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 ◽  
...  

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.

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Hamid Raieszadeh ◽  
Vahid Noaman ◽  
Mehrdad Yadegari

270 Ross broiler chickens of twenty days old were housed in 18-floor pens in a completely randomized design with six treatment groups and three replicate groups and fifteen chicks per each pen. The treatment groups (1–6) consisted of 0, 10, 20, 30, 50, and 70 ppm of nanocide in drinking water, respectively. At 26 days of age, 3 chickens were selected randomly for echocardiography using a 7.5 MHz linear probe, and the left ventricular internal diameter at the end of diastole (LVIDd), left ventricular internal diameter at the end of systole (LVIDs), left ventricular fractional shortening (LVFS), ejection fraction (EF), stroke volume (SV), interventricular septum thickness at the end of systole (IVSTs), and interventricular septum thickness at the end of diastole (IVSTd) were evaluated. LVIDd and LVIDs in group six were of higher rate than other groups and showed statistically significant differences with groups two, three, and four (P<0.05). LVFS, percentage of EF, and IVSTd were minimum in group six and had significant difference with other groups (P<0.05). The results of this study showed that prescription of high dosage of nanocide leads to cardiovascular problems with decrease in myocardial contractility and increase in the internal diameter of left ventricle.


2016 ◽  
Vol 45 (4) ◽  
pp. 171
Author(s):  
Ria Nova ◽  
Bambang Madiyono ◽  
Sudigdo Sastroasmoro ◽  
Damayanti R Sjarif

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


1998 ◽  
Vol 275 (5) ◽  
pp. H1879-H1885 ◽  
Author(s):  
Abe DeAnda ◽  
Masashi Komeda ◽  
Marc R. Moon ◽  
G. Randall Green ◽  
Ann F. Bolger ◽  
...  

Left ventricular (LV) wall stress is an important element in the assessment of LV systolic function; however, a reproducible technique to determine instantaneous local or regional wall stress has not been developed. Fourteen dogs underwent placement of twenty-six myocardial markers into the ventricle and septum. One week later, marker images were obtained using high-speed biplane videofluoroscopy under awake, sedated, atrially paced baseline conditions and after inotropic stimulation (calcium). With a model taking into account LV pressure, regional wall thickness, and meridional and circumferential regional radii of curvature, we computed average midwall stress for each of nine LV sites. Regional end-systolic and maximal LV wall stress were heterogeneous and dependent on latitude (increasing from apex to base, P < 0.001) and specific wall (anterior > lateral and posterior wall stresses; P = 0.002). Multivariate ANOVA demonstrated only a trend ( P = 0.056) toward increased LV stress after calcium infusion; subsequent univariate analysis isolated significant increases in end-systolic LV wall stress with increased inotropic state at all sites except the equatorial regions. The model used in this analysis incorporates local geometric factors and provides a reasonable estimate of regional LV wall stress compared with previous studies. LV wall stress is heterogeneous and dependent on the particular LV site of interest. Variation in wall stress may be caused by anatomic differences and/or extrinsic interactions between LV sites, i.e., influences of the papillary muscles and the interventricular septum.


2004 ◽  
Vol 40 (5) ◽  
pp. 359-363 ◽  
Author(s):  
Rosemary A. Henik ◽  
Rebecca L. Stepien ◽  
Hattie B. Bortnowski

A retrospective study was performed in 75 hypertensive cats to determine the spectrum and frequency of M-mode echocardiographic abnormalities. Results indicated that 21.3% of the cats had M-mode measurements within normal reference ranges. For cats with echocardiographic abnormalities, changes were variable. Thirty-nine percent of hypertensive cats had hypertrophy of the interventricular septum in diastole, and 41.3% had hypertrophy of the left ventricular (LV) posterior wall in diastole. One cat in five had a dilated left atrium, while fractional shortening and LV internal dimension in diastole were normal in 82.7% and 86.7% of the cats, respectively. The marked variability of echocardiographic findings in hypertensive cats made echocardiography an unreliable screening test for hypertension.


2021 ◽  
Vol 11 ◽  
Author(s):  
Yandong Liu ◽  
Jiawei Cai ◽  
Lefeng Qu

Background: Carotid atherosclerotic disease is associated with aortic stenosis and reduced cardiac function. The causality between carotid and cardiac pathologies is unknown. We aim to explore the effects of carotid stenosis or occlusion on cardiac pathology and function.Methods and Results: We produced carotid obstruction or stenosis in 36 atherogenic mice with 150- or 300-μm tandem surgery or sham surgery. The structure and function of the heart were assessed by histology and animal ultrasound. The 150-μm group had larger plaque burden and thicker valve leaflets in the aortic root than did the control group. Also, the two surgery groups had a thicker left ventricular posterior wall and smaller internal diameter compared with controls. Increased myocardial fibrosis was also found in the 150-μm group compared with controls, although the surgery groups had preserved systolic function compared with that of controls.Conclusions: In a mouse model, carotid occlusion accentuated the formation of aortic stenosis and promoted ventricular remodeling without impairing systolic function. Carotid atherosclerotic plaque may be a pathogenic factor for aortic stenosis and ventricular remodeling.


2004 ◽  
Vol 286 (3) ◽  
pp. H1070-H1075 ◽  
Author(s):  
Fumito Ichinose ◽  
Kenneth D. Bloch ◽  
Justina C. Wu ◽  
Ryuji Hataishi ◽  
H. Thomas Aretz ◽  
...  

To investigate the role of endothelial nitric oxide synthase (NOS3) in left ventricular (LV) remodeling induced by chronic pressure overload, the impact of transverse aortic constriction (TAC) on LV structure and function was compared in wild-type (WT) and NOS3-deficient (NOS3–/–) mice. Before TAC, LV wall thickness, mass, and fractional shortening were similar in the two mouse strains. Twenty-eight days after TAC, both WT and NOS3–/– mice had increased LV wall thickness and mass as well as decreased fractional shortening. Although the pressure gradient across the TAC was similar in both strains of mice 28 days after TAC, LV mass and posterior wall thickness were greater in NOS3–/– than in WT mice, whereas fractional shortening and the maximum rate of developed LV pressure were less. Diastolic function, as measured by the time constant of isovolumic relaxation and the maximum rate of LV pressure decay, was impaired to a greater extent in NOS3–/– than in WT mice. The degree of myocyte hypertrophy and LV fibrosis was greater in NOS3–/– than in WT mice at 28 days after TAC. Mortality was greater in NOS3–/– than in WT mice 28 days after TAC. Long-term administration of hydralazine normalized the blood pressure and prevented the LV dilation in NOS3–/– mice but did not prevent the LV hypertrophy, dysfunction, and fibrosis associated with NOS3 deficiency after TAC. These results suggest that the absence of NOS3 augments LV dysfunction and remodeling in a murine model of chronic pressure overload.


Biomolecules ◽  
2018 ◽  
Vol 8 (3) ◽  
pp. 63 ◽  
Author(s):  
Martin Bahls ◽  
Dorothee Atzler ◽  
Marcello Markus ◽  
Nele Friedrich ◽  
Rainer Böger ◽  
...  

Low homoarginine is an independent marker of mortality in heart failure patients and incident cardiovascular events. Whether homoarginine is related with healthier cardiac structure and function is currently unclear. We used data of the population-based “Study of Health in Pomerania” (SHIP-Trend) to assess this relation. Homoarginine was measured in serum using liquid chromatography-tandem mass spectrometry. Linear regression models assessed the relation between homoarginine and several structural as well as functional parameters and N-terminal pro B-type natriuretic peptide (NTproBNP). All models were adjusted for age, sex, body mass index, and renal function. A total of 3113 subjects (median age 48 (25th percentile 37 to 75th percentile 60) years, 46% male) were included. A standard deviation decrease in homoarginine was associated with a larger left ventricular diastolic diameter (0.3; 95%-confidence interval (CI): 0.2 to 0.5 mm; p < 0.001), left ventricular systolic diameter (0.38; 95%-CI: −0.22 to 0.54 mm; p < 0.001) as well as a less relative wall thickness (–0.003 95%-CI: −0.006 to −0.0008; p = 0.01), left ventricular ejection fraction (–0.47; 95%-CI: –0.79 to −0.15%; p < 0.01) and fractional shortening (−0.35; 95%-CI: −0.62 to 0.07%; p = 0.01). Low homoarginine was also related to higher NTproBNP (−0.02 95%-CI: −0.034 to −0.009 log pg/mL; p < 0.01). Lower serum homoarginine is associated with dilatation of the heart and decreased function. Prospective clinical studies should assess if homoarginine supplementation improves cardiac health in subjects with low serum concentrations.


2007 ◽  
Vol 292 (5) ◽  
pp. H2387-H2396 ◽  
Author(s):  
Yukiko Abe ◽  
Koh Ono ◽  
Teruhisa Kawamura ◽  
Hiromichi Wada ◽  
Toru Kita ◽  
...  

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.


Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Hongmei Peng ◽  
Jiang Xu ◽  
Xiao-Ping Yang ◽  
Xiangguo Dai ◽  
Edward Petersion ◽  
...  

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.


2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Buyan-Ochir Orgil ◽  
Fuyi Xu ◽  
Undral Munkhsaikhan ◽  
Neely R Alberson ◽  
Jason Johnson ◽  
...  

Background: Causal and modifier genes, genetic background and environment underlie clinical heterogeneity in cardiomyopathy (CM). The BXD recombinant inbred (RI) family represents a murine genetic reference population (GRP) that are descendants from crosses between C57BL/6J (B6) and DBA/2J (D2) mice. The parental D2 mouse is a natural model of hypertrophic CM (HCM). The study aimed to dissect genetic architecture of cardiac traits in BXD GRP using systems genetics analysis. Methods: Echocardiography was performed in 88 strains of male (M) and female (F) BXDs (N>5/sex) at 4-5 months of age. Cardiac traits were then associated with heart transcriptome, and expression quantitative trait loci ( eQTL) mapping was performed. Results: More than 2-fold variance in ejection fraction (EF%), fractional shortening (FS%), left ventricular (LV) volumes at end-systole and end-diastole (Vol;s and Vol;d), internal dimensions (ID;s and ID;d), posterior wall (PW), and interventricular septum (IVS) thickness was found among BXDs. Traits seen in dilated CM (DCM) patients such as reduced EF%, FS%, and LVPW and increased Vol;s and ID;s are found in BXD78 (M, F), BXD32, 111, and 68 (F) strains. Strains D2, BXD90 and 155 (M, F), BXD44 and 65 (M), and BXD113, 16, 77 (F) had significantly greater LV mass, LVPW and IVS thickness compared to sex-matched controls, suggestive for traits seen in HCM patients. A 6.4 Mb QTL (peak LRS=18.50) was identified on chromosome (Chr) 8 to be significantly associated with ID;s, ID;d, Vol;s and Vol;d among male BXDs. eQTL mapping for each of 131 genes on Chr8 QTL identified 6 genes ( Coq9 , Ndrg4 , Crnde, Irx3, Rpgrip1l, and Rbl2 ) being cis -regulated and Ndrg, Slc6a2 and Ces1d being significantly (p < 0.05) correlated with LV volumes. In female BXDs, a significant QTL on Chr7 (40.2 Mb) with 9 genes that significantly correlated with LVPW;d was identified. A suggestive 92.6 Mb QTL on Chr3 with Snapin , Tpm3 , and Wars2 correlated with EF% and FS% (p < 0.05). Conclusions: Our study found cardiomyopathy-associated traits are segregated among BXD family and these traits vary among BXD lines. Multiple associated QTLs demonstrate that the BXD family is suitable to map gene variants and identify genetic factors and modifiers that influence cardiomyopathy phenotypes.


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