two mice MI models were formed: 1) permanent coronary ligation (non-reperfused MI), 2) transient 45-min coronary occlusion followed by reperfusion (reperfused MI); in both models, animals underwent echocardiography before euthanasia at day 21 after MI induction. Serum and myocardial VEGF-A165b levels were determined. In both experimental MI models, functional and structural implication of VEGF-A165b blockade was assessed. In a cohort of 104 ST-segment elevation MI patients, circulating VEGF-A165b levels were correlated with cardiovascular magnetic resonance-derived left ventricular ejection fraction at 6-months and with the occurrence of adverse events (death, heart failure and/or re-infarction). Results In both models, circulating and myocardial VEGF-A165b presence was increased 21 days after MI induction. Serum VEGF-A165b levels inversely correlated with systolic function evaluated by echocardiography. VEGF-A165b blockage increased capillary density, reduced infarct size, and enhanced left ventricular function in reperfused, but not in non-reperfused MI experiments. In patients, higher VEGF-A165b levels correlated with depressed ejection fraction and worse outcomes. Conclusions In experimental and clinical studies, higher serum VEGF-A165b levels associates with a worse systolic function. Its blockage enhances neoangiogenesis, reduces infarct size, and increases ejection fraction in reperfused, but not in non-reperfused MI experiments. Therefore, VEGF-A165b neutralization represents a potential co-adjuvant therapy to coronary reperfusion. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): This study was funded by “Instituto de Salud Carlos III” and “Fondos Europeos de Desarrollo Regional FEDER” (Exp. PIE15/00013, PI17/01836, PI18/00209 and CIBERCV16/11/00486).

Effects of avertin versus xylazine-ketamine anesthesia on cardiac function in normal mice

2001 ◽  
Vol 281 (5) ◽  
pp. H1938-H1945 ◽  
Author(s):  
Chari Y. T. Hart ◽  
John C. Burnett ◽  
Margaret M. Redfield
Keyword(s):  
Cardiac Function ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Lv Function ◽  
Ketamine Anesthesia ◽  
The Difference ◽  
And Function ◽  
Derivatives Of

Anesthetic regimens commonly administered during studies that assess cardiac structure and function in mice are xylazine-ketamine (XK) and avertin (AV). While it is known that XK anesthesia produces more bradycardia in the mouse, the effects of XK and AV on cardiac function have not been compared. We anesthetized normal adult male Swiss Webster mice with XK or AV. Transthoracic echocardiography and closed-chest cardiac catheterization were performed to assess heart rate (HR), left ventricular (LV) dimensions at end diastole and end systole (LVDd and LVDs, respectively), fractional shortening (FS), LV end-diastolic pressure (LVEDP), the time constant of isovolumic relaxation (τ), and the first derivatives of LV pressure rise and fall (dP/d t max and dP/d t min, respectively). During echocardiography, HR was lower in XK than AV mice (250 ± 14 beats/min in XK vs. 453 ± 24 beats/min in AV, P < 0.05). Preload was increased in XK mice (LVDd: 4.1 ± 0.08 mm in XK vs. 3.8 ± 0.09 mm in AV, P < 0.05). FS, a load-dependent index of systolic function, was increased in XK mice (45 ± 1.2% in XK vs. 40 ± 0.8% in AV, P < 0.05). At LV catheterization, the difference in HR with AV (453 ± 24 beats/min) and XK (342 ± 30 beats/min, P < 0.05) anesthesia was more variable, and no significant differences in systolic or diastolic function were seen in the group as a whole. However, in XK mice with HR <300 beats/min, LVEDP was increased (28 ± 5 vs. 6.2 ± 2 mmHg in mice with HR >300 beats/min, P < 0.05), whereas systolic (LV dP/d t max: 4,402 ± 798 vs. 8,250 ± 415 mmHg/s in mice with HR >300 beats/min, P < 0.05) and diastolic (τ: 23 ± 2 vs. 14 ± 1 ms in mice with HR >300 beats/min, P < 0.05) function were impaired. Compared with AV, XK produces profound bradycardia with effects on loading conditions and ventricular function. The disparate findings at echocardiography and LV catheterization underscore the importance of comprehensive assessment of LV function in the mouse.

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