scholarly journals Investigating Insulin Resistance in Pediatric Cardiomyopathy - A Pilot Study

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A660-A661
Author(s):  
Daniel Mak ◽  
Kaitlin A Ryan ◽  
Joan C Han
Keyword(s):  
Insulin Resistance ◽  
Dilated Cardiomyopathy ◽  
Wall Thickness ◽  
Cardiac Dysfunction ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Inverse Association ◽  
Septal Thickness ◽  
Posterior Wall Thickness ◽  
Pediatric Cardiomyopathy

Abstract Children with cardiomyopathy are a vulnerable population and understanding the factors that contribute to cardiac dysfunction are of great importance. At the biochemical level, energy utilization by cardiomyocytes during stress may provide insight into the progression of cardiomyopathy. There is a large body of literature that describes insulin resistance in adults with cardiomyopathy (1,2). Extensive literature on the topic in adult individuals exists however investigation in the pediatric population is sparse. The pathophysiology of disease in children and adolescents is unique. To study the role of insulin resistance in pediatric cardiomyopathy, we measured the homeostasis model assessment-estimated insulin resistance (HOMA-IR) at baseline in pre-pubertal patients (age 13-18 years old; mean 16 years old; n = 8) with either hypertrophic cardiomyopathy (HCM) or dilated cardiomyopathy (DCM). In patients with HCM, greater insulin resistance was positively correlated with greater left ventricular (LV) septal thickness (r = 0.55; p = 0.33; n = 5) and LV posterior wall thickness (r = 0.7; p = 0.19; n = 5) during diastole. As expected, insulin resistance was strongly correlated with BMI (r = 0.84; p = 0.08; n = 5) though greater BMI was not as strongly associated with LV septal thickness (r = 0.59; p = 0.3; n = 5) or posterior wall thickness (r = 0.59; p = 0.3; n = 5). In patients with DCM, insulin resistance was positively correlated with LV end diastolic volume (r = 0.59; p = 0.59; n = 3). Interestingly, there was an observed inverse association between insulin resistance and BMI in DCM (r = -0.85; p = 0.34; n =3). Though our sample population is limited, thus affecting statistical significance, results showed that there was a trend towards greater insulin resistance in patients with poorer cardiac measurements. These findings are consistent with adult literature and the proposition that cardiac dysfunction is an insulin resistant state. References: (1) Riehle C, Abel ED. Insulin Signaling and Heart Failure. Circulation research. 2016;118(7):1151-1169. (2) Shah A, Shannon RP. Insulin resistance in dilated cardiomyopathy. Reviews in cardiovascular medicine. 2003;4 Suppl 6:S50-57

scholarly journals Diagnostic Utility of Electrocardiogram and Transthoracic Echocardiography in Diagnosis of Left Ventricular Hypertrophy among Known Hypertensive Patients

2020 ◽  
pp. 28-32
Author(s):  
Amit C. Botre ◽  
U. T. Mane ◽  
Dilip P. Patil ◽  
A. T. Pardesi ◽  
Anil Bhattad
Keyword(s):  
Wall Thickness ◽  
Ventricular Hypertrophy ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Age Group ◽  
Hypertensive Patients ◽  
Septal Thickness ◽  
Posterior Wall Thickness ◽  
Males And Females ◽  
The Mean

The purpose of the study is to find out presence of LVH by 2D Echo in all cases of hypertension in relation to their duration and severity. In this study it was observed that 59% subjects were males and 41% were females and the mean age of males and females was 64 yrs. Majority of them 36.5% were in the age group of 61-70 yrs, out of them majority of females 48.6% were from age group 71-80 yrs and majority of males 76.5% were from age group of >80 yrs. Study showed that occurrence of LVH by Interventricular septal thickness criteria and Left ventricular posterior wall thickness criteria of 2D Echo in relation to duration of hypertension was statistically not significant. Occurrence of LVH by interventricular septal thickness criteria and Left ventricular posterior wall thickness criteria of 2D Echo in relation to severity of hypertension was statistically not significant.

scholarly journals Evaluation of LVEF with Changing left Ventricular Morphology in Hypertrophic Cardiomyopathy

2019 ◽  
Vol 15 (1) ◽  
pp. 12-15
Author(s):  
Md Mohiuddin Masum ◽  
Rayhan Shahrear ◽  
Zinnat Ara Yesmin ◽  
Latifa Nishat ◽  
Laila Anjuman Banu
Keyword(s):  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Wall Thickness ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Septal Thickness ◽  
Posterior Wall Thickness

Background:Hypertrophic cardiomyopathy (HCM) is the most frequent type of cardiomyopathy. HCM is a disease of changing cardiac morphology that causes various form of cardiac dysfunction. HCM patients may remain asymptomatic and undiagnosed for a long time. If they become symptomatic, they commonly present with breathlessness, chest discomfort, and exertion. It is also responsible for the sudden cardiac death.Proper assessment of the functional status of the heart is required for proper management strategies of HCM. Objective: The objective of the study was to assess the IVS, PWT and LVEF in different cardiac phenotypes as well as to draw correlation among them. Materials and method:A descriptive cross-sectional study was undertaken on thirty-four adult Bangladeshi hypertrophic cardiomyopathy patients (thirty-one male, three female). The study was carried out in the Department of Anatomy, BSMMU. Diagnoses adult HCM patients were selected as study patients. Transthoracic echocardiography was done to assess the interventricular septal thickness (IVS), left ventricular posterior wall thickness (PWT) and left ventricular ejection fraction (LVEF). Result: The changes in the value of the left ventricular ejection fraction shows significant correlation with left ventricular posterior wall thickness,rather than the interventricular septal thickness. Conclusion:Though significant correlation between left ventricular ejection fraction and left ventricular posterior wall thickness was found, a large cohort study could be done to see the long term outcome of such correlation. University Heart Journal Vol. 15, No. 1, Jan 2019; 12-15

scholarly journals Cardiac remodeling indicators in adolescent athletes

2017 ◽  
Vol 63 (5) ◽  
pp. 427-434 ◽  
Author(s):  
Joaquim Castanheira ◽  
João Valente-dos-Santos ◽  
Daniela Costa ◽  
Diogo Martinho ◽  
Jorge Fernandes ◽  
...  
Keyword(s):  
Wall Thickness ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Basketball Players ◽  
Mean Values ◽  
Septal Thickness ◽  
Posterior Wall Thickness ◽  
Comparison Results ◽  
Hockey Players ◽  
Judo Athletes

Summary Objective: The idea that different sports and physical training type results in different cardiac adaptations has been widely accepted. However, this remodelling process among different sport modalities is still not fully understood. Thus, the current study aims to investigate the heart morphology variation associated with a set of different modalities characterized by distinct models of preparation and different methods and demands of training and completion. Method: The sample comprises 42 basketball players, 73 roller hockey players, 28 judo athletes and 21 swimmers. Anthropometry was assessed by a single and experienced anthropometrist and the same technician performed the echocardiographic exams. Analysis of variance was used to study age, body size and echocardiograph parameters as well as different sport athlete's comparison. Results: Basketball players are taller (F=23.448; p<0.001; ES-r=0.553), heavier (F=6.702; p<0.001; ES-r=0.334) and have a greater body surface area (F=11.896; p<0.001; ES-r=0.427). Basketball and hockey players have larger left auricle diameters compared with judo athletes (F=3.865; p=0.011; ES-r=0.316). Interventricular end-diastolic septal thickness (F=7.287; p<0.001; ES-r=0.347) and left ventricular posterior wall thickness (F=8.038; p<0.001; ES-r=0.362) of the judokas are smaller compared to the mean values of other sports participants. In addition, relative left parietal ventricular wall thickness is lower among swimmers compared with judokas (F=4.127; p=0.008; ES-r=0.268). Conclusion: The major contributors to changes in heart morphology are for the most part associated with sport-specific training and competition and the specific dynamics and adaptive mechanisms imposed by each sport.

Abstract 12078: Obese Girls With PCOS Have Evidence of Vascular Stiffening and Left Ventricular Hypertrophy Which Relate to Insulin Resistance

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Melanie Cree-Green ◽  
Uyen Truong ◽  
Jennifer L. Dorosz ◽  
Kerri Moreau ◽  
Gregory Coe ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Profile ◽  
Vascular Disease ◽  
Wall Thickness ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Plaque Formation ◽  
Vascular Stiffness ◽  
Posterior Wall Thickness ◽  
Vascular Stiffening

Introduction: Women with polycystic ovarian syndrome (PCOS) have evidence of greater plaque formation and vascular disease by the third decade of life compared to women without PCOS. We previously reported that obese girls with PCOS have a more atherogenic lipoprotein particle size profile compared to controls. It was unknown these youth also already had evidence of cardiac or vascular disease and plaque development. Hypothesis: We hypothesized that adolescent girls with PCOS have evidence of vascular stiffness and plaque formation. Methods: Sedentary, non-diabetic, obese girls with PCOS (OBP; N=38, age 14.9±0.2 years, BMI% 98.1±0.3) and without PCOS (OB; N=14, age 14±0.5 years, BMI% 97.4±0.7) were enrolled. Girls with clinical hypertension, renal disease or structural cardiac abnormalities were excluded. Measures included carotid IMT (CIMT), resting echocardiogram, blood pressure, serum lipid profile, and insulin sensitivity assessed with a hyperinsulinemic euglycemic clamp. Calculated measures included carotid beta- stiffness index and distention. Results: Resting blood pressures were normal for age and similar between groups. OBP had greater carotid vascular stiffness than OB (βstiffness 1.91±0.08U OB vs 2.19±0.09 OBP, p=0.01; Distention 0.23±0.17mm OB vs 0.18±0.01 OBP, P=0.0007), and there was evidence of greater left ventricular posterior wall thickness (0.79±0.03cm OB vs 0.88±0.02 OBP; P=0.02) and intraventricular wall thickness (0.77±0.04cm OB vs 0.86±0.02 OBP; P=0.04). There was no difference in CIMT between OBP and OB (0.45±0.02cm OB vs 0.48±0.01 OBP, P>0.1). However, OBP were also more insulin resistant than OB (glucose infusion rate 18.3±2.3 mg/leankg/min OB vs 10.4±1.6 OBP, P=0.0007), which correlated with left ventricular posterior wall thickness (R=-0.50, P<0.001). Conclusions: Obese normotensive girls with PCOS have vascular stiffening and left ventricular remodeling which relate to insulin resistance. They do not yet have increased CIMT, however, they have insulin resistance and a more atherogenic lipid profile, indicating that the substrate for imtimal-medial thickening and plaque formation is present. Interventions to prevent cardiovascular disease should begin in adolescence.

scholarly journals Leptin Improves Cardiac Structure and Function in Patients With Generalized Lipodystrophy

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A315-A316
Author(s):  
My-Le Nguyen ◽  
Vandana Sachdev ◽  
Thomas Burklow ◽  
Wen Li ◽  
Rebecca J Brown
Keyword(s):  
Metabolic Disease ◽  
Insulin Resistance ◽  
Wall Thickness ◽  
Hemoglobin A1c ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Open Label ◽  
Posterior Wall Thickness ◽  
Lv Mass ◽  
And Function

Abstract Lipodystrophy (LD) syndromes are rare disorders of deficient adipose tissue and severe metabolic disease, including insulin resistance, diabetes, and hypertriglyceridemia. LD may affect all adipose depots (generalized LD, GLD) or only some depots (partial LD, PLD). Low adipose mass leads to very low leptin in GLD, and variable leptin in PL. Treatment with exogenous leptin (metreleptin) improves metabolic disease in LD, particularly GLD. Left ventricular (LV) hypertrophy is frequent in LD, especially GLD. The mechanism for hypertrophy in LD is not known and may relate to glucose or lipotoxicity. We hypothesized that metreleptin would improve cardiac abnormalities in LD, and that this would be mediated by improvements in glucose and triglycerides (TG). We analyzed echocardiograms (echo), blood pressure (BP), heart rate (HR), and metabolic parameters in 38 subjects with LD (18 GLD, 20 PLD) who were treated with metreleptin in open-label clinical studies at the National Institutes of Health. 27 had repeat echo after 1y of metreleptin (mean 1.0 ± 0.2y), and 23 after 3 to 5y (mean 3.7±0.6y). In GLD, metreleptin significantly improved metabolic disease, including reduced TG (median(IQR) 740(403–1239), 138(88–196), 211(136–558) mg/dL at baseline, 1y, & 3-5y, P&lt;0.0001), hemoglobin A1c (9.5±3.0, 6.5±1.6, 6.5±1.9% at baseline, 1y, & 3-5y, P&lt;0.001), and insulin resistance by HOMA-IR (34.1 (15.2–43.5), 8.7 (2.4–16.0), 8.9 (2.1–16.4), P&lt;0.001). Only HOMA-IR improved in PLD (P&lt;0.01). Systolic BP and HR decreased after metreleptin in GLD (BP 120±11, 117±10, 109±16 mmHg, P=0.046; HR 89±9, 82±12, 80±16 bpm, P=0.018; at baseline, 1y, 3-5y, respectively) but not PLD. Metreleptin improved cardiac parameters in patients with GLD, including reduced posterior wall thickness (9.8±1.7, 9.1±1.3, 8.3±1.7 at baseline, 1y, & 3-5y, P&lt;0.01), LV mass (140.7±45.9, 128.7±37.9, 110.9±29.1 at baseline, 1y, & 3-5y, P&lt;0.01), and LV mass index (88.6±22.0, 81.6±16.9, 81.6±16.9 at baseline, 1y, & 3-5y, P&lt;0.01). Metreleptin also improved septal e’ velocity, a measure of early diastolic cardiac function, in GLD (8.6±1.7, 10.0±2.1, 10.7±2.4 at baseline, 1y, & 3-5y, P&lt;0.01). All changes remained significant after adjustment for BP. In GLD, multivariate variable selection models suggested that changes in posterior wall thickness and LV mass index related to metreleptin-induced reductions in TG, and changes in septal e’ velocity related to metreleptin-induced reductions in hemoglobin A1c. No changes in echo parameters were seen in PLD. These findings suggest that metreleptin improves cardiac hypertrophy and diastolic function in patients with GLD, and these improvements may be mediated by reduced lipotoxicity and glucose toxicity. The applicability of these findings to a broader, leptin-sufficient population with LV hypertrophy and/or diabetic cardiomyopathy remains to be determined.

Combination of Huangqi Granule and Rosuvastatin Improves the Cardiac Function in Heart Failure

2020 ◽  
Vol 19 (2) ◽  
pp. 181-187
Author(s):  
Jing Li ◽  
Yun Zhang ◽  
Weizhong Huangfu ◽  
Yuhong Ma
Keyword(s):  
Heart Failure ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Wall Thickness ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Model Group ◽  
Ventricular Ejection Fraction ◽  
Posterior Wall Thickness

Using rat models of heart failure, we evaluated the effects of rosuvastatin and Huangqi granule alone and in combination on left ventricular end-diastolic dimension, left ventricular end-systolic dimension, left ventricular ejection fraction, left ventricular posterior wall thickness at end-diastole, and left ventricular posterior wall thickness at end-systole. Results showed that left ventricular end-diastolic dimension, left ventricular end-systolic dimension in the rosuvastatin + Huangqi granule group were significantly decreased (P ‹ 0.01), while left ventricular ejection fraction, left ventricular posterior wall thickness at end-diastole and left ventricular posterior wall thickness at end-systole were significantly increased (P ‹ 0.05). The serum IL-2, IFN-β, and TNF-α in rosuvastatin + Huangqi granule group were significantly lower than those in model group (P ‹ 0.05). However, the levels of S-methylglutathione and superoxide dismutase in rosuvastatin + Huangqi granule group were significantly higher, while nitric oxide was significantly lower than that in the model group (P ‹ 0.05). Also, compared to the model group, the apoptosis rate, and the autophagy protein LC3-II in the cardiomyocytes of rosuvastatin + Huangqi granule group was significantly decreased (P ‹ 0.01), while the level of p62 protein was significantly increased (P ‹ 0.01). The levels of AMPK and p-AMPK in cardiomyocytes were significantly lower in rosuvastatin + Huangqi granule group; however, the levels of mTOR and p-mTOR showed an opposite trend (P ‹ 0.05). To sum up, rosuvastatin + Huangqi granule could improve the cardiac function, decrease the level of oxidative stress, and inflammatory cytokines in rats with HF. The possible underlying mechanism might be inhibition of autophagy and reduced apoptosis in cardiomyocytes by regulating AMPK-mTOR signaling pathway.

scholarly journals Superoxide production by NAD(P)H oxidase and mitochondria is increased in genetically obese and hyperglycemic rat heart and aorta before the development of cardiac dysfunction. The role of glucose-6-phosphate dehydrogenase-derived NADPH

2009 ◽  
Vol 297 (1) ◽  
pp. H153-H162 ◽  
Author(s):  
Sabrina Serpillon ◽  
Beverly C. Floyd ◽  
Rakhee S. Gupte ◽  
Shimran George ◽  
Mark Kozicky ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Rat Heart ◽  
Mitochondrial Respiratory Chain ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Posterior Wall Thickness ◽  
Patients With Diabetes ◽  
Protein Kinase C Inhibitor ◽  
Glucose 6 Phosphate Dehydrogenase

Increased oxidative stress is a known cause of cardiac dysfunction in animals and patients with diabetes, but the sources of reactive oxygen species [e.g., superoxide anion (O2−)] and the mechanisms underlying O2− production in diabetic hearts are not clearly understood. Our aim was to determine whether NADPH oxidase (Nox) is a source of O2− and whether glucose-6-phosphate dehydrogenase (G6PD)-derived NADPH plays a role in augmenting O2− generation in diabetes. We assessed cardiac function, Nox and G6PD activities, NADPH levels, and the activities of antioxidant enzymes in heart homogenates from young (9–11 wk old) Zucker lean and obese (fa/fa) rats. We found that myocardial G6PD activity was significantly higher in fa/fa than in lean rats, whereas superoxide dismutase and glutathione peroxidase activities were decreased ( P < 0.05). O2− levels were elevated (70–90%; P < 0.05) in the diabetic heart, and this elevation was blocked by the Nox inhibitor gp-91ds-tat (50 μM) or by the mitochondrial respiratory chain inhibitors antimycin (10 μM) and rotenone (50 μM). Inhibition of G6PD by 6-aminonicotinamide (5 mM) and dihydroepiandrosterone (100 μM) also reduced ( P < 0.05) O2− production. Notably, the activities of Nox and G6PD in the fa/fa rat heart were inhibited by chelerythrine, a protein kinase C inhibitor. Although we detected no changes in stroke volume, cardiac output, or ejection fraction, left ventricular diameter was slightly increased during diastole and systole, and left ventricular posterior wall thickness was decreased during systole ( P < 0.05) in Zucker fa/fa rats. Our findings suggest that in a model of severe hyperlipidema and hyperglycemia Nox-derived O2− generation in the myocardium is fueled by elevated levels of G6PD-derived NADPH. Similar mechanisms were found to activate O2− production and induce endothelial dysfunction in aorta. Thus G6PD may be a useful therapeutic target for treating the cardiovascular disease associated with type 2 diabetes, if second-generation drugs specifically reducing the activity of G6PD to near normal levels are developed.

scholarly journals The impact of obesity on left ventricular mass and left ventricular systolic function in children

2016 ◽  
Vol 45 (4) ◽  
pp. 171
Author(s):  
Ria Nova ◽  
Bambang Madiyono ◽  
Sudigdo Sastroasmoro ◽  
Damayanti R Sjarif
Keyword(s):  
Wall Thickness ◽  
Systolic Function ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Internal Diameter ◽  
Obese Children ◽  
Normal Children ◽  
Posterior Wall Thickness ◽  
Lv Mass ◽  
Lv Systolic Function

Background Obesity causes cardiovascular disturbances. Theincidence of cardiovascular disease is higher even in mildly obesepatients than in lean subjects.Objectives The purpose of this study was to compare left ven-tricular (LV) mass, LV internal dimensions, and LV systolic func-tion between obese and normal children; and to determine the as-sociation of the degree of obesity with LV mass and LV systolicfunction.Methods This cross-sectional study was conducted on elemen-tary school students in Jakarta from February to April 2003. Wemeasured the subjects’ body weight and height, and performedlipid profile and echocardiography examinations. Measurementsof LV mass, LV internal dimensions with regard to septum thick-ness, LV internal diameter, and LV posterior wall thickness; andLV systolic function as indicated by shortening fraction and ejec-tion fraction, were performed echocardiographically. The differ-ences in measurements between obese and normal children aswell as between obese children with and without lipid abnormalitywere analyzed. The correlation between the degree of obesity withLV size and systolic function was determined.Results Twenty-eight normal children and 62 obese children wereenrolled in the study. Mean LV mass was 35.7 (SD 5.16) g/cm 3 inobese children versus 24.0 (SD 3.80) g/cm 3 in normal children(P<0.0001). Mean septum thickness was 0.8 (SD 0.14) mm inobese children versus 0.6 (SD 7.90) mm in normal children (P<0.0001). Mean posterior wall thickness was 0.9 (SD 0.14) mm inobese children versus 0.6 (SD 9.97) mm in normal children(P<0.0001). Mean LV internal diameter was 4.0 (SD 0.34) mm inobese children versus 3.9 (SD 0.29) mm in normal children(P=0.300). There was strong correlation between the degree ofobesity and LV mass (r=0.838, P<0.0001). LV systolic function(shortening fraction) was 37.1 (SD 4.20) percent in obese childrenversus 35.8 (SD 4.99) percent in normal children (P=0.19). Ejec-tion fraction was 67.4 (SD 5.32) percent in obese children versus65.5 (SD 6.29) percent in normal children (P=0.13). There wasweak correlation between LV systolic function and the degree ofobesity (shortening fraction r=0.219, P=0.038; ejection fractionr=0.239, P=0.023).Conclusions Obese children had significantly greater LV mass,septum thickness, and posterior wall thickness than normal chil-Backgrounddren. Such significant difference was absent for LV internal diam-eter and measures of LV systolic function. There was no signifi-cant difference in LV mass and LV systolic function between obesechildren with or without abnormality of lipid profile. A strong corre-lation exists between the degree of obesity and LV mass, but thecorrelation between degree of obesity and LV systolic function wasweak

Anatomical Accuracy of Echocardiographically Assessed Left Ventricular Wall Thickness

1979 ◽  
Vol 57 (s5) ◽  
pp. 55s-57s ◽  
Author(s):  
H. Larkin ◽  
D. C. Johnson ◽  
S. N. Hunyor ◽  
P. Caspari ◽  
R. Kaplan
Keyword(s):  
Direct Measurement ◽  
Wall Thickness ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Left Ventricular Wall Thickness ◽  
Echocardiographic Measurement ◽  
Posterior Wall Thickness ◽  
Ventricular Wall Thickness

1. A comparison of direct measurement and M-mode echocardiography in the determination of posterior left ventricular wall thickness was performed in 26 subjects, of whom 21 underwent cardiac bypass surgery; the remainder came to necropsy. 2. In the surgical group a close correlation was demonstrated between direct measurement of posterior wall thickness and the echocardiographic end-diastolic dimension (r = 0·76, P &lt; 0·001). 3. The necropsy measurement of posterior wall thickness correlated with the echocardiographic end-systolic dimension (r = 0·99, P &lt; 0·001). 4. These findings confirm that the echocardiographic measurement of posterior wall thickness accurately reflects the anatomical dimension.

Fgl2 deficiency causes neonatal death and cardiac dysfunction during embryonic and postnatal development in mice

2007 ◽  
Vol 31 (1) ◽  
pp. 53-62 ◽  
Author(s):  
Junwu Mu ◽  
Dawei Qu ◽  
Agata Bartczak ◽  
M. James Phillips ◽  
Justin Manuel ◽  
...  
Keyword(s):  
Postnatal Development ◽  
Cardiac Dysfunction ◽  
Neonatal Death ◽  
Posterior Wall ◽  
Ultrasound Biomicroscopy ◽  
Left Ventricular ◽  
Mode Analysis ◽  
Posterior Wall Thickness ◽  
Perinatal Lethality ◽  
And Function

We hypothesized that cardiac dysfunction was responsible for the high perinatal lethality that we previously reported in fibrinogen-like protein 2 ( Fgl2) knockout (KO) mice. We therefore used ultrasound biomicroscopy to assess left ventricular (LV) cardiac structure and function during development in Fgl2 KO and wild-type (WT) mice. The only deaths observed between embryonic day (E)8.5 (onset of heart beating) and postnatal day (P)28 (weaning) were within 3 days after birth, when 33% of Fgl2 KO pups died. Histopathology and Doppler assessments suggested that death was due to acute congestive cardiac failure without evidence of valvular or other obvious cardiac structural abnormalities. Heart rates in Fgl2 KO embryos were significantly reduced at E8.5 and E17.5, and irregular heart rhythms were significantly more common in Fgl2 KO (21/26) than WT (2/21) embryos at E13.5. Indexes of systolic and/or diastolic cardiac function were also abnormal in KO mice at E13.5 and E17.5, in postnatal mice studied at P1, and in KO mice surviving to P28. M-mode analysis showed no difference in LV diastolic chamber dimension, although posterior wall thickness was thinner at P7 and P28 in Fgl2 KO mice. We conclude that Fgl2 deficiency is not associated with obvious structural cardiac defects but is associated with a high incidence of neonatal death as well as contractile dysfunction and rhythm abnormalities during embryonic and postnatal development in mice.

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